期刊
JOURNAL OF IMMUNOLOGY
卷 185, 期 6, 页码 3140-3148出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.0902487
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资金
- Institut National de la Sante et de la Recherche Medicale
- Institut Paoli Calmettes
- Groupement des Entreprises Francaises dans la Lutte Contre le Cancer
- Infrastructures en Biologie Sante et Agronomie
- Association pour la Recherche sur le Cancer
B and T lymphocyte attenuator (BTLA), like its relative programmed cell death-1 (PD-1), is a receptor that negatively regulates murine T cell activation. However, its expression and function on human T cells is currently unknown. We report in this study on the expression of BTLA in human T cell subsets as well as its regulation on virus-specific T cells during primary human CMV infection. BTLA is expressed on human CD4(+) T cells during different stages of differentiation, whereas on CD8(+) T cells, it is found on naive T cells and is progressively downregulated in memory and differentiated effector-type cells. During primary CMV infection, BTLA was highly induced on CMV-specific CD8(+) T cells immediately following their differentiation from naive cells. After control of CMV infection, BTLA expression went down on memory CD8(+) cells. Engagement of BTLA by mAbs blocked CD3/CD28-mediated T cell proliferation and Th1 and Th2 cytokine secretion. Finally, in vitro blockade of the BTLA pathway augmented, as efficient as anti-PD-1 mAbs, allogeneic as well as CMV-specific CD8(+) T cell proliferation. Thus, our results suggest that, like PD-1, BTLA provides a potential target for enhancing the functional capacity of CTLs in viral infections. The Journal of Immunology, 2010, 185: 3140-3148.
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