科研之友
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摘要
Recognition of viral antigenic peptides bound to major histocompatibility complex class I molecules (MHCI) by TCR is critical for initiating the responses of CD8(+) T cells that ultimately lead to elimination of virus-infected cells. This antigen recognition is enhanced by the CD8 coreceptor through its interaction with the peptide-MHCI complexes (pMHCI). Mouse CD8 alpha beta can form two different complexes with pMHCI via either the CD8 alpha- or CD8 beta-dominated interaction. To understand the functional significance of these complexes in vivo, we generated Tg mice carrying a variant CD8 alpha beta (CD8 alpha(m3)beta) capable of forming only the CD8 beta-dominated CD8 alpha beta/pMHCI complex. These mice show sub-optimal thymic differentiation with reduced populations of CD8(+) single-positive thymocytes. Tg CD8(+) T cells exhibit a compromised developmental capacity when competing with CD8(+) T cells from B6 mice in mixed bone marrow chimera experiments. However, once these CD8(+) T cells have emigrated to the peripheral lymphoid organs, they exhibit normal effector function against viral infection. Our observations indicate that, in addition to the CD8 activity conferred by CD8 beta-dominated CD8 alpha beta/pMHCI complexes, full thymocyte differentiation requires additional coreceptor activities conferred by CD8 alpha alpha and/or CD8 alpha beta with CD8 alpha-dominated CD8/pMHCI complexes.
- 出版日期2010-3
- 单位Biogen Idec
