Immunologic Research[JOURNAL]
Sun
200 papers
A case of autoimmune hemolytic anemia with acquired functional mutation of the TLR7.
Han Y, Chen H, Li Y … +3 more , Yin Y, Zhu X, Wu X
Immunol Res · 2026 May · PMID 42067661 · Full text
This article presents a case of recurrent autoimmune hemolytic anemia in a child with a gain-of-function (GOF) mutation of the TLR7. This patient's condition contrasts with the six previously documented cases of GOF muta...
This article presents a case of recurrent autoimmune hemolytic anemia in a child with a gain-of-function (GOF) mutation of the TLR7. This patient's condition contrasts with the six previously documented cases of GOF mutations in the TLR7, thereby expanding the phenotypic spectrum of such mutations and enhancing clinical comprehension of childhood systemic lupus erythematosus (cSLE). The article discusses the mechanisms by which TLR7 GOF mutations can result in autoimmune hemolytic anemia, explores the influence of cytomegalovirus (CMV) infection on the disease's development and progression, and emphasizes the therapeutic potential of hematopoietic stem cell transplantation for cases of TLR7 GOF mutations.
Immune cell annotation in the single-cell studies: technologies, challenges, and integrative solutions.
George S, Johdi NA
Immunol Res · 2026 May · PMID 42062653 · Full text
Single-cell RNA sequencing has transformed immunological research by enabling high-resolution transcriptional profiling of individual immune cells. Despite its transformative impact, annotating immune cells based solely...
Single-cell RNA sequencing has transformed immunological research by enabling high-resolution transcriptional profiling of individual immune cells. Despite its transformative impact, annotating immune cells based solely on transcriptomic data remains challenging. These difficulties arise from biological factors, including gene expression heterogeneity and post-transcriptional regulation, as well as technical limitations that contribute to mismatches between mRNA and protein expression. Such discrepancies may lead to cell misclassification and obscure functional insights, particularly in heterogeneous populations such as peripheral blood mononuclear cells. This review highlights the major challenges in immune cell annotation by detailing the mechanisms underlying mRNA-protein discrepancies, examining both the biological factors and technical artifacts that drive this divergence, and emphasizing their implications for accurate cell classification. A critical overview of current single-cell profiling technologies follows, with evaluation of the respective advantages and limitations of transcriptomic, proteomic, and multimodal approaches. In particular, technologies such as Cellular Indexing of Transcriptomes and Epitopes by Sequencing integrate transcriptomic and proteomic data, addressing the shortcomings of single-modality analyses. Further examination focuses on computational strategies for immune cell annotation, with emphasis on automated methods and bioinformatics frameworks tailored to multi-omics datasets. The unique computational challenges of integrating mRNA and protein data, together with solutions for improved annotation accuracy, are discussed. This review integrates key challenges, technologies, and computational tools, highlighting the need for standardized multimodal profiling of immune cells. Such integration enhances annotation reliability and advances disease understanding and therapy discovery.
ANKFN1 in skin fibroblasts may modulate mast cell activity and is associated with dupilumab response in atopic dermatitis.
Wei QJ, Lu JR, Xiang WY … +7 more , Liang HQ, Zhang SQ, Huang SY, Peng JW, Zhou ZF, Li QJ, Zheng WJ
Immunol Res · 2026 May · PMID 42062651 · Publisher ↗
BACKGROUND: Atopic dermatitis (AD) is a prevalent chronic inflammatory skin disease. Dupilumab is a new targeted drug used to treat moderate to severe AD. However, some patients with AD exhibit poor response to dupilumab...
BACKGROUND: Atopic dermatitis (AD) is a prevalent chronic inflammatory skin disease. Dupilumab is a new targeted drug used to treat moderate to severe AD. However, some patients with AD exhibit poor response to dupilumab treatment. OBJECTIVE: This study aims to investigate the potential role and mechanisms of ANKFN1 in the development of resistance to dupilumab in AD. METHODS: This study conducted a comprehensive analysis of bulk RNA, single-cell RNA (scRNA-seq), and spatial transcriptome sequencing data. A prospective cohort of 54 AD patients treated with dupilumab was analyzed. Based on the SCORAD score, we measured whether the AD patients responded to 16 weeks of dupilumab treatment. By analyzing differentially expressed genes between the pre-treatment response group and the resistant group, drug resistance-associated genes were identified and externally validated in an independent dataset. Subsequently, biological function enrichment analysis, immune cells assessment, scRNA-seq analysis, and spatial transcriptomics were employed to investigate ANKFN1's biological functions, cellular localization, and association with the immune microenvironment. Additionally, we constructed a ceRNA regulatory network. RESULTS: Four key genes ANKFN1, HTR3A, HLA-DQA1, and ALOX15B were identified, with ANKFN1 exhibiting the strongest predictive efficacy (AUC = 0.938) and showing significantly upregulated expression in the resistant group, a finding confirmed in the validation cohort. High ANKFN1 expression positively correlated with resting mast cell infiltration levels and negatively correlated with immune stimulatory factors, chemokines, and IL-4/IL-13 pathway receptors (IL4R, IL13RA1, IL13RA2), suggesting its association with an immunosuppressive microenvironment. scRNA-seq analysis revealed ANKFN1 was specifically overexpressed in fibroblasts, particularly within the COL6A5⁺ fibroblast subpopulation. Spatial transcriptomics analysis further validated this finding. The ceRNA network suggested ANKFN1 may be regulated by the lncRNA NEAT1/miR-224 axis and transcription factors AR and GRHL2. CONCLUSION: ANKFN1 may be associated with dupilumab non-response and warrants further validation.
