Immunology[JOURNAL]
Sun
200 papers
MicroRNA-18a-3p as a biomarker for neonatal respiratory distress syndrome and its effects in alveolar epithelial type II cells.
Shi Y, Jin Y, Yu H
BMC Immunol · 2026 Jun · PMID 42316012 · Full text
BACKGROUND: Neonatal respiratory distress syndrome (NRDS) is a major cause of significant morbidity and mortality among neonates, particularly in preterm infants. Existing studies have highlighted various microRNAs (miRN...
BACKGROUND: Neonatal respiratory distress syndrome (NRDS) is a major cause of significant morbidity and mortality among neonates, particularly in preterm infants. Existing studies have highlighted various microRNAs (miRNAs) implicated in NRDS, yet the precise molecular mechanisms, particularly regarding miR-18a-3p, remain incompletely understood. This research aimed to elucidate the role of miR-18a-3p as a potential biomarker for NRDS and to explore its functional mechanisms in alveolar type II epithelial cells. METHOD: A total of 35 NRDS patients and 35 healthy controls were enrolled, with samples of amniotic fluid and neonatal blood collected for expression analysis of miR-18a-3p. Utilizing cell culture, transfection, qRT-PCR techniques, CCK-8 assay, and ELISA assay, the function of miR-18a-3p in alveolar epithelial type II cells (an immortalized cell line, IHPEC-II, and AEC2-like cells derived from human pluripotent stem cells) was investigated. The binding relationship between miR-18a-3p and surfactant pulmonary-associated protein C (SFTPC) was predicted and validated using a dual-luciferase reporter assay. RESULTS: Elevated levels of miR-18a-3p levels were observed in the serum of NRDS cases, with an area under the ROC curve (AUC) of 0.86 for distinguishing NRDS from healthy controls. Increased miR-18a-3p levels were also detected in amniotic fluid from these NRDS cases, yielding an ROC AUC of 0.82 for discriminating between NRDS cases and healthy controls. A positive correlation between serum miR-18a-3p levels and those in amniotic fluid was observed. Functional assays demonstrated that inhibition of miR-18a-3p significantly enhanced cell viability and increased SPC secretion in alveolar epithelial type II cells following surfactant stimulation. Dual-luciferase reporter assays confirmed that miR-18a-3p modulated SFTPC expression. CONCLUSION: MiR-18a-3p was increased in NRDS cases. MiR-18a-3p can inhibit alveolar epithelial type II cell function, suggesting its potential role in fetal lung development.
Long-Acting Cabotegravir/Rilpivirine Reduces Immune-Activation and -Senescence in People With HIV With CMV Co-Infection.
Guardiani M, Tortellini E, Carraro A … +14 more , Zingaropoli MA, Ansaldo L, Grimaldi A, Vita S, Dominelli F, Mengoni F, Pasquazzi C, Turriziani O, Ciardi MR, Vullo V, Mastroianni CM, Marocco R, Borgo CD, Lichtner M
Immunology · 2026 Jun · PMID 42300985 · Publisher ↗
Despite the effectiveness of combined antiretroviral therapy (ART), HIV infection remains a chronic condition characterised by persistent inflammation and immune activation, likely associated with viral persistence and o...
