Premium
Pivotal Advance: CTLA‐4 + T cells exhibit normal antiviral functions during acute viral infection
Author(s) -
Raué HansPeter,
Slifka Mark K.
Publication year - 2007
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1189/jlb.0806535
Subject(s) - lymphocytic choriomeningitis , biology , ctla 4 , cytotoxic t cell , effector , cd8 , t cell , immunology , immune system , vaccinia , virus , virology , interleukin 21 , in vitro , recombinant dna , biochemistry , gene
Previous studies have shown that T cells, which are genetically deficient in CTLA‐4/CD152 expression, will proliferate uncontrollably, resulting in lethal autoimmune disease. This and other evidence indicate that CTLA‐4 plays a critical role in the negative regulation of effector T cell function. In contrast to expectations, BrdU incorporation experiments demonstrated that CTLA‐4 expression was associated with normal or even enhanced in vivo proliferation of virus‐specific CD4 + and CD8 + T cells following acute lymphocytic choriomeningitis virus or vaccinia virus infection. When compared with CTLA‐4 – T cells directly ex vivo, CTLA‐4 + T cells also exhibited normal antiviral effector functions following stimulation with peptide‐coated cells, virus‐infected cells, plate‐bound anti‐CD3/anti‐CTLA‐4, or the cytokines IL‐12 and IL‐18. Together, this indicates that CTLA‐4 does not directly inhibit antivral T cell expansion or T cell effector functions, at least not under the normal physiological conditions associated with either of these two acute viral infections.