Antineutrophil cytoplasmic antibody-associated pachymeningitis: a systematic review of clinical features, diagnosis and treatment outcomes.
Faria GAS, Silva PBR, Allioni GA … +4 more , Lucato LT, Adoni T, Castro LHM, Silva GD
Immunol Res · 2026 May · PMID 42062638 · Full text
Antineutrophil cytoplasmic antibody (ANCA)-associated pachymeningitis is a rare inflammatory disorder of the dura mater that may occur in isolation or as part of systemic vasculitis. The clinical features and outcomes of...
Antineutrophil cytoplasmic antibody (ANCA)-associated pachymeningitis is a rare inflammatory disorder of the dura mater that may occur in isolation or as part of systemic vasculitis. The clinical features and outcomes of proteinase 3 (PR3)- and myeloperoxidase (MPO)-ANCA-associated pachymeningitis remain poorly defined. We aimed to synthesize clinical presentation, investigations, and treatment outcomes to improve diagnosis and guide management. A systematic review was conducted in accordance with PRISMA guidelines. PubMed, Embase, and Scopus were searched to June 15, 2023. Eligible studies were case reports or series of patients with imaging-confirmed pachymeningitis and positive ANCA serology. Individual patient data were extracted, including demographics, clinical features, pathology, and outcomes. We identified 230 patients from 177 reports, including 108 MPO-ANCA-positive, 71 PR3-ANCA-positive, and 3 dual MPO/PR3-positive cases; 46 ANCA-positive cases had unspecified antigen specificity, and 2 were ELISA-negative but ANCA IIF-positive. Median age was 60 years; 53% were male. Headache and cranial neuropathies-particularly hearing loss, visual impairment, and diplopia-were predominant. Systemic involvement was present in 89% of cases, primarily affecting the ear, nose, throat, lungs, orbits and kidneys. Imaging often showed tentorium/falx, middle cranial fossa, and frontal convexities involvement. Inflammatory markers were raised in > 90%, and cerebrospinal fluid pleocytosis in 50%. Typical pathological features such as granulomas, vasculitis, or necrosis were documented in 66% of biopsied patients. At a median 9-month follow-up, mortality rate was 3.9% and relapse rate 23.5%. Rituximab (25%) was associated with lower rates of refractory disease. PR3- and MPO-ANCA-associated pachymeningitis typically presents with headache and cranial neuropathies, usually with systemic involvement. Relapse and incomplete recovery remain common despite treatment, underscoring the need for early recognition, targeted immunotherapy, and long-term follow-up.
ELF3/miR-9-5p/NFKB1 axis promotes the progression of osteoarthritis by triggering NLRP3-mediated cell pyroptosis.
Gong B, He M, Shen X … +2 more , Wang S, Tan L
Immunol Res · 2026 May · PMID 42062631 · Publisher ↗
Pyroptosis promotes the progression of osteoarthritis (OA). This study aims to explore the functions and regulating mechanisms of E74-like factor 3 (ELF3) in chondrocyte pyroptosis. A mouse model of OA and lipopolysaccha...
