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Differences in the Reactivity of CD4 + T‐Cell Lines Generated against Free Versus Nucleosome‐Bound SV40 Large T Antigen
Author(s) -
Bredholt G.,
Rekvig O.P.,
Andreassen K.,
Moens U.,
Marion T.N.
Publication year - 2001
Publication title -
scandinavian journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.934
H-Index - 88
eISSN - 1365-3083
pISSN - 0300-9475
DOI - 10.1046/j.1365-3083.2001.00873.x
Subject(s) - antigen , anti nuclear antibody , biology , immune system , microbiology and biotechnology , antibody , immunology , virology , autoantibody
Previous results have revealed a strong correlation between polyomavirus BK reactivation and disease activity and antinuclear auto‐antibody production in the human autoimmune disease systemic lupus erythematosus. BK virus establishes a latent infection in most humans, and reactivation requires the production of the DNA‐binding large T antigen. Experimentally induced expression of the polyomavirus SV40 large T antigen in mice induces both an immune response to large T antigen and autoimmune response to nuclear antigens and antinuclear antibody production. Previous results have indicated that human T‐antigen‐specific CD4 + T‐cell lines are stimulated equally by free, soluble and nucleosome‐bound T antigen. This study was designed to determine how antigen processing of nucleosomes containing bound SV40 large T antigen may affect the specificity and response characteristics of experimentally induced T‐antigen‐specific CD4 + T cells. The results indicated that CD4 + T‐cell lines generated from mice immunized with soluble, free T antigen responded very poorly in response to stimulation with T antigen bound to nucleosomes. CD4 + T‐cell lines generated from mice immunized with nucleosomes that had bound T antigen in situ responded to both free and nucleosome‐bound T antigen. The T‐antigen‐specific, CD4 + memory T cells induced by latent polyomavirus infections in humans may be uniquely suited to initiate autoimmunity to nuclear antigens upon virus reactivation.