Despite the effectiveness of combined antiretroviral therapy (ART), HIV infection remains a chronic condition characterised by persistent inflammation and immune activation, likely associated with viral persistence and other factors such as cytomegalovirus (CMV) co-infection. Long-acting (LA) injectable formulations, a newer class of ART with improved and sustained bioavailability, may help modulate the HIV-associated immunoinflammatory state. Therefore, we analysed dynamic changes in lymphoid immune-activation and -senescence markers in people with HIV (PWH) switching to LA injectable cabotegravir and rilpivirine (CAB/RPV-LA), compared with PWH who continued oral ART by choice. The relationship between CMV-specific immune responses and phenotypic T-cell alterations was also evaluated. T-cell immune-activation (CD38 + HLA-DR+) and -senescence (CD28-CD57+) were measured at baseline (T0), at 4 (T4), 28 (T28), 48 (T48) and at 72 (T72) weeks after switching to CAB/RPV-LA. A control group (CG) of PWH (PWH-CG) on daily oral ART was studied at T0 and at 48 weeks (T48). Furthermore, CMV-specific cellular and humoral immune responses were assessed. Thirty-seven PWH switching to CAB/RPV-LA and nine PWH-CG were enrolled. In PWH-LA, total CD4 levels remained stable over time, while CD8 levels decreased significantly at T72 versus T0 and T4. In CG, an increasing CD4 and decreasing CD8 trend was observed. The CD4/CD8 ratio remained stable in both PWH-LA and -CG and showed a nonsignificant increase at T48 in PWH-CG. Immune-activation decreased in PWH-LA: CD4 activation levels were significantly lower at T48 and T72 versus earlier time points and CD8 activation was reduced at T72 versus T0 and T4. Immune-senescence declined in both compartments, with a significant reduction in CD8 senescence at T28, T48 and T72 compared to earlier time-points. Delta analysis confirmed a greater reduction in immune-activation and -senescence in PWH-LA compared to PWH-CG. Regarding CMV immune response, anti-CMV antibody levels remained stable with only a minor decline over time, whereas CMV-specific T-cell responses transiently increased at T28 before returning to baseline at T48 and T72. Switching to CAB/RPV-LA is associated with reduced T-cell activation and senescence, particularly in CD8 T-cell, suggesting improved immune homeostasis beyond viral suppression alone. However, despite these promising immunological changes, CMV coinfection remains a key driver of residual immune dysfunction.
The clinical significance of serum complement fibroblast growth factor 21 in patients with rheumatoid arthritis.
Chen M, Fu Y, Li X … +5 more , Zhou T, Liu L, Gu J, Li H, Zu B
BMC Immunol · 2026 Jun · PMID 42298397 · Full text
OBJECTIVE: This study aimed to assess serum fibroblast growth factor 21 (FGF-21) levels and explore their clinical significance in patients with rheumatoid arthritis (RA). METHODS: A total of 187 patients with RA, who we...
OBJECTIVE: This study aimed to assess serum fibroblast growth factor 21 (FGF-21) levels and explore their clinical significance in patients with rheumatoid arthritis (RA). METHODS: A total of 187 patients with RA, who were treated at Xuzhou Central Hospital between January 2023 and December 2024, were enrolled in this study. Based on carotid intima-media thickness (cIMT) measurements, they were categorized into a plaque group (n = 118) and a plaque-free group (n = 69). Additionally, 139 healthy individuals undergoing routine physical examinations were recruited as healthy controls (HC). Clinical data were collected from all participants, including lipid profiles, HOMA-IR, ESR, CRP, RF, anti-CCP antibody levels, and serum FGF-21 concentrations. We analyzed the associations between serum FGF-21 levels and both disease activity and atherosclerotic status in RA patients. Statistical analyses, including the chi-square test, Student's t-test, Pearson correlation analysis, and logistic regression, were performed to evaluate these relationships. RESULTS: Serum levels of FGF-21 were significantly elevated in patients with RA compared with healthy controls (805.7 ± 188.68 vs. 203.8 ± 50.7 pg/mL, p < 0.001). Among RA patients, those with carotid plaques exhibited higher FGF-21 levels than those without plaques (840.7 ± 203.6 vs. 745.6 ± 142.2 pg/mL, p < 0.001). Correlation analyses revealed that serum FGF-21 levels were positively associated with LDL-C (r = 0.544), HOMA-IR (r = 0.625), anti-CCP antibodies (r = 0.617), rheumatoid factor (r = 0.366), DAS28 (r = 0.309), and cIMT (r = 0.604) (all p < 0.001). Conversely, FGF-21 levels were negatively correlated with the use of disease-modifying antirheumatic drugs (DMARDs) (r = - 0.569, p < 0.001) and flow-mediated dilation (FMD) (r = - 0.294, p < 0.001). Multivariate logistic regression analysis identified the serum FGF-21 level as an independent factor associated with increased cIMT (odds ratio [OR] = 1.003, 95% confidence interval [CI]: 1.001-1.006, p = 0.006). CONCLUSIONS: Our findings suggest a potential correlation between elevated FGF-21 levels and RA disease activity as well as certain metabolic parameters. Further replication studies are needed to clarify whether FGF-21 might serve as a research biomarker in the context of cardiovascular comorbidity in RA.