Pyroptosis promotes the progression of osteoarthritis (OA). This study aims to explore the functions and regulating mechanisms of E74-like factor 3 (ELF3) in chondrocyte pyroptosis. A mouse model of OA and lipopolysaccharide (LPS)-induced chondrocytes were employed. Adenovirus sh-ELF3, miR-9-5p inhibitor or oe-Nuclear Factor kappa B subunit 1 (NFKB1) were administered to OA mice via intra-articular injection. LPS-induced chondrocytes were transfected with sh-ELF3, oe-NFKB1, miR-9-5p mimic/inhibitor or negative controls. Articular cartilage tissues were assessed using H&E staining, Safranin O/fast green staining, and Osteoarthritis Research Society International (OARSI) grading system. Pyroptosis was assessed by flow cytometry combined with Western blot analysis of key markers, while apoptosis was detected by TUNEL staining. Levels of interleukin-1 beta (IL-1β) and Interleukin-18 (IL-18) were measured by enzyme linked immunosorbent assay (ELISA). Interactions among ELF3, miR-9-5p, and NFKB1 were validated using chromatin immunoprecipitation (ChIP) and luciferase reporter assays. We found that pyroptosis was enhanced and ELF3 expression was elevated in both the OA mouse model and LPS-induced chondrocytes. Depletion of ELF3 inhibited pyroptosis, apoptosis, extracellular matrix (ECM) degeneration, and inflammation in LPS-injured chondrocytes. Mechanistically, ELF3 suppressed miR-9-5p transcription, which targeted NFKB1, and NFKB1 interacted with ELF3 to form a regulatory loop. miR-9-5p inhibition or NFKB1 overexpression reversed the protective effects of ELF3 knockdown on pyroptosis and ECM degradation. In vivo study further confirmed that silencing ELF3 attenuated articular cartilage injury through miR-9-5p/NFKB1/ NLR Family Pyrin Domain Containing 3 (NLRP3) axis. Overall, the ELF3/miR-9-5p/NFKB1 axis accelerated OA progression by promoting NLRP3-mediated chondrocyte pyroptosis.
Immune checkpoint landscape in CD4⁺ T cells stratifies HIV-infected individuals by clinical progression.
Spampinato S, Scuderi G, Di Rosa M … +2 more , Fagone P, Nunnari G
Immunol Res · 2026 Apr · PMID 42053743 · Full text
Immune checkpoint (IC) pathways play a central role in modulating HIV-specific T cell responses and may influence the degree of viral control. Here, we performed a comparative transcriptomic analysis of CD4⁺ T cells from...
Immune checkpoint (IC) pathways play a central role in modulating HIV-specific T cell responses and may influence the degree of viral control. Here, we performed a comparative transcriptomic analysis of CD4⁺ T cells from HIV-infected individuals classified as elite controllers (EC), viremic controllers (VC), and chronic progressors (CP), aiming to identify IC signatures associated with viral control. ECs exhibited distinct expression profiles, characterized by significant upregulation of CEACAM1 and CD274 (PD-L1), and downregulation of CD200, TIGIT, CTLA4, BTLA, and ADGRG1 relative to CPs. VC samples displayed intermediate expression levels. Principal component analysis (PCA) of IC genes revealed clear separation between ECs and CPs, driven largely by the differential expression of PDCD1, CTLA4, TIGIT, and CD28. ECs were also enriched in effector memory and Th2 CD4⁺ T cell subsets, which correlated positively with CEACAM1 and PD-L1, and inversely with TIGIT and CTLA4. Co-expression network analysis identified two distinct gene modules: one (M2) containing CEACAM1 and PD-L1, enriched for interferon signaling and NF-κB pathways, and another (M4) comprising TIGIT, CD200, and BTLA, enriched for TCR signaling and metabolic processes. Finally, comparison of ECs, ART-naïve, and ART-treated individuals showed that pre-ART subjects displayed significantly elevated ADGRG1 expression, which decreased following ART initiation, resembling the EC profile. These findings reveal checkpoint-related molecular signatures and cell subset compositions that stratify HIV-infected individuals by disease control phenotype, and highlight potential targets for immunomodulatory therapies aimed at achieving functional cure.
Innovative biomaterial solutions for enhancing the efficacy of tumor immunotherapy.
Zhu P
Immunol Res · 2026 Apr · PMID 42043740 · Full text
Cancer remains a significant global health issue, exacerbated by population growth and aging. Immunotherapy has emerged as a promising treatment by leveraging the immune system to eliminate tumors. However, challenges su...
Cancer remains a significant global health issue, exacerbated by population growth and aging. Immunotherapy has emerged as a promising treatment by leveraging the immune system to eliminate tumors. However, challenges such as inadequate immune activation, poor targeting, and side effects persist. Recent advancements in biomaterials, including liposomes, nanoparticles, micelles, and hydrogels, offer innovative solutions to these limitations. These engineered materials enhance the delivery and efficacy of immunotherapeutic agents, improve pharmacokinetics, enable controlled release, facilitate immune cell interactions, and reduce off-target toxicity. This review discusses the synergy between biomaterials and tumor immunotherapy, exploring current technologies, mechanisms, and future directions for personalized cancer treatments. Ongoing research in this interdisciplinary domain aims to develop next-generation immunotherapies with improved precision and therapeutic outcomes.
Engineered IL1R1-CD3 Tregs modulate neuroimmune responses and attenuate neuropathic pain in a rat CCI model.
