Flexible migration program regulates γδ T-cell involvement in humoral immunity
Flexible migration program regulates γδ T-cell involvement in humoral immunity
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DOI：
10.1182/blood-2003-04-1016
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发表时间：
2003-11-15
期刊：
影响因子：
20.3
通讯作者：
Moser, B
中科院分区：
文献类型：
--
作者：
Brandes, M;Willimann, K;Moser, B
γ δ T细胞在它们的迁移潜力和对抗微生物免疫的贡献方面都没有充分的定义。在这里，我们研究了人血γ δ T细胞和相关细胞系的迁移概况，并将这些发现与它们在次级淋巴组织中的分布及其在B细胞共培养物中的功能相关联。我们发现，静息γ δ T细胞的特征在于类似于先天免疫系统的细胞的炎性迁移程序。然而，T细胞受体（TCR）触发导致淋巴结（LN）归巢程序的快速但短暂的诱导，如通过功能性CCR 7表达和伴随的CCR 5以及较小程度的CCR 2的表达和功能的降低所证明的。此外，LN归巢程序反映在胃肠道淋巴组织中存在γ δ T细胞，特别是在B细胞滤泡的生发中心内的簇中。与这些发现一致，V γ Vdelta-TCR触发再适合于必需B细胞共刺激分子（包括CD 40 L、OX 40、CD 70和ICOS）的显著表达。此外，γ δ T细胞显示在体外抗体产生期间提供有效的B细胞帮助。总的来说，我们的研究结果同意γ δ T细胞在抗微生物反应早期的体液免疫中的作用。(C)2003年，美国血液学会。
gammadelta T cells are inadequately defined both in terms of their migration potential and contribution to antimicrobial immunity. Here, we have examined the migration profile of human blood gammadelta T cells and related cell lines and correlated these findings with their distribution in secondary lymphoid tissues and their function in B-cell cocultures. We find that resting gammadelta T cells are characterized by an inflammatory migration program similar to cells of the innate immune system. However, T-cell receptor (TCR) triggering resulted in the rapid but transient induction of a lymph node (LN)-homing program, as evidenced by functional CCR7 expression and concomitant reduction in expression and function of CCR5 and, to a lesser degree, CCR2. Moreover, the LN-homing program was reflected by the presence of gammadelta T cells in gastrointestinal lymphoid tissues, notably in clusters within germinal centers of B-cell follicles. In line with these findings, VgammaVdelta-TCR triggering re-suited in prominent expression of essential B-cell costimulatory molecules, including CD40L, OX40, CD70, and ICOS. Furthermore, gammadelta T cells were shown to provide potent B-cell help during in vitro antibody production. Collectively, our findings agree with a role for gammadelta T cells in humoral immunity during the early phase of antimicrobial responses. (C) 2003 by The American Society of Hematology.