Type II membrane protein CD69 regulates the formation of resting T-helper memory
Type II membrane protein CD69 regulates the formation of resting T-helper memory
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DOI：
10.1073/pnas.1118539109
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发表时间：
2012-04
期刊：
影响因子：
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通讯作者：
K. Shinoda;K. Tokoyoda;A. Hanazawa;Koji Hayashizaki;S. Zehentmeier;H. Hosokawa;C. Iwamura;H. Koseki;D. Tumes;A. Radbruch;T. Nakayama
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文献类型：
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作者：
K. Shinoda;K. Tokoyoda;A. Hanazawa;Koji Hayashizaki;S. Zehentmeier;H. Hosokawa;C. Iwamura;H. Koseki;D. Tumes;A. Radbruch;T. Nakayama
记忆性辅助性T淋巴细胞（Th）对于维持获得性免疫以消除感染性病原体至关重要。我们以前已经证明，大多数记忆Th淋巴细胞驻留和休息的骨髓（BM）的基质壁龛。然而，关于BM记忆Th淋巴细胞的产生和维持的分子基础知之甚少。在这里，我们表明，CD69缺陷的效应CD4 T淋巴细胞不能重新定位到并坚持在BM中，因此分化成记忆细胞。因此，CD69缺陷型CD4 T细胞不能促进高亲和力抗体的产生和在免疫应答的后期BM长寿浆细胞的产生。因此，CD69对于专业记忆Th淋巴细胞的产生和维持至关重要，其可以有效地帮助晚期体液免疫。CD69缺陷小鼠的免疫记忆缺陷也突出了BM在Th记忆建立中的重要作用。
Memory T-helper (Th) lymphocytes are crucial for the maintenance of acquired immunity to eliminate infectious pathogens. We have previously demonstrated that most memory Th lymphocytes reside and rest on stromal niches of the bone marrow (BM). Little is known, however, regarding the molecular basis for the generation and maintenance of BM memory Th lymphocytes. Here we show that CD69-deficient effector CD4 T lymphocytes fail to relocate into and persist in the BM and therefore to differentiate into memory cells. Consequently, CD69-deficient CD4 T cells fail to facilitate the production of high-affinity antibodies and the generation of BM long-lived plasma cells in the late phase of immune responses. Thus, CD69 is critical for the generation and maintenance of professional memory Th lymphocytes, which can efficiently help humoral immunity in the late phase. The deficit of immunological memory in CD69-deficient mice also highlights the essential role of BM for the establishment of Th memory.