Gamma delta T cells assist alpha beta T cells in adoptive transfer of contact sensitivity.
Gamma delta T cells assist alpha beta T cells in adoptive transfer of contact sensitivity.
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DOI：
10.4049/jimmunol.149.11.3503
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发表时间：
1992-12
影响因子：
4.4
通讯作者：
W. Ptak;P. Askenase
中科院分区：
文献类型：
--
作者：
W. Ptak;P. Askenase
对接触致敏剂如苦基氯或恶唑酮的皮肤免疫应答是体内T细胞介导的免疫的经典表现。事实上，T细胞介导的免疫的第一个文件是过继转移接触敏感性（CS）反应的能力。虽然现在已经清楚Ag/MHC限制性α β TCR阳性效应T细胞负责24至48 h CS应答，但小鼠中Thy-1+细胞的其他亚群也参与CS的诱发。因此，需要Thy-1+、CD 5+、CD 3-、B220+、半抗原特异性、非MHC限制性的早期作用细胞通过导致局部5-羟色胺释放来启动CS应答，这允许血管外募集晚期作用的α β TCR+、CS效应T细胞。这项研究描述了另一种T细胞群，这是通过α β T细胞过继转移CS所需的。在体外处理的CS效应细胞的混合物与仓鼠单克隆抗体的γ δ TCR，与兔补体，或通过淘选抗仓鼠Ig包被的培养皿，大大减少了CS反应性的后续转移，而不影响CS起始细胞，或后期作用，α β TCR+ CS效应T细胞。用抗α β TCR mAb处理的免疫细胞，或在抗γ δ TCR淘选后作为贴壁细胞从培养皿中回收的免疫细胞（即，γ δ TCR富集细胞），重建了抗γ δ TCR处理的免疫细胞的能力（即，α β TCR富集的细胞）以转移24小时CS应答性。辅助CS效应子α β T细胞的γ δ T细胞的表型为：CD 3+、CD 4-和CD 8+。辅助α β T细胞的γ δ T细胞不是Ag特异性的，因为来自苦酰氯免疫的供体的抗α β-TCR处理的细胞（γ δ T富集的）辅助来自恶唑酮免疫的供体的α β T细胞（抗γ δ TCR处理的），相反，来自恶唑酮免疫的供体的γ δ T细胞辅助来自苦酰氯免疫的供体的α β T细胞。此外，CS调节γ δ T细胞不是MHC限制性的，因为来自H2 d或H2 b供体的γ δ T细胞可以辅助来自H2k供体的α β T细胞。得出的结论是，在CS的过继转移中，需要非Ag特异性、非MHC限制性γ δ T细胞的调节群体来辅助免疫效应物、Ag/MHC特异性α β T细胞。
Cutaneous immune responses to contact sensitizers such as picryl chloride or oxazolone, are classical manifestations of T cell-mediated immunity in vivo. In fact, the first documentation of T cell-mediated immunity was the ability to adoptively transfer contact sensitivity (CS) responses. Although it is now clear that Ag/MHC-restricted alpha beta TCR positive effector T cells are responsible for 24 to 48 h CS responses, other subsets of Thy-1+ cells in mice also participate in the elicitation of CS. Thus, Thy-1+, CD5+, CD3-, B220+, hapten-specific, non-MHC-restricted early-acting cells are required to initiate CS responses by leading to local serotonin release, which allows for extravascular recruitment of the late-acting, alpha beta TCR+, CS effector T cells. This study describes another T cell population that is needed for the adoptive transfer of CS by alpha beta T cells. In vitro treatment of a mixture of CS effector cells with hamster mAb to gamma delta TCR, together with rabbit complement, or by panning on anti-hamster Ig-coated dishes, diminished substantially the subsequent transfer of CS reactivity without affecting either CS-initiating cells, or the later-acting, alpha beta TCR+ CS effector T cells. Immune cells treated with anti-alpha beta TCR mAb, or recovered as adherent cells from petri dishes after anti-gamma delta TCR panning (i.e., gamma delta TCR-enriched cells), reconstituted the ability of anti-gamma delta TCR-treated immune cells (i.e., alpha beta TCR-enriched cells) to transfer 24-h CS responsiveness. The phenotype of the gamma delta T cells that assisted CS effector alpha beta T cells was: CD3+, CD4-, and CD8+. The gamma delta T cells that assisted alpha beta T cells were not Ag-specific since anti-alpha beta-TCR-treated cells (gamma delta T-enriched) from picryl chloride immunized donors aided alpha beta T cells (anti-gamma delta TCR-treated) from oxazolone-immunized donors, and conversely gamma delta T cells from oxazolone-immunized donors aided alpha beta T cells from picryl chloride immunized donors. Furthermore, the CS-regulating gamma delta T cells were not MHC-restricted because gamma delta T cells from H2d or H2b donors could assist alpha beta T cells from H2k donors. It was concluded that a regulatory population of non-Ag specific, non-MHC-restricted gamma delta T cells was needed to assist immune effector, Ag/MHC-specific alpha beta T cells in the adoptive transfer of CS.