Chen J, Li J, Qin Q … +1 more , Zheng L
Immunol Res · 2026 Apr · PMID 42043727 · Publisher ↗
Neuropathic pain is a chronic and disabling disorder driven by persistent neuroimmune activation in addition to aberrant neuronal signaling. Regulatory T cells (Tregs) play a central role in restraining inflammation; how...
Neuropathic pain is a chronic and disabling disorder driven by persistent neuroimmune activation in addition to aberrant neuronal signaling. Regulatory T cells (Tregs) play a central role in restraining inflammation; however, their therapeutic potential in neuropathic pain is limited by poor stability and survival within cytokine-rich inflammatory environments, particularly those dominated by interleukin-1 (IL-1) signaling. This study investigated whether redirecting IL-1 signaling through an engineered IL1R1-CD3 fusion receptor could enhance Treg persistence and restore their immunoregulatory capacity in a rat model of chronic constriction injury (CCI). CD4⁺CD25⁺ Tregs were isolated from rats and transduced with a lentiviral construct encoding an IL1R1-CD3ζ-IRES-GFP fusion receptor. Engineered Tregs were evaluated in vitro for migratory capacity, proliferation, and apoptosis in response to IL-1 stimulation. Neuropathic pain was induced by sciatic nerve CCI, followed by adoptive transfer of unmodified or IL1R1-CD3–engineered Tregs. Mechanical hypersensitivity was assessed behaviorally, while flow cytometry and molecular analyses were used to characterize immune cell infiltration, inflammatory mediator production, and intracellular signaling pathways within the spinal cord. Endogenous Tregs were unable to adequately control CCI-induced neuroinflammation: depletion aggravated mechanical hypersensitivity, and transfer of unmodified Tregs failed to confer analgesic benefit due to IL-1–induced apoptosis. In contrast, IL1R1-CD3 Tregs preserved IL-1–dependent chemotaxis, exhibited enhanced proliferative responses, and resisted apoptosis under inflammatory conditions, resulting in preferential accumulation within the spinal cord. Adoptive transfer of IL1R1-CD3 Tregs significantly alleviated mechanical hypersensitivity and reduced macrophage infiltration while promoting an anti-inflammatory phenotype. Microglial activation and production of pro-inflammatory mediators, including TNF, IL-1β, IL-6, and iNOS, were markedly suppressed, accompanied by attenuation of NF-κB and MAPK signaling. Furthermore, IL1R1-CD3 Tregs limited neutrophil recruitment and diminished neutrophil-derived cytokines, matrix metalloproteinases, and oxidative stress. By reinterpreting IL-1 signaling, IL1R1-CD3–engineered Tregs exhibit enhanced persistence and exert immunoregulatory effects across multiple innate immune populations, leading to attenuation of neuropathic pain. These findings suggest that signal-reprogrammed Treg therapy may represent a potential strategy for modulating IL-1–driven neuroinflammation and may provide a conceptual framework for future translational studies targeting chronic pain.
FTO-mediated m6A demethylation of TRIM21 regulates macrophage polarization and attenuates myocardial ischemia-reperfusion injury.
Wan Z, Ding Y
Immunol Res · 2026 Apr · PMID 42033549 · Publisher ↗
Myocardial infarction (MI) and ischemia-reperfusion injury (IRI) are critical challenges in clinical practice. The function of macrophage in this process has gained increasing attention. Macrophage polarization from pro-...
Myocardial infarction (MI) and ischemia-reperfusion injury (IRI) are critical challenges in clinical practice. The function of macrophage in this process has gained increasing attention. Macrophage polarization from pro-inflammatory (M1) to reparative (M2) phenotypes is crucial for cardiac repair. However, the regulatory mechanisms behind macrophage polarization, particularly involving m6A modification are not well understood. We utilized a mouse model of myocardial IRI to study m6A modifications and related enzymes in a mouse model of myocardial IRI. We co-cultured bone marrow-derived macrophages with conditioned medium from HL-1 cells to assess the role of FTO in macrophage polarization. Through bioinformatics analysis and m6A methylated RNA immunoprecipitation (MeRIP), TRIM21 was identified as a target gene of FTO. Finally, we investigated the effects of FTO and TRIM21 on myocardial injury in macrophages using transgenic mice. After IRI, FTO expression was reduced in cardiac macrophages, which was associated with enhanced m6A modification and a shift toward M1 polarization. Overexpression of FTO promotes M2 polarization, reduces inflammatory cytokine levels, and attenuates myocardial injury. In addition, TRIM21 knockdown inhibited activation of the NF-κB pathway, thereby suppressing M1 polarization. In vivo experiments using transgenic mice expressing FTO and TRIM21 specifically in macrophages demonstrated that FTO attenuated myocardial injury, whereas TRIM21 exacerbated myocardial injury through an opposite effect on macrophage polarization. These findings emphasize the critical roles of FTO and TRIM21 in macrophage-mediated myocardial repair and provide potential therapeutic targets for attenuating IRI.
