Increased frequency of late‐senescent T cells lacking CD127 in chronic hepatitis C disease

Abstract

Chronic HCV infection results in increased turnover of late-senescent T cells that lack survival potentials, possibly contributing to viral persistence. Our findings challenge the prominence of senescent T-cell phenotypes in clinical hepatitis C infection.

Hepatitis C Virus Infection in the Older Patient

“…HCV infection itself might be associated with loss of early-differentiated T cells and progressive accumulation of chronically-activated, late-differentiated senescent T cells. One small study 20 comparing HCV-infected individuals with healthy controls, all of whom were less than 54 years of age, found that the CD4 and CD8 T cells from HCV-infected individuals showed a significant increase in the T cell immunosenescent phenotype that is more commonly associated with advancing age. Whether or not this increase is associated with the premature onset of not only liver but also non-liver clinical outcomes related to aging in HCV-infected persons is unclear.…”

Peripheral loss of CD8+CD161++TCRVα7·2+ mucosal‐associated invariant T cells in chronic hepatitis C virus‐infected patients

“…Although T-cell activation is essential for effector functions such as cytotoxicity and suppression of viral replication, persistent activation of the immune system is related to HCV disease progression [34,35]. We recently found significant increase of HCV-specific CD4 + and CD8 + T cells coexpressing HLA-DR and CD38 during chronic HCV infection [34].…”

Concurrent loss of co-stimulatory molecules and functional cytokine secretion attributes leads to proliferative senescence of CD8+ T cells in HIV/TB co-infection

“…Decrease in CD127 may be directly associated with T-cell activation in HIV infection, and has previously been correlated with HIV disease progression [46,47]. Further, co-infection may harness an advanced stage of immune deterioration where survival of T cells is significantly affected [48][49][50]. We also showed that CD127 expression was inversely associated with surrogate markers of disease progression, immune activation markers and CD57, suggesting the essential role of CD127 in maintaining T-cell homeostasis and survival [8].…”