ArticleFrontiers in immunology2026
CXCL10 rs8878 identifies a genotype-associated immune phenotype linked to T-lymphocyte preservation and survival in sepsis.
Article in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Sepsis is characterized by a dysregulated host response to infection, leading to concurrent hyperinflammation and immunosuppression, including profound alterations in T lymphocyte homeostasis. The chemokine CXCL10, an interferon-γ-inducible mediator of T cell trafficking, has been implicated in immune activation and tissue injury. However, it remains unclear whether genetic variation in CXCL10 contributes to T cell dysregulation and clinical outcomes in sepsis. Methods: In a prospective cohort of septic patients (n=278), we analyzed CXCL10 rs8878 genotypes, circulating immune cell counts, cytokine concentrations, and CXCL10 protein and mRNA expression in whole blood. Associations between genotype, immune parameters, plasma proteomics and 30-day survival were assessed using group comparisons and Kaplan-Meier analyses. Correlation analyses were performed to evaluate relationships between CXCL10 concentrations, cytokines, and clinical parameters. Results: Variants in the CXCL10 gene were associated with T cell dysregulation. Carriers of the rs8878 AA genotype exhibited higher circulating T cell counts and improved survival compared with G-allele carriers. Higher total and CD8 Conclusion: The CXCL10 rs8878 genotype is associated with T cell dynamics and 30-day survival in sepsis, suggesting a genotype-dependent modulation of the adaptive immune response. While the AA genotype is linked to preserved T cell counts and improved outcomes, increased CXCL10 expression in non-survivors points to a context-dependent role in inflammation-driven immune dysregulation. These findings identify CXCL10 as a potential biomarker for risk stratification and a candidate target for immunomodulatory therapies in sepsis.
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