Epitope prediction and immunogenicity assessment of Leishmania donovani TryS protein as a potential vaccine candidate.
Khan E, Kumar S, Sarma M … +4 more , Madhukar P, Sundar S, Kumar R, Dubey VK
Immunol Res · 2026 Apr · PMID 41999514 · Publisher ↗
Leishmaniasis, a vector-borne tropical disease, is caused by the bite of Leishmania-infected sand flies. Currently, chemotherapy is the only available option because of the absence of any approved vaccine. Vaccines are c...
Leishmaniasis, a vector-borne tropical disease, is caused by the bite of Leishmania-infected sand flies. Currently, chemotherapy is the only available option because of the absence of any approved vaccine. Vaccines are considered decisive for the complete eradication of the disease. In this study, we have designed a multiepitope-based vaccine and evaluated its potential immunogenicity using immunoinformatic tools. We selected Leishmania donovani trypanothione synthetase (LdTryS) for the development and analysis of potential immunogenic epitopes. A total of 4 CTL, 3 HTL and 2 LBL epitopes were identified from LdTryS. The immunogenicity, toxicity, and allergenicity of the vaccine construct, comprising all the selected epitopes joined by a linker sequence and adjuvant at the N-terminal, were assessed. Furthermore, LdTryS was also included in the immune simulation. Molecular docking and MD simulations were performed between LdTryS and TLR9, given the high antibody titers observed against the vaccine construct. The results confirmed stable docking of the complex, with localized flexibility observed during molecular dynamics simulations. In addition, MTT assay of LdTryS showed no toxicity in human THP-1 cells, with cell viability always being over 90% even at the maximum concentration tested (20 µg), implying that the protein is safe for subsequent in-vitro and in-vivo validation. Further in vitro or in vivo studies are needed to validate the immunoinformatic predictions for LdTryS.
Inverse relationship between Epstein-Barr virus serostatus and anti-glutamic acid decarboxylase autoantibody levels.
Debuysschere C, Ouafi M, Nekoua MP … +4 more , Lobert D, Pigny P, Alidjinou EK, Hober D
Immunol Res · 2026 Apr · PMID 41999458 · Full text
Epstein-Barr virus (EBV) is suspected of being involved in the pathogenesis of several autoimmune diseases. However, its role in pancreatic islet autoimmunity remains to be determined. In the present study, the relations...
Epstein-Barr virus (EBV) is suspected of being involved in the pathogenesis of several autoimmune diseases. However, its role in pancreatic islet autoimmunity remains to be determined. In the present study, the relationship between EBV serostatus and serum level of glutamic acid decarboxylase autoantibodies (GADA), a common marker of pancreatic islet autoimmunity, was investigated. Serum samples were collected from 158 individuals (aged 2–25 years) with GADA levels ≥ 0.7 U/mL and the EBV serostatus of each individual was determined. EBV seropositive (EBV+) individuals were defined as positive for both serum VCA IgG and EBNA IgG and EBV seronegative (EBV-) individuals were negative for these antibodies. Univariate and multivariate analyses were performed to investigate the association between EBV serostatus and GADA levels. EBV+ individuals tend to have lower GADA levels than EBV- individuals (p = 0.053). After adjustment for gender and age, mean GADA levels were significantly lower in EBV+ individuals than in EBV- individuals (9.34 U/mL versus 17.49 U/mL, respectively, p = 0.015). The lower GADA levels in EBV+ individuals suggest that there is an inverse relationship between pancreatic islet autoimmunity and EBV serostatus. Further studies are needed to investigate the role of EBV in pancreatic islet autoimmunity.
Lewis Y (Le) orchestrates leukocyte trafficking and inflammatory remodeling in leprosy patients from the Brazilian Amazon.
Almeida S, da Cruz EDRM, de Loiola RDSP … +1 more , Corvelo TCO
Immunol Res · 2026 Apr · PMID 41957202 · Full text
Leprosy is characterized by a complex inflammatory microenvironment in which host-related factors play a decisive role in disease progression. However, the contribution of tissue glycans to inflammatory remodeling remain...
