Premium
Non‐antigenic signals alter memory CD8 T cell development during chronic infection
Author(s) -
Shin Haina,
Beiting Daniel,
Roos David,
Wherry E. John
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.663.7
Subject(s) - immunology , cytotoxic t cell , cd8 , antigen , effector , biology , memory t cell , chronic infection , t cell , immune system , microbiology and biotechnology , in vitro , biochemistry
Memory CD8 T cells are a critical component of protective immunity. After an acute infection or vaccination, a small pool of antigen‐specific CD8 T cells differentiate from effector to memory CD8 T cells. They acquire several properties, including the ability to rapidly produce anti‐viral cytokines and a high proliferative capacity, that allow them to confer protection. During chronic infection, however, CD8 T cells undergo altered memory differentiation and do not acquire the properties that are attributed to memory CD8 T cells. While antigen load has been shown to correlate with the severity of CD8 T cell dysfunction, it is not clear if persistent antigen signaling alone is responsible for all the defects that occur during chronic infection. We have found that the non‐antigenic signals present during chronic infection influence the survival, phenotype and proliferative capacity of antigen‐specific CD8 T cells differentiating from the effector to memory stage, but did not have a profound effect on cytokine production. Furthermore, the chronic inflammatory environment may be sufficient to delay the differentiation of effector memory CD8 T cells to central memory. These findings indicate that TCR and non‐TCR signals may alter different aspects of memory differentiation during chronic infection.