Development of Mycobacterium tuberculosis post in vitro fertilization and embryo transfer: A case series derived from a multi-omics analysis and literature review.

Transcriptomic signatures predict severe linezolid-induced peripheral neuropathy and reveal pre-treatment immune and antioxidant dysregulation.

Persistent T cell phenotypic alterations and early innate immune dysregulation as potential biomarkers of Long COVID.

Background/Objectives: Oocyte donation (OD) pregnancies involve complete maternal–fetal genetic disparity and are associated with increased placental dysfunction and adverse perinatal outcomes. However, a unified histopathological framework to characterize alloimmune-mediated placental injury in OD gestations is lacking. This study evaluates immune and vascular alterations in OD triplet placentas and proposes a structured scoring system, the Placental Allograft Rejection-like Score (PARS), to quantify immunovascular dysregulation. Methods: This retrospective study included all OD triplet pregnancies with placental examination performed during 24 years at a tertiary referral center. Maternal, obstetric, fetal, neonatal, and pathological variables were analyzed at the pregnancy level. Histological and immunohistochemical features previously shown to differ between OD and non-OD pregnancies were grouped into six domains: innate immunity, adaptive immunity, checkpoint regulation, vascular remodeling, complement activation, and trophoblastic behavior. Binary thresholds, immunoreactive scores or established morphological cut-offs, were applied to construct a 20-point score classified into three grades. Results: Forty-five OD triplet pregnancies were analyzed. Intra-pregnancy concordance for PARS components was high, with intraclass correlation coefficient ≥0.70 in 87.3% pregnancies. Increasing PARS grades demonstrated a clear clinical gradient. Grade 3 pregnancies had significantly lower birthweight, higher rates of prematurity (<34 weeks), and increased fetal growth restriction. Placental weight decreased progressively with higher PARS. Histologically, grade 3 placentas showed significantly increased accelerated villous maturation and intervillous fibrin deposition. Conclusions: PARS integrates immune and vascular placental lesions into a structured and reproducible framework that correlates with clinically relevant perinatal outcomes and may support future clinical risk stratification, although further validation in larger, multicenter prospective cohorts is required.

Background and Aims: Tuberculosis remains a major public health problem, and the emergence of drug-resistant forms significantly complicates its management, particularly in resource-limited countries such as the Republic of Guinea. Thus, this study is to assess the management of patients with drug-resistant pulmonary tuberculosis at the Matam Tuberculosis Center (CAT), in order to identify shortcomings and propose areas for improvement. Methodology: During 12 months, a descriptive and analytical cross-sectional study was conducted at the Matam Tuberculosis Center (CAT). Sociodemographic, clinical, bacteriological, and treatment-related data were collected. A total of 152 sputum samples were analyzed using the GeneXpert MTB/RIF assay and fluorescence microscopy. Results: Among the152 pulmonary tuberculosis patients, GeneXpert MTB/RIF detected 32% of cases compared to 22% by fluorescence microscopy, confirming its superior diagnostic performance. Hematological findings revealed a high prevalence of anemia (98%), mainly microcytic along with leukocytosis and lymphopenia, reflecting chronic inflammation and immune alterations. Biochemical abnormalities, including elevated transaminases and creatinine (31%), suggest treatment-related hepatic and renal effects. The treatment success rate reached 94%, exceeding WHO targets, indicating effective patient management despite persistent challenges related to drug resistance and adherence. Conclusion: Drug-resistant tuberculosis remains a major challenge in Conakry. Strengthening early detection, improving treatment monitoring, and ensuring strict adherence to treatment protocols are essential to improving patient care.

Corrigendum “immune cell alterations in a pristane‐induced lupus model in C57BL/6J mice”

The ageing population faces numerous physiological changes, among which immunosenescence plays a central role. Understanding the mechanisms underlying immunosenescence remains a priority. Within this framework, the contribution of comorbidities to immune dysfunction is still poorly characterized, despite growing evidence suggesting that it may represent a critical determinant in the evaluation of immunosenescence. The main objective of this report was to disentangle the respective impacts of age and comorbidities. To this end, we focused on immunological parameters originally developed in the context of sepsis, a condition that shares many immunological defects with immunosenescence. Data were obtained from two cohorts: the REALISM cohort, including healthy elderly individuals, and the SENIOR-HLA-DR cohort, consisting of a real-life hospitalized geriatric population. Immunological parameters assessed were circulating IL-6, percentage of immature neutrophils, monocyte HLA-DR expression (mHLA-DR), neutrophil-to-lymphocyte ratio (NLR), T lymphocyte count, and interferon-γ release assay (IGRA) in response to phytohemagglutinin (PHA). In the absence of comorbidities, age had no detectable effect on immune parameters in the REALISM cohort (n = 174 individuals). The SENIOR-HLA-DR cohort (n = 76 patients) revealed that cardiovascular comorbidities exerted the greatest influence, being associated with significantly reduced mHLA-DR expression and increased NLR. Infections further triggered substantial alterations in inflammation and innate immunity, characterized by elevated percentages of immature neutrophils and decreased mHLA-DR expression. Our findings indicate a limited impact of chronological age and comorbidities on the selected immunological parameters. These results suggest that routine clinical tools may be insufficient to fully capture the complexity of immunosenescence.