The potential role of the gut microbiota in the development of autoantibodies associated with Spondyloarthritis: a narrative review.
Elsaghir A, Wadan AS, Witte T
BMC Immunol · 2026 Jun · PMID 42298377 · Full text
Spondyloarthritis (SpA) is a set of immune-inflammatory conditions characterized by musculoskeletal and extra-articular manifestations. Increasing evidence indicates that alterations in the gut microbiota (dysbiosis) may...
Spondyloarthritis (SpA) is a set of immune-inflammatory conditions characterized by musculoskeletal and extra-articular manifestations. Increasing evidence indicates that alterations in the gut microbiota (dysbiosis) may influence both mucosal and systemic immune responses, potentially contributing to the loss of tolerance and the development of autoantibodies in SpA.This narrative review examines the current evidence linking gut dysbiosis to autoantibody development in SpA, with particular focus on ankylosing spondylitis (AS) and psoriatic arthritis (PsA).We summarized key mechanistic pathways, including Th17 axis activation, molecular mimicry, increased intestinal permeability ("leaky gut"), and altered microbial metabolite signaling. We discussed the potential relevance of these mechanisms to SpA-associated autoantibodies such as anti-CD74, anti-HSP65, and anti-Kaiso. Where direct evidence in SpA is limited, findings from other autoimmune diseases are considered as mechanistic analogies rather than definitive parallels.We further review microbiome-targeted therapeutic strategies, including probiotics, prebiotics, and bacterially based therapies, and highlight differences between preclinical findings and available clinical data. Although biologically plausible mechanisms, direct causal evidence linking gut dysbiosis to autoantibody production in SpA remains limited, and clear methodological heterogeneity persists across microbiome studies.Overall, while modulation of the gut-immune axis represents a promising research direction in SpA, further mechanistic and longitudinal human studies are required before microbiota-targeted interventions can be considered applicable for autoantibody modulation.
Nuclear STING compromises replication fidelity.
El-Daher MA, Crow YJ
Nat Rev Immunol · 2026 Jun · PMID 42298082 · Publisher ↗
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MOG-Peptide Synergizes With Rapamycin to Drive CD4 T Cells Into Protective Antigen-Specific Tregs in EAE.
Zafar MA, Lamba T, Tehseen A … +9 more , Sarkar R, Nanda S, Prajapati S, Khan MA, Malik JA, Benamar M, Charbonnier LM, Sehrawat S, Agrewala JN
Immunology · 2026 Jun · PMID 42297731 · Publisher ↗
During multiple sclerosis, immune responses directed against myelin oligodendrocyte glycoprotein (MOG) contribute to demyelination and neuroinflammation. Among these, Th17 cells play an important role in promoting inflam...
During multiple sclerosis, immune responses directed against myelin oligodendrocyte glycoprotein (MOG) contribute to demyelination and neuroinflammation. Among these, Th17 cells play an important role in promoting inflammatory damage to the myelin sheath and disrupting the integrity of blood brain barrier fibres. Despite advances in immunotherapy, there is no vaccine or durable cure for the disease. Regulatory T cells (Tregs) play a protective role against Th17-mediated damage of myelin sheath. In this study, we investigated whether rapamycin, a well-characterized mTOR inhibitor known to favour differentiation and metabolic reprogramming of Tregs, could synergize with MOG-peptide to convert naïve T cells into protective, MOG-specific Tregs. To test this, mice were immunized with a combination of NOAEL (No Observed Adverse Effect Level) dose of MOG and rapamycin. Remarkably, upon subsequent challenge with a disease-inducing (morbific) dose of MOG, the immunized animals showed pronounced resistance to clinical symptoms of experimental autoimmune encephalomyelitis (EAE). While the unimmunized group showed severe EAE symptoms. Notably, there was a significant increase in the population of memory Tregs that primarily expressed an immunosuppressive phenotype (FoxP3, TGF-β, IL-10). This was accompanied by a decline in Th17 cells. Additionally, a substantial increase in the pool of myeloid-derived suppressor cells (MDSCs) was observed in the rapamycin treated group, further contributing immunoregulatroy landscape. The underlying mechanism of this phenomenon was associated with the modulation of autophagic pathways by rapamycin, encouraging the differentiation of naïve CD4 T cells into MOG-specific Tregs, as evidenced by tetramer staining. These findings provide a conceptual framework for exploring strategies aimed at promoting antigen-specific tolerance in autoimmune diseases.