Leprosy is characterized by a complex inflammatory microenvironment in which host-related factors play a decisive role in disease progression. However, the contribution of tissue glycans to inflammatory remodeling remains poorly understood. In this study, we investigated the expression of Lewis blood group antigens in skin biopsies from patients with different clinical forms of leprosy in the Brazilian Amazon, a region marked by persistent hyperendemic transmission. Using immunohistochemistry, we demonstrate that the difucosylated epitope Lewis Y (Ley) is preferentially expressed in inflamed lesions, particularly in endothelial cells, histiocytes, lymphocytes, and neural structures, while being absent in healthy skin. Quantitative and spatial analyses revealed that Ley displays the broadest and most intense expression pattern among the investigated Lewis antigens, whereas Lewis X (Lex) and sialyl-Lewis x (sLex) exhibited restricted, tissue-dependent expression profiles. Statistical analyses showed that Ley expression varies significantly according to the clinical spectrum of leprosy, while Lewis X and sialyl-Lewis X are primarily dependent on tissue compartment rather than clinical classification. Mechanistically, our findings support a model in which endothelial Ley functions as a central glycan regulator of the inflammatory microenvironment, promoting leukocyte recruitment, endothelial activation, angiogenesis, and immune–vascular interactions. We propose a Ley-driven glyco-immune axis, involving DC-SIGN–mediated interactions with dendritic cells and macrophages, as a unifying mechanism linking glycan remodeling, immune cell trafficking, vascular remodeling, and tissue reorganization in leprosy lesions. Together, these results identify Ley as a tissue-specific glycan signature of inflammatory remodeling and highlight glycan remodeling as a previously underexplored organizing principle in leprosy immunopathology, with translational implications for biomarker discovery, risk stratification, and therapeutic targeting in endemic settings.
Subcutaneous Sweet Syndrome as an uncommon mucocutaneous manifestation in systemic lupus erythematosus: a case report and literature review.
Cimé-Aké E, Arriaga Escamilla D, Ríos-Valencia J … +2 more , Saeb-Lima M, Fragoso-Loyo H
Immunol Res · 2026 Apr · PMID 41945165 · Publisher ↗
The Sweet Syndrome (SS) as a mucocutaneous manifestation of systemic lupus erythematosus (SLE) has been rarely reported in the literature. The subcutaneous variant of SS in SLE patients is extremely rare. We present a ca...
The Sweet Syndrome (SS) as a mucocutaneous manifestation of systemic lupus erythematosus (SLE) has been rarely reported in the literature. The subcutaneous variant of SS in SLE patients is extremely rare. We present a case of a subcutaneous SS occurring as a manifestation of SLE and we discuss the findings reported in the literature regarding this association. The patient was a 31-year-old woman with a recently diagnosis of SLE. On admission she presented with malaise, fever, and skin lesions consisting with tender and warmth large plaques with a violaceous erythema on the right thigh. Laboratory studies showed leukocytosis, neutrophilia, elevated high-sensitive C-reactive protein, hypocomplementemia and increased levels of anti-dsDNA. Others differential diagnosis were ruled out. The skin biopsy revealed a superficial and deep perivascular and periadnexal infiltrate, with neutrophils surrounding adipocytes, concluding the diagnosis of subcutaneous SS. She had a good response to treatment with prednisone 0.5 mg/kg/day, and dapsone 100 mg/day. A structured literature search was performed in PubMed, Web of Science and Scopus, identifying 17 published cases of SS associated with SLE. SS in SLE tends to occur early in the disease course and typically presents as painful violaceous erythematous plaques, accompanied by constitutional SLE manifestations and elevated anti-dsDNA and anti-Sm levels. SS should be considered as a possible manifestation in SLE patients.
Epigenetic regulators and inflammation antagonists in familial Mediterranean fever: the role of hsa-miR-335-5p, hsa-miR-26b-5p, hsa-miR-16-5p miRNAs and IL-36Ra levels in pathogenesis.
Erdik S, Solmaz Avcikurt A, Bolat H
Immunol Res · 2026 Apr · PMID 41942806 · Publisher ↗
Familial Mediterranean Fever (FMF) is a hereditary autoinflammatory disease characterized by mutations in the MEFV and an over-activation of the pyrin inflammatory cascade. In this study, the roles of three specific micr...
Familial Mediterranean Fever (FMF) is a hereditary autoinflammatory disease characterized by mutations in the MEFV and an over-activation of the pyrin inflammatory cascade. In this study, the roles of three specific microRNAs (miRNAs) and the inflammatory cytokine antagonist IL-36Ra in the pathogenesis of FMF were investigated due to their potential roles in chronic inflammation. 40 FMF patients and 45 healthy control individuals who applied to the Balikesir University Genetic Disorders Evaluation Center between February 2021 and June 2024 were included in the study. miRNA expression levels were determined by Quantitative Real-Time Polymerase Chain Reaction (qRT-PCR), and IL-36Ra protein levels were determined using the ELISA method. Gene expression levels were analyzed by the 2-ΔΔCt method. A significant decrease (p < 0.005) in hsa-miR-335-5p and hsa-miR-26b-5p expression levels and a significant increase (p < 0.005) in hsa-miR-16-5p and IL-36Ra protein levels were observed in FMF patients. These findings point to the existence of a two-way molecular mechanism in FMF pathogenesis: on one hand, there is a deficit in epigenetic regulators with anti-inflammatory properties, such as hsa-miR-335-5p and hsa-miR-26b-5p, while on the other hand, molecules like hsa-miR-16-5p and IL-36Ra increase as a compensatory response to balance the inflammatory load. These molecules show promise as potential biomarkers for the diagnosis and follow-up of FMF.