Immunotherapy with immune checkpoint inhibitors (ICIs) has revolutionized treatment for non-small cell lung cancer (NSCLC) and head and neck squamous cell carcinoma (HNSCC), yet resistance limits durable responses in many patients. Emerging evidence implicates the intratumoral microbiome – comprising bacteria, fungi, and viruses within tumor tissues – as a key modulator of tumor biology, immune infiltration, and ICI sensitivity, beyond traditional tumor-intrinsic and immune factors. In HNSCC, human papillomavirus (HPV)-negative tumors exhibit higher oncobacteria abundance than HPV-positive ones, with elevated levels linked to worse survival in HPV-positive oropharyngeal cases, suggesting an immunosuppressive tumor microenvironment that may influence ICI outcomes. In NSCLC, intratumoral taxa such as Fusobacterium nucleatum and Bacteroides fragilis promote progression and evasion via immune checkpoint modulation (PD-1/PD-L1), pro-inflammatory pathways (toll-like receptors and cytokines like interleukin-6/tumour necrosis factor-alpha), metabolic reprogramming (PI3K/AKT), and recruitment of suppressive cells (neutrophils and myeloid-derived suppressor cells). Pan-cancer studies show microbial enrichments and compositional shifts in responders versus non-responders to ICI, with metabolites (e.g., lactate and succinic acid) driving M2 macrophage polarization, T-cell suppression, and resistance. The gut–tumor axis further exacerbates refractoriness through systemic dysbiosis and immune alterations. Preclinical models indicate that targeted microbiome interventions – such as fecal microbiota transplantation, specific probiotics (e.g., Bifidobacterium spp. and Akkermansia muciniphila ), or selective antibiotics – can restore antitumor immunity, enhance ICI efficacy, and minimize broad dysbiosis risks. Integrating intratumoral microbial profiling into HNSCC and NSCLC clinical trials could refine patient stratification, uncover predictive biomarkers, and accelerate microbiome-directed adjunct therapies, advancing precision oncology and expanding immunotherapy benefits.

Background Rothia is an oral commensal bacterium increasingly detected in the respiratory tract, and recent studies have highlighted changes in its abundance in respiratory infections. Objective This study aimed to investigate the species distribution of Rothia, its co-occurrence with respiratory pathogens, and the immune alterations associated with Rothia co-infection in respiratory infections. Design We developed real-time PCR to differentiate R. aeria, R. dentocariosa, and R. mucilaginosa. Sputum samples from 447 hospitalized patients were tested for 35 respiratory pathogens and three Rothia species using customized TaqMan Array Card. Co-infection murine models were established. Results All three Rothia species were frequently detected (39.4% to 72.3%). R. mucilaginosa showed positive associations with SARS-CoV-2 among patients with respiratory symptoms (odds ratio 4.0, p < 0.0001) or pneumonia (OR 2.7, p = 0.019) and influenza A virus (IAV; OR 8.4, p = 0.004) in patients with pneumonia during an influenza season, but was negatively associated with Klebsiella pneumoniae (OR 0.3, p < 0.05). These inverse associations were confirmed in murine models. Increased mortality and bacterial burden were observed in IAV and R. mucilaginosa co-infection, while K. pneumoniae and R. mucilaginosa co-infection was attenuated. Both models showed increased neutrophils. Functionally, IAV co-infection impaired bactericidal activity whereas prior K. pneumoniae exposure enhanced bacterial clearance. Conclusions This study uncovers distinct pathogen associations of Rothia in respiratory infections, which may provide evidence for their roles in shaping disease outcomes.