Identification of characteristic genes of pressure ulcers based on angiogenesis-related genes and construction of miRNA, transcription factor, and molecular drug regulatory networks.
Wang N, Xiao H, Wu L … +6 more , Bao D, Ma Y, Wang Q, Xu Q, Xu X, Zhang X
BMC Immunol · 2026 Jun · PMID 42286465 · Full text
This study aimed to analyze transcriptomic changes in pressure ulcer (PU) samples, identify angiogenesis-related differentially expressed genes (AR-DEGs), and explore their potential as diagnostic and therapeutic targets...
This study aimed to analyze transcriptomic changes in pressure ulcer (PU) samples, identify angiogenesis-related differentially expressed genes (AR-DEGs), and explore their potential as diagnostic and therapeutic targets for PU, with a particular focus on the role of CDKN1A. Transcriptomic data from dataset GSE137897, which included 381 PU samples and 391 healthy controls, were utilized to investigate these changes. Differential expression analysis was performed to identify AR-DEGs, which were subsequently analyzed for enrichment in regulatory and signaling pathways. Protein-protein interaction (PPI) network analysis was carried out to highlight key hub AR-DEGs. In addition, correlation analysis was performed to examine the relationships between these genes. Regulatory networks involving microRNAs (miRNAs), transcription factors (TFs), and targeted drugs were constructed using miRNet and DGIdb. A rat PU model was established to validate the expression of CDKN1A in vivo and to investigate the effects of CDKN1A knockout on PU healing. Through differential expression analysis, 128 AR-DEGs were identified and found to be enriched in various regulatory and signaling pathways. PPI network analysis identified seven hub AR-DEGs (JUN, HIF1A, CCND1, FOS, HDAC1, CDKN1A, CCL2), which exhibited strong diagnostic potential for PU. Correlation analysis revealed that CDKN1A was negatively correlated with CCND1, CCL2, and FOS, while HIF1A was positively correlated with CDKN1A and HDAC1. Validation experiments in a rat PU model confirmed that CDKN1A was significantly upregulated at both the mRNA and protein levels in wound tissues. Furthermore, silencing CDKN1A in dermal fibroblasts enhanced cell viability, migration (wound healing), and collagen secretion in vitro. In vivo, CDKN1A knockout significantly accelerated wound healing in PU rats, as evidenced by improved wound closure, reduced inflammation, and increased collagen deposition. This study demonstrates that CDKN1A plays a pivotal role in modulating inflammation and collagen synthesis in PUs. The findings suggest that CDKN1A holds promise as a therapeutic target for PU treatment, providing novel insights into the management of this condition.
Pathological potential of autoantibodies in long COVID.
Bird L
Nat Rev Immunol · 2026 Jul · PMID 42286128 · Publisher ↗
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IL-6 (-174 G/C) and IL-10 (-1082 G/A) polymorphisms and serum levels in Sudanese patients with end-stage renal disease and overt hepatitis B infection: a pilot comparative study.
Shmed OBM, Hussein WA
BMC Immunol · 2026 Jun · PMID 42277653 · Full text
BACKGROUND: Patients with end-stage renal disease (ESRD) undergoing maintenance hemodialysis are at increased risk for persistent hepatitis B virus (HBV) infection. Host immunogenetic variations, particularly in cytokine...
