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Analysis of the costimulatory requirements for generating human virus-specific in vitro T helper and effector responses.

Abstract：

:The present study analyzes the role of CD28-B7-mediated costimulation during in vitro human peripheral blood memory T cell activation by influenza A virus. Inhibition studies using the B7-binding fusion protein CTLA4Ig and antibodies against CD80 and CD86 demonstrate that CTLA4Ig and anti-CD86 inhibited influenza-specific T cell proliferation, interleukin (IL)-2 and interferon (IFN)-gamma production, and generation of influenza-specific CD8+ CTL. The production of IL-10 and IL-18, which are known to modulate T cell immune responses, were not affected by blocking the CD28-B7 costimulatory pathway. Inhibition of diverse influenza-specific T cell functions could be reversed by the addition of exogenous IL-2 or IL-12 but not by the addition of IFN-gamma or IL-18. Although IL-2 is known to overcome CD28-B7 costimulatory requirements, this is the first report showing that exogenous IL-12 is able to bypass CD28-B7 costimulatory blockade induced by CTLA4Ig in vitro. The induction of IFN-gamma production with the recently described IFN-gamma inducing cytokine IL-18 was not detected. In conclusion, these results demonstrate that CD86 represents a major costimulatory signal for the activation of resting peripheral blood memory T cells with recall antigens. These observations may have important implications for the development of immunotherapeutic strategies in diverse immunodeficiency diseases as well as in tumor immunotherapy.

journal_name

J Clin Immunol

journal_title

Journal of clinical immunology

authors

Blazevic V,Trubey CM,Shearer GM

doi

10.1023/a:1010987426835

subject

Has Abstract

pub_date

2001-07-01 00:00:00

pages

293-302

issue

4

eissn

0271-9142

issn

1573-2592

journal_volume

21

pub_type

杂志文章

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