Strenuous endurance exercise imposes substantial physiological stress on the cardiovascular system and has been associated with transient elevations in cardiac biomarkers. Vitamin D₃ has been suggested to influence oxidative stress and immune responses. In this study, we investigated the effects of vitamin D₃ supplementation on biomarkers of cardiac, muscle, and immune responses following a marathon race. Twenty-one amateur runners were allocated to either a vitamin D₃ supplementation group (receiving vitamin D₃ for 8 weeks) or a placebo group. All participants completed an official full marathon (42.195 km). Blood biomarkers were measured from 24 h before to 24 h after the race. Post-race increases in markers of muscle damage and cardiac stress were observed. Vitamin D₃ supplementation was associated with attenuated elevations in selected biomarkers demonstrating significant interaction effects. Compared with the placebo group, the vitamin D₃ group demonstrated attenuation of protein carbonyls (PC), the only oxidative stress marker showing a significant Group × Time interaction. No significant interaction effects were observed for thiobarbituric acid reactive substances (TBARS) or antioxidant enzymes. Both groups showed post-race increases in white blood cell counts, particularly neutrophils, whereas lymphocyte counts significantly decreased at 0.5 h and 2 h post-race. Immunoprofiling revealed time-dependent alterations in selected immune cell subsets, although no significant interaction effects were detected. Descriptive differences in recovery patterns were observed between groups, and exploratory correlation analyses suggested time-specific associations between immune cell subsets and biochemical markers during recovery. Vitamin D₃ supplementation may attenuate PC responses and was associated with lower creatine kinase (CK) and creatine kinase-MB (CK-MB) levels at 24 h post-race following marathon running. Immune alterations were time-dependent, with descriptive differences in recovery patterns between groups.

Ageing is associated with profound and progressive alterations in immune structure and function that collectively reshape host defence across the lifespan. These changes, broadly described as immunosenescence, reflect not merely immune decline but a complex remodelling of both innate and adaptive immunity. Immunosenescence contributes to increased susceptibility to infections, diminished vaccine responsiveness, heightened cancer risk, and the paradoxical emergence of chronic inflammatory and autoimmune conditions in older adults. This review integrates current evidence on the biological drivers of immune ageing, focusing on thymic involution, lymphocyte repertoire contraction, cellular senescence, and dysregulated cytokine signalling. Particular attention is given to the clinical implications of these immune alterations and their relevance to infectious disease outcomes, cancer surveillance, and age-associated comorbidities. Emerging therapeutic and preventive strategies, including tailored vaccination approaches and immunomodulatory interventions, are critically examined. Understanding immune ageing as a dynamic and potentially modifiable process provides a foundation for developing integrated strategies to extend health span and improve quality of life in ageing populations.

Intracerebral hemorrhage (ICH) is a life-threatening neurological disorder with high mortality and limited treatment options. Inflammation and metabolic dysregulation contribute to ICH pathology, yet their molecular underpinnings remain poorly understood. Lactylation, a recently discovered post-translational modification, is known to regulate immune and metabolic pathways. This study investigated lactylation-related genes in ICH, their relationship with immune cell infiltration, and their diagnostic potential. Gene expression data from two public datasets (GSE73378 and GSE36791) were integrated after batch correction. Differentially expressed genes (DEGs) were identified with "limma" and lactylation-related genes were curated from the literature. Functional enrichments were conducted via GO and KEGG. Diagnostic genes were selected using XGBoost, Random Forest, and LASSO regression. Immune cell infiltration was analyzed by ssGSEA, and unsupervised clustering defined molecular subtypes. Hemorrhage-associated genes were validated by RT-qPCR in a mouse model of hemorrhage. A total of 111 lactylation-related DEGs were identified. Seven core genes demonstrated strong diagnostic performance (AUC = 0.80-0.92). ssGSEA revealed significant immune alterations associated with lactylation-related gene expression. Unsupervised clustering identified two distinct ICH subtypes with different immune and transcriptional profiles. Upstream regulators predicted PTBP1 and HNRNPD as potential transcriptional regulators. Six of the seven genes were validated in hemorrhagic mice. These findings suggest that lactylation links metabolic dysregulation to immune responses in ICH, contributes to molecular heterogeneity, and may enable patient stratification and precision therapeutic strategies. Lactylation-related genes are closely linked to immune dysregulation in ICH and show promise as diagnostic biomarkers and therapeutic targets.

Bipolar disorder (BD) is a major psychiatric condition with a multifaceted and largely unknown pathophysiology. Mania, the defining feature of BD, remains underinvestigated. Proteomics offers a powerful, data-driven, unbiased approach to uncover biological alterations. Blood platelets provide a stable and comprehensive reflection of the body's internal milieu. This proof-of-concept study explores platelet proteomic alterations in mania. High-resolution proteomic profiling was performed on platelet samples from hospitalized patients with severe mania (n = 11) and 1:1 age- and sex-matched healthy controls (n = 11) using liquid chromatography-tandem mass spectrometry. Platelet proteins were quantified, differentially expressed proteins identified, and functional enrichment analyses conducted to characterize associated biological pathways. Key proteomic predictions were validated by enzyme-linked immunosorbent assay (ELISA) in platelet and plasma samples. Proteomic analysis revealed that mania is associated with proteins primarily enriched in immune activation while lacking those enriched in cell homeostasis. Among shared proteins, mania exhibited a prominent cluster of downregulated proteins, primarily converging on immune-related pathways. The most robust alteration involved deficits in MHC Class I-mediated antigen processing. Key immune regulatory hubs - transforming growth factor (TGF)-β and interleukin-4 (IL-4) - were identified, with the association of increased TGF-β levels with mania validated by ELISA. This study highlights platelet proteomics as a valuable tool for investigating biological alterations in psychiatric disorders. Our findings indicate deficits in MHC Class I-related pathways and immune alterations consistent with chronic low-grade inflammation, suggesting potential roles for latent viral and autoimmune-related mechanisms in BD. These results support and refine the concept of immune dysregulation in mania and BD.