BACKGROUND: Patients with end-stage renal disease (ESRD) undergoing maintenance hemodialysis are at increased risk for persistent hepatitis B virus (HBV) infection. Host immunogenetic variations, particularly in cytokines regulating pro- and anti-inflammatory responses, may influence viral chronicity. This study evaluated the association of IL-6 - 174G/C and IL-10 - 1082G/A polymorphisms and their corresponding serum levels in Sudanese patients with overt HBV and ESRD-HBV. METHODS: A case-control study was conducted among 68 HBV-infected individuals (31 ESRD-HBV and 37 overt HBV). Genotyping was performed using sequence-specific primer PCR (SSP-PCR), and serum cytokine concentrations were measured by ELISA. Statistical analyses were conducted using R software, applying non-parametric Wilcoxon rank-sum and Kruskal-Wallis tests. RESULTS: No significant differences were observed between groups in IL-6 serum levels (p = 0.29) or genotype frequencies (p = 0.738), nor in IL-10 genotype distribution (p = 0.194). In contrast, IL-10 serum levels were significantly higher in the ESRD-HBV group compared to the overt HBV group (p = 0.00024). A significant genotype-phenotype association for IL-10 was identified within the ESRD-HBV cohort (p = 0.018), where carriers of the GA genotype exhibited higher serum IL-10 levels compared to AA and GG genotypes. This association was not observed in the overt HBV group (p = 0.33). CONCLUSION: No significant variation in IL-6 or IL-10 genotype frequencies was detected between the groups. Nevertheless, the IL-10 (- 1082G/A) polymorphism was related to differences in serum IL-10 concentrations among patients with concurrent HBV infection and ESRD. However, given the limited sample size and absence of key clinical confounders, these findings should be interpreted as exploratory and require validation in larger, well-characterized cohorts.
Protective and pathological roles of immunothrombosis in sepsis.
Minton K
Nat Rev Immunol · 2026 Jul · PMID 42265355 · Publisher ↗
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Extrafollicular plasma cells suppress T cell priming in tumour-draining lymph nodes.
Cai Y, Aggelakopoulou M
Nat Rev Immunol · 2026 Jul · PMID 42259971 · Publisher ↗
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Lower respiratory microbiota as modulators of tumor immunity in lung adenocarcinoma.
Chen Y, Kuang M, Li Q … +2 more , Chen Z, Zhou H
BMC Immunol · 2026 Jun · PMID 42243682 · Full text
BACKGROUND: Lung adenocarcinoma is common type of cancer with high morbidity and mortality. Emerging evidence suggests that microbial colonization in the lower respiratory airways may modulate immune activation and respo...
BACKGROUND: Lung adenocarcinoma is common type of cancer with high morbidity and mortality. Emerging evidence suggests that microbial colonization in the lower respiratory airways may modulate immune activation and response to immunotherapy. However, the immunologic relevance of microbiome diversity in lung cancer remains unclear. METHODS: We analyzed bronchoalveolar lavage fluid (BALF), serum cytokines, immune cell subsets, and checkpoint molecule expression from 350 patients with lung adenocarcinoma. Microbiome diversity was quantified by phylum- and genus-level richness derived from binary detection of specific bacterial groups. Associations between microbial diversity, immune parameters, and clinical prognosis were evaluated using correlation and comparative statistical analyses. RESULTS: Among 350 samples, there was no major compositional difference between patients who died and those who recovered. Microbial diversity showed no significant associations with systemic cytokines, including IL-6, IL-1β, TNF-α, IL-10, and IFN-γ. Genus richness showed positive correlation with PD-1 expression, while phylum richness correlated inversely with PD-L1. Specific taxa demonstrated distinct immune associations: TM7 correlated with increased regulatory T cells, Actinobacteria and Veillonella correlated with lower IL-1β, while Neisseria correlated with CTLA-4 expression. CONCLUSION: Lower airway microbiota in lung adenocarcinoma display moderate diversity and meaningful immunologic associations, particularly with PD-1/PD-L1 pathways, Tregs, and IL-1β regulation. Although diversity alone is not prognostic, specific microbial taxa may shape immune landscapes relevant to immunotherapy response and represent potential targets for future microbiome-based interventions. CLINICAL TRIAL NUMBER: Not applicable.
Early diagnostic value of serum procalcitonin, C-reactive protein, white blood cell count and the neutrophil percentage in bacterial and fungal bloodstream infections.
Zhai S, Luo C
BMC Immunol · 2026 Jun · PMID 42243654 · Full text
BACKGROUND: Bloodstream infections (BSIs) are severe systemic disorders caused by pathogenic microorganisms, including bacteria and fungi, invading the bloodstream. Associated with high morbidity and mortality, BSIs repr...
