B7-h1 expressed by activated CD8 T cells is essential for their survival

An immunoinhibitory role of B7 homologue 1 (B7-H1) expressed by non-T cells has been established; however, the function of B7-H1 expressed by T cells is not clear. Peak expression of B7-H1 on Ag-primed CD8 T cells was observed during the contraction phase of an immune response. Unexpectedly, B7-H1 b...

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Bibliographic Details
Published in:The Journal of immunology (1950) 2011-12, Vol.187 (11), p.5606-5614
Main Authors: Pulko, Vesna, Harris, Kimberley J, Liu, Xin, Gibbons, Rachel M, Harrington, Susan M, Krco, Christopher J, Kwon, Eugene D, Dong, Haidong
Format: Article
Language:English
Subjects:
Adoptive Transfer
Animals
Apoptosis - immunology
B7-H1 Antigen - immunology
B7-H1 Antigen - metabolism
CD8-Positive T-Lymphocytes - cytology
CD8-Positive T-Lymphocytes - immunology
CD8-Positive T-Lymphocytes - metabolism
Cell Separation
Cell Survival - immunology
Female
Flow Cytometry
Lymphocyte Activation - immunology
Mice
Mice, Inbred C57BL
Mice, Transgenic
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Summary:An immunoinhibitory role of B7 homologue 1 (B7-H1) expressed by non-T cells has been established; however, the function of B7-H1 expressed by T cells is not clear. Peak expression of B7-H1 on Ag-primed CD8 T cells was observed during the contraction phase of an immune response. Unexpectedly, B7-H1 blockade at this stage reduced the numbers of effector CD8 T cells, suggesting B7-H1 blocking Ab may disturb an unknown function of B7-H1 expressed by CD8 T cells. To exclusively examine the role of B7-H1 expressed by T cells, we introduced B7-H1 deficiency into TCR transgenic (OT-1) mice. Naive B7-H1-deficient CD8 T cells proliferated normally following Ag stimulation; however, once activated, they underwent more robust contraction in vivo and more apoptosis in vitro. In addition, B7-H1-deficient CD8 T cells were more sensitive to Ca-dependent and Fas ligand-dependent killing by cytotoxic T lymphocytes. Activation-induced Bcl-x(L) expression was lower in activated B7-H1-deficient CD8 T cells, whereas Bcl-2 and Bim expression were comparable to the wild type. Transfer of effector B7-H1-deficient CD8 T cells failed to suppress tumor growth in vivo. Thus, upregulation of B7-H1 on primed T cells helps effector T cells survive the contraction phase and consequently generate optimal protective immunity.
ISSN:0022-1767
1550-6606
DOI:10.4049/jimmunol.1003976