CD27 promotes survival of activated T cells and complements CD28 in generation and establishment of the effector T cell pool.
CD27, like CD28, acts in concert with the T cell receptor to support T cell expansion. Using CD27(-/-) mice, we have shown earlier that CD27 determines the magnitude of primary and memory T cell responses to influenza virus. Here, we have examined the relative contributions of CD27 and CD28 to generation of the virus-specific effector T cell pool and its establishment at the site of infection (the lung), using CD27(-/-), CD28(-/-), and CD27/CD28(-/-) mice. We find that primary and memory CD8+ T cell responses to influenza virus are dependent on the collective contribution of both receptors. In the primary response, CD27 and CD28 impact to a similar extent on expansion of virus-specific T cells in draining lymph nodes. CD27 is the principle determinant for accumulation of virus-specific T cells in the lung because it can sustain this response in CD28(-/-) mice. Unlike CD28, CD27 does not affect cell cycle activity, but promotes survival of activated T cells throughout successive rounds of division at the site of priming and may do so at the site of infection as well. CD27 was found to rescue CD28(-/-) T cells from death at the onset of division, explaining its capacity to support a T cell response in absence of CD28.
Division of Immunology, The Netherlands Cancer Institute, 1066 CX Amsterdam, Netherlands.
Jenny
J
Hendriks
Yanling
Y
Xiao
Jannie
J
Borst
D019264:Adoptive Transfer; D000818:Animals; D017209:Apoptosis; D018106:CD28 Antigens / Q000276:immunology*; D008213:Lymphocyte Activation; D051379:Mice; D018345:Mice, Knockout; D013601:T-Lymphocytes / Q000276:immunology*; D018127:Tumor Necrosis Factor Receptor Superfamily, Member 7 / Q000235:genetics / Q000276:immunology*
D018106:CD28 Antigens; D018127:Tumor Necrosis Factor Receptor Superfamily, Member 7