BACKGROUND: Bloodstream infections (BSIs) are severe systemic disorders caused by pathogenic microorganisms, including bacteria and fungi, invading the bloodstream. Associated with high morbidity and mortality, BSIs represent one of the leading causes of death globally. There is an urgent demand for simple, rapid, and accurate laboratory biomarkers to facilitate the diagnosis and differential diagnosis of patients with suspected BSIs, thereby guiding timely and targeted antimicrobial therapy. OBJECTIVE: To evaluate the value of serum procalcitonin (PCT), C-reactive protein (CRP), white blood cell count (WBC), and neutrophil percentage (NEUT%) for early and differential diagnosis of bacterial vs. fungal bloodstream infections (BSIs), a cross-sectional study was conducted. METHODS: A total of 1649 patients with suspected BSI were included in this retrospective study. Of these, 1357 patients with positive blood cultures were classified as the BSI group (experimental group), and 292 patients with negative blood cultures were assigned to the non-BSI group (control group). Serum PCT, CRP, WBC/NEUT% were measured using a bioMerieux VIDAS 30 analyzer, SIEMENS ADVIA 2400 and by Sysmex XN-9000, respectively. Microbial identification was based on bioMerieux VITEK 2 systems. The diagnostic performance of these biomarkers in the discrimination in bacterial and fungal bloodstream infections were compared using receiver operating characteristic (ROC) curves. RESULTS: For BSI discrimination, a PCT level > 0.687 ng/mL could demonstrate the optimal performance (AUC = 0.788, sensitivity 61.7%, specificity 80.1%). The PCT level < 0.5 ng/mL for 3 consecutive days could effectively rule out BSI (sensitivity 98.1%, specificity 79.5%). Elevated PCT (> 1.78 ng/mL) and CRP (> 79.76 mg/L) levels were associated with bacterial BSIs (AUC = 0.686 for the combined markers). A PCT level > 1.98 ng/mL suggested Gram-negative BSI (sensitivity 68.4%). The positive diagnostic rates of the PCT + CRP+NEUT% combined test for G- bacterial and G+ bacterial BSIs reached 96.17% and 92.86% respectively, which significantly improved the diagnostic positive rate compared with single diagnosis. CONCLUSIONS: PCT could reliably excludes BSI (3-day < 0.5 ng/mL rule) and aids differentiation (bacterial/fungal: PCT + CRP; G-/G+: PCT+NEUT%). Multi-parameter approaches optimize diagnostic accuracy for timely intervention.
The immune engram: a spatial model of immunological memory.
Takaba H
Nat Rev Immunol · 2026 Jun · PMID 42243322 · Publisher ↗
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G protein-coupled receptor autoantibody expression patterns in adults with decelerated biological aging mirror pediatric profiles.
Paniskaki K, Stervbo U, Goretzki S … +9 more , Hufnagel D, Anft M, Heidecke H, Westhoff TH, Rohn H, Felderhoff-Mueser U, Witzke O, Dohna-Schwake C, Babel N
BMC Immunol · 2026 Jun · PMID 42237231 · Full text
BACKGROUND: G protein-coupled receptors (GPCRs) represent the largest and most diverse family of membrane proteins. In addition to their endogenous ligands, functional natural autoantibodies (Aab) have also been shown to...
BACKGROUND: G protein-coupled receptors (GPCRs) represent the largest and most diverse family of membrane proteins. In addition to their endogenous ligands, functional natural autoantibodies (Aab) have also been shown to bind and modulate GPCRs. Aab concentration is known to increase with chronological age, and several studies demonstrated an association of certain GPCR-binding Aab with chronic inflammation, concretely with specific autoimmune diseases in adults. However, prevalence of GPCR-Aab in pediatric population is not known so far. METHODS: In this descriptive study, we investigated the levels of Aab targeting 14 distinct GPCRs across individuals (pediatric, n = 83, adults n = 198) taking into consideration chronological and biological age, as defined by PhenoAge clock. RESULTS: Our findings suggest, that anti-GPCR Aab are present from childhood through adulthood; however, their expression patterns undergo significant changes over the course of life. Specifically, we observed a significant increase in Aab targeting ACE2, CXCR3, and BDKRB1 in adults and older individuals. Conversely, concentrations of Aab against ATR1, ADRA1A, ADRB2, and ETAR were significantly higher in children compared to adults. We also assessed the impact of age acceleration on Aab levels, defined by a positive Δ age score based on the PhenoAge clock. Distinct GPCR Aab expression signatures correlated with accelerated aging, differing notably from patterns seen in pediatric and adult cohorts. Concretely, the expression profile of GPCR Aab in -Δage adults exhibits similarity to that observed in the pediatric cohort. Furthermore, we found a concordant presence of CXCR3-Aab and expansion of CXCR3 + T cells with increased chronological age. CONCLUSIONS: Because systemic chronic inflammation is a known driver of accelerated aging, we hypothesize that the altered Aab expression profiles observed in biologically older adults may reflect this underlying inflammatory state. Although future research will be essential to evaluate the therapeutic potential of targeting these GPCRs in the context of inflammaging and autoimmune pathophysiology, chronological as well as biological age should be considered when assessing GPCR-Aab patterns.