Effectiveness and safety of ravulizumab in anti-acetylcholine receptor antibody-positive (AChR-Ab+) generalized myasthenia gravis: a systematic review and meta-analysis.
Sabet H, Abbas A, AbuHamdia A … +5 more , Salama EY, Abo-Elnour DE, Alanazi SM, Saleh MGA, Negida Y
Immunol Res · 2026 Apr · PMID 41936007 · Publisher ↗
OBJECTIVE: To evaluate the effectiveness and safety of ravulizumab in patients with anti-acetylcholine receptor antibody-positive generalized myasthenia gravis (AChR-Ab+ gMG). METHODS: A systematic search was conducted i...
OBJECTIVE: To evaluate the effectiveness and safety of ravulizumab in patients with anti-acetylcholine receptor antibody-positive generalized myasthenia gravis (AChR-Ab+ gMG). METHODS: A systematic search was conducted in PubMed, Scopus, Web of Science, and Cochrane CENTRAL up to May 3, 2025. Eligible studies included clinical trials and observational studies assessing ravulizumab in MG. Two independent reviewers performed study selection and data extraction. Outcomes included the Quantitative Myasthenia Gravis (QMG) score, Myasthenia Gravis Activities of Daily Living (MG-ADL) score, Myasthenia Gravis Quality of Life 15-item revised scale (MG-QoL15r), corticosteroid dose, clinically meaningful improvement (≥ 2-point reduction in MG-ADL score), and adverse events (AEs). We used random-effects models to calculate pooled mean differences (MD) and proportions with 95% confidence intervals (CIs), and heterogeneity was assessed via I2 statistics. RESULTS: Six studies involving 321 patients (mean age: 56.27 ± 18.78 years) were included. Ravulizumab significantly improved QMG (MD: -2.91 points, 95% CI: [-4.50 to -1.32]), MG-ADL (MD: -2.64 points, 95% CI: [-3.75 to -1.54]), and MG-QoL15r (MD: -4.61 points, 95% CI: [-8.44 to -0.77]) scores. Clinically meaningful improvement was observed in 69% of patients (95% CI: [42% to 96%]). The corticosteroid dose was reduced by 5.98 mg/day (95% CI: [-7.71 to -4.25]). AEs were reported in 80.52% of patients; 28.5% experienced serious AEs. CONCLUSIONS: Ravulizumab significantly improved QMG and MG-ADL scores and quality of life in AChR-Ab+ gMG patients, with a minimal steroid-sparing effect. Given the generally favorable safety profile, these findings support ravulizumab as a treatment option for patients with AChR-Ab+ gMG.
From PD-L1 downregulation to biomarker-driven immunotherapy design: advancing translational application of SALL4-targeted PEN-FFW in breast cancer.
Vijayasimha M, Srikanth M
Immunol Res · 2026 Apr · PMID 41925953 · Publisher ↗
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Critique on "Elevated levels of advanced glycation end-products AGE10 in patients with reactive arthritis caused by Chlamydia trachomatis and Epstein-Barr virus infection".
Bibi Z, Ali K
Immunol Res · 2026 Mar · PMID 41912964 · Publisher ↗
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Using B-cell-targeting drugs to achieve marked efficacy in anti-signal recognition particle myopathy: two case reports.
Song Z, Zhong J, Cui H … +3 more , Zheng X, Luo X, Xiong A
Immunol Res · 2026 Mar · PMID 41906052 · Publisher ↗
Anti-signal recognition particle (anti-SRP) antibody-associated myopathy is a severe immune-mediated necrotizing myopathy characterized by elevated serum creatine kinase (CK), rapidly progressive proximal weakness, and s...
Anti-signal recognition particle (anti-SRP) antibody-associated myopathy is a severe immune-mediated necrotizing myopathy characterized by elevated serum creatine kinase (CK), rapidly progressive proximal weakness, and specific pathological features on muscle biopsy. Cardiac involvement and even paralysis may occur in some patients. Response to steroid monotherapy and conventional immunosuppressants is often suboptimal, whereas B-cell-targeted therapies represent the potential advantages. We report two patients with anti-SRP myopathy treated with B-cell-targeted drugs individually. One achieved remission with low-dose rituximab (RTX), and the other responded to telitacicept (RC-18) at the lowest effective dose. During follow-up, both patients improved substantially and maintained long-term remission without relapse or infection. These cases support the feasibility of individualized B-cell-targeted strategies, including low-dose RTX and RC-18, for anti-SRP myopathy. Given the limited evidence, prospective studies are needed to assess the efficacy and safety.