Immune-mediated necrotizing myopathy (IMNM) is a severe autoimmune myopathy causing proximal muscle weakness. Its underlying immunopathogenesis remains incompletely understood, limiting the development of targeted therapies. To elucidate disease mechanisms and inform therapeutic strategies, this study characterized the peripheral immune profile of treatment-naïve IMNM patients. This retrospective study analyzed serum cytokine levels, complement proteins (C3, C4), immunoglobulins (IgA, IgG, and IgM), and peripheral blood lymphocyte subsets in 28 treatment-naïve IMNM patients during the active disease phase and 25 healthy controls at Tongji Hospital from August 2023 to March 2025. Compared with healthy controls, IMNM patients showed significantly elevated serum concentrations of interleukin-6 and interferon-γ (both p < 0.001). IgG and IgM levels were also markedly higher in the IMNM group (p = 0.003; p = 0.002). The number and percentage of B cells were significantly increased in IMNM patients (both p = 0.004). The number and percentage of CD8+ T cells were similarly elevated (p = 0.009; p = 0.004). In contrast, the proportion of CD4+ T cells was significantly reduced (p = 0.002), and the absolute count of natural killer cells was also significantly reduced (p = 0.004). IMNM exhibits a distinct peripheral immune landscape, characterized by enhanced humoral immunity potentially driven by CD8+ T cell-mediated mechanisms, accompanied by reduced circulating natural killer cells. These findings suggest potential biomarkers for disease activity and may inform targeted immunotherapies. Further studies are needed to validate these immune alterations and clarify their role in IMNM pathogenesis.

To characterize immune alterations in PLWH across disease stages and identify laboratory indicators for diagnosing fungal co-infections. We conducted a comprehensive cross-sectional study comparing laboratory immunological parameters-including lymphocyte subsets, activation/exhaustion markers, and plasma cytokines-across patient groups stratified by co-infection type and CD4⁺ T cell count. Statistical significance was assessed using false discovery rate correction. The most severe immunological compromise was observed in patients with advanced HIV disease (CD4⁺ ≤199 cells/µL) and co-infections, who exhibited profound pan-lymphopenia and a dissociated T cell profile featuring both hyperactivation (HLA-DR/CD38) and exhaustion (loss of CD28). Compared to patients with other opportunistic infections, those with fungal co-infections displayed a distinct immune phenotype characterized by significantly lower CD4⁺ T cell counts (51.32 ± 47.41 vs. 134.27 ± 130.12 cells/µL, q = 0.004) and B cell counts (65.74 ± 56.13 vs. 108.30 ± 101.10 cells/µL, q = 0.024), alongside elevated CD8⁺ T cell activation. Patients with localized Talaromyces marneffei infection had significantly higher CD4⁺ T, CD8⁺ T, and natural killer cell counts than those with disseminated disease, underscoring the importance of preserved cellular immunity in pathogen containment. No significant differences were observed across fungal pathogens or sites of cryptococcal disease. Correlation analysis revealed a strong positive association between HIV viral load and interleukin-10(R² = 0.587, r = 0.632, 95% CI: 0.473 to 0.755, P = 0.014). Specific immunological parameters-particularly severe CD4⁺ and B cell lymphopenia with concurrent CD8⁺ T cell hyperactivation-provide an objective basis for identifying PLWH at high risk for fungal infections. These findings highlight the potential value of adjunctive immunomodulatory strategies alongside antiviral therapy in this patient population. Not applicable.

Smoking and systemic Th17/Treg immune alterations in periodontitis: A cross-sectional study.

Bisphenol S toxicity in zebrafish: Endocrine, neurobehavioural, and metabolic disruptions.

Perinatal HIV exposure is associated with long-term alterations in immune marker levels in children.

Evolution of circulating respiratory syncytial virus lineages before and after the COVID-19 pandemic, 2017-2024, Taiwan.

Single-cell transcriptomics combined with spatial proteomics defines phagocytes type-specific immune regulation in diabetic cataract.