Glial cells in chronic inflammation: diversity, dysfunction and therapeutic targeting.
Lee HG, Rone JM, Lee JH … +1 more , Quintana FJ
Nat Rev Immunol · 2026 Jun · PMID 42236914 · Publisher ↗
Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system (CNS). Current therapies for relapsing MS primarily target the peripheral immune system but have consistently failed to address mech...
Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system (CNS). Current therapies for relapsing MS primarily target the peripheral immune system but have consistently failed to address mechanisms underlying disease progression, which are thought to involve CNS-resident glial cells such as astrocytes, microglia and oligodendrocytes. Recent technological advances have revealed the functional heterogeneity of these glial cells, highlighting their crucial roles in inflammation, demyelination, remyelination and neurodegeneration. In this Review, we summarize emerging insights into the diversity, function and regulation of glial cells in MS and inflammation in general, highlight their interactions with immune cells and non-immune cells in the CNS, and discuss potential strategies for their therapeutic modulation.
Hallmarks and correlates of effective adoptive cell immunotherapy for cancer.
Krishna S, Robbins PF, Lowery FJ … +1 more , Rosenberg SA
Nat Rev Immunol · 2026 Jun · PMID 42230788 · Publisher ↗
Cancer immunotherapies have shown promise and success in a number of different types of tumours, yet many solid epithelial tumours remain recalcitrant. Somatic mutations in tumour cells can lead to the expression of neoa...
Cancer immunotherapies have shown promise and success in a number of different types of tumours, yet many solid epithelial tumours remain recalcitrant. Somatic mutations in tumour cells can lead to the expression of neoantigens, which are potent targets of the human antitumour immune response. These can be targeted through adoptive cell transfer (ACT) of neoantigen-specific T cells, including tumour-infiltrating lymphocytes (TILs) or T cell receptor (TCR)-engineered T cells (TCR-T cells), an approach that has been shown to achieve tumour regression in patients with different types of metastatic solid tumours including melanoma, breast and gastrointestinal cancer. Immunogenomics, systems immunology and genome editing now provide multidisciplinary tools to design cell therapies against solid cancer. Here, we review historical efforts and our current conceptual understanding of ACT using TILs or TCR-T cells. Moreover, we highlight emerging correlates of response to ACT and novel strategies that integrate tumour immunology, cancer genomics, computational biology and T cell engineering for the development of next-generation cellular immunotherapies.
Immunological Reprogramming by Radiation Therapy: Implications for Precision Cancer Treatment.
Singh AK, Sharma VC, Kumar M … +1 more , Mishra MK
Immunology · 2026 Jun · PMID 42228408 · Publisher ↗
Radiation therapy (RT) is a main part of cancer treatment and is known mostly for its ability to directly kill cancer cells. However, recent studies have shown that RT can have potent immunomodulatory properties, which i...