Integrated analysis and functional validation of PEG3, SYNPO2, and DCN as regulators of tumor suppression and cellular stress in cervical cancer.
Han C, Zhao Y, Yang X … +1 more , Sun F
Immunol Res · 2026 Mar · PMID 41880062 · Publisher ↗
Autophagy has a context-dependent role in cervical cancer (CC). This study aimed to identify and functionally validate autophagy-related genes contributing to cervical cancer progression.Transcriptome data were analyzed...
Autophagy has a context-dependent role in cervical cancer (CC). This study aimed to identify and functionally validate autophagy-related genes contributing to cervical cancer progression.Transcriptome data were analyzed to screen DEGs, followed by Gene Ontology, Kyoto Encyclopedia of Genes and Genome, and protein-protein interaction network analysis. Candidate autophagy-associated DEGs were validated using GEPIA and ENCORI databases. Expression levels were further examined in clinical CC specimens. Functional assays were performed in SiHa cells transfected with overexpression or silencing vectors for PEG3, SYNPO2, and DCN. Cellular phenotypes (proliferation, colony formation, invasion, apoptosis, and cell cycle) were assessed, and the expression of autophagy- and ferroptosis-associated proteins was examined. Reactive oxygen species (ROS) and intracellular Fe²⁺ were detected by fluorescence probes. Finally, a xenograft model was established to evaluate tumor growth and cells proliferation. Two thousand, seven hundred forty DEGs were identified (1,109 upregulated, 1,631 downregulated), of which PEG3, SYNPO2, and DCN were selected as autophagy-associated candidates. Database analyses and patient samples confirmed their reduced expression in CC. In vitro, overexpression of PEG3, SYNPO2, or DCN suppressed colony formation and invasion and increased apoptosis and G0/G1 arrest, while silencing produced the opposite effects. Autophagosome markers (LC3-II, Beclin-1) were lower in overexpression groups and ferroptosis-related profiles (GPX4, FTH, ACSL4, ROS, Fe²⁺) were consistent with reduced lipid/iron-stress propensity. In vivo, overexpression reduced tumor growth and Ki-67/p16 staining.PEG3, SYNPO2, and DCN act as cytostatic tumor suppressors that modulate cellular stress in CC and represent potential therapeutic targets pending further validation.
Factors influencing post-vaccination antibody levels to measles and rubella in children with inflammatory bowel disease.
Samolygo IS, Kostinov MP, Manina MA … +7 more , Pestova AS, Antishin AS, Novikov AV, Stribul PA, Yablokova EA, Tinkov AA, Erdes SI
Immunol Res · 2026 Mar · PMID 41851559 · Publisher ↗
Children with inflammatory bowel disease are at increased risk of infectious diseases, including vaccine-preventable infections, due to immune dysregulation and immunosuppressive therapy. Data on the persistence of prote...
Children with inflammatory bowel disease are at increased risk of infectious diseases, including vaccine-preventable infections, due to immune dysregulation and immunosuppressive therapy. Data on the persistence of protective antibodies against measles and rubella in this population remain limited. To evaluate the seroprotective levels of IgG antibodies to measles and rubella in children with IBD and identify factors associated with antibody loss. A prospective observational study included 93 pediatric patients with IBD. IgG antibodies against measles and rubella were measured using ELISA. Vaccination status, clinical activity indices (PUCAI, PCDAI), and immunosuppressive therapies were documented. Survival analysis using Cox regression assessed factors influencing antibody persistence. Seroprotection rates were 65.5% for measles and 76% for rubella. Complete vaccination was achieved by 68.2% and 72% of patients for measles and rubella, respectively. Patients with full vaccination had significantly higher antibody levels. Younger age (<6 years) was associated with an increased risk of antibody loss: for measles, HR 21.58 (95% CI 4.46 – 104.40, p < 0.001), and for rubella in univariate analysis, HR 6.44 (95% CI 1.47–28.19, p=0.013). Incomplete vaccination increased the risk of antibody loss for measles (HR 2.76; 95% CI 1.31 – 5.79; p=0.007) and rubella (HR 2.53; 95% CI 1.06 – 6.01; p=0.036) in univariate analyses, but lost significance after adjustment in multivariate models. Immunosuppressive therapy did not significantly affect antibody levels. The highest risk groups for antibody loss were identified as High risk for measles (70% loss) and Intermediate-High risk for rubella (50% loss). In children with IBD, completed vaccination does not always guarantee protective antibody levels. Younger age and incomplete vaccination are key predictors of antibody loss. These findings highlight the need for personalized vaccination strategies and regular serological monitoring in this vulnerable population.
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