Peptide immunization indicates that CD8+ T cells are the dominant effector cells in trinitrophenyl-specific contact hypersensitivity
Peptide immunization indicates that CD8+ T cells are the dominant effector cells in trinitrophenyl-specific contact hypersensitivity
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DOI：
10.1046/j.1523-1747.2000.00038.x
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发表时间：
2000-08-01
影响因子：
6.5
通讯作者：
Weltzien, HU
中科院分区：
文献类型：
--
作者：
Martin, S;Lappin, MB;Weltzien, HU
参与接触性超敏反应的效应T细胞群体的身份仍然是有疑问的，有证据表明促进CD 4（+）或CD 8（+）T细胞。以前的实验研究依赖于使用抗体体内耗竭T细胞亚群，或使用具有CD 4（+）或CD 8（+）T细胞介导的免疫缺陷的敲除小鼠。为了解决I类和II类介导的T细胞活化途径在免疫系统完整的小鼠接触性超敏反应中的作用，我们利用了各种三硝基苯基衍生肽，其与H-2 K（B）（主要组织相容性复合物I类）或H-2 I-A（B）（主要组织相容性复合物II类）特异性结合。皮下注射主要组织相容性复合物II类特异性，但不是I类结合，半抗原衍生肽在不完全弗氏佐剂诱导特异性，虽然低，接触性超敏反应三硝基氯苯。当骨髓来源的树突状细胞，但是，脉冲与相同的肽和皮内给药，观察到相反的结果，即I类结合肽诱导的接触性超敏反应后观察到的类似于表皮三硝基氯苯应用。与此相反，树突状细胞脉冲与主要组织相容性复合物II类结合肽没有可重复的敏感性接触超敏反应。令人惊讶的是，两种免疫方案都有效地诱导了CD 8（+）效应T细胞。这些结果支持了CD 8（+）T细胞是介导接触性超敏反应的主要效应细胞群的观点，并且CD 4（+）T细胞亚群仅贡献很少。
The identity of the effector T cell population involved in contact hypersensitivity is still questionable with evidence promoting both CD4(+) or CD8(+) T cells. Previous experimental studies have relied on the in vivo depletion of T cell subsets using antibody, or the use of knock-out mice with deficiencies in either CD4(+) or CD8(+) T cell-mediated immunity. To address the role of the class I- and class II-mediated pathways of T cell activation in contact hypersensitivity responses in mice with an intact immune system, we utilized various trinitrophenyl-derivatized peptides, which bind specifically with H-2K(b) (major histocompatibility complex class I) or H-2I-A(b) (major histocompatibility complex class II). The subcutaneous injection of major histocompatibility complex class II-specific, but not of class I-binding, hapten-derivatized peptides in incomplete Freund's adjuvant induced specific, albeit low, contact hypersensitivity responsiveness to trinitrochlorobenzene. When bone-marrow-derived dendritic cells, however, were pulsed with the same peptides and administered intradermally, the opposite result was observed, namely that the class I binding peptides induced contact hypersensitivity responses similar to that observed after epicutaneous trinitrochlorobenzene application. In contrast, dendritic cells pulsed with major histocompatibility complex class II binding peptides did not reproducibly sensitize for contact hypersensitivity responses. Surprisingly, both immunization protocols efficiently induced CD8(+) effector T cells. These results support the notion that CD8(+) T cells are the dominant effector population mediating contact hypersensitivity responsiveness and that the CD4(+) T cell subset only contributes little if at all.