Radiation therapy (RT) is a main part of cancer treatment and is known mostly for its ability to directly kill cancer cells. However, recent studies have shown that RT can have potent immunomodulatory properties, which include both the ability to re-program the tumour microenvironment (TME) and the activation of systemic anti-tumour immune responses. It reviews the immune mechanisms involved in the killing of tumours after irradiation, such as immunogenic cell death (ICD), activation of the cGAS-STING (cyclic GMP-AMP synthase-stimulator of interferon genes) pathway, dendritic cell (DC) maturation, priming of cytotoxic T lymphocytes (CTLs), and the abscopal effect, which refers to the regression of non-irradiated tumours following local irradiation. We also discuss how RT induces immunosuppressive counterforces such as regulatory T cells (Tregs), myeloid-derived suppressor cells (MDSCs), and programmed death-ligand 1 (PD-L1) upregulation. The synergy between RT and immune checkpoint inhibitors (ICIs) such as anti-programmed cell death protein 1 (anti-PD-1), anti-programmed death-ligand 1 (anti-PD-L1), and anti-cytotoxic T-lymphocyte-associated protein 4 (anti-CTLA-4) agents is critically assessed. We also discuss possible clinically relevant enhancement of side effects of immunotherapies by RT. The induction of neo-antigens and immune activation by chemotherapy (ChX) versus RT is compared/contrasted. Particular focus is paid to dose fractionation approaches, such as stereotactic body radiation therapy (SBRT) and stereotactic radiosurgery (SRS), and their differential immunogenic effects. The different tumour types that are most susceptible to radiotherapy-induced immunologic responses are covered in great detail, particularly malignant melanoma. The field is contextualised with relevant clinical trials, emerging patents, and translational case studies. In this review, we seek to give an integrative framework for how radiation-induced immune reprogramming can be harnessed in the design of next-generation precision oncology strategies.
Senescent B cells accumulate in germinal centre niches of the aged human lymph node.
Wang X, Kim BYS
Nat Rev Immunol · 2026 Jul · PMID 42225883 · Publisher ↗
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Characterisation of HIV-1 Gag Cytotoxic T-Lymphocyte Epitopes in the Southern African Region-A Systematic Review.
Fortuin TL, Nkone P, Loubser S … +2 more , Tiemessen CT, Mayaphi SH
Immunology · 2026 May · PMID 42219374 · Publisher ↗
During early HIV-1 infection, robust Cytotoxic T-lymphocyte (CTL) responses are mostly targeted at immunodominant Gag p24 epitopes to reduce HIV-1 viraemia to a set-point. The aim of this study was to review the current...
During early HIV-1 infection, robust Cytotoxic T-lymphocyte (CTL) responses are mostly targeted at immunodominant Gag p24 epitopes to reduce HIV-1 viraemia to a set-point. The aim of this study was to review the current body of knowledge on HIV-1 Gag CTL epitopes in the southern African region where subtype C is prevalent. Peer-reviewed records were obtained from three databases: PubMed Central, Web of Science Core Collection, and Scopus, using the following search terms: HIV subtype C Gag epitopes, and HIV clade C Gag epitopes. The search results were restricted to countries within the southern African region, and only data published in English and between the years 2000-2025 were considered for this review. The search from the three databases produced a total of 2103 peer-reviewed records, and 49 records were included in the review. The majority of studies (58.44%) were conducted in South Africa, followed by Botswana (15.58%), Zambia (10.39%), Malawi (7.79%), Zimbabwe (6.49%) and Angola (1.30%). There were no studies identified from other southern African countries. A total of 60 Gag CTL epitopes were identified, of which 17 (28.33%) were located within the matrix protein (p17), 33 (55.00%) within the capsid protein (p24), and 4 (6.67%) within the Gag polyprotein (p2p7p1p6). The commonly detected immunodominant epitopes were mostly located within the Gag p24 protein; and included TPQDLNTML (TL9, Gag p24 48-56) and TSTLQEQIGW (TW10, Gag p24 108-117) present at 16.00% and 13.3%, respectively. The proportion of HLA-A, B and C allotypes in this systematic review were 18%, 78%, and 4%, respectively. The more common HLA-B allotypes that restrict immunodominant Gag epitopes and facilitate better control of HIV-1 were HLA-B*57, -B*58:01, -B*42:01 and -B*81:01. This systematic review has provided important insights into the description of immunodominant Gag epitopes and HLA-I alleles that contribute to the control of HIV-1 viraemia in the southern African region. It has also exposed that some CTL epitopes identified in the southern African studies are not reported on the Los Alamos HIV database (LANL HIV database). This highlights a need to have this database updated with this information as it is used as a reference for epitopes. This review could provide insights into the design of an epitope-based HIV-1 vaccine that would also be effective in the southern African region.
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