Lichenoid tissue reaction (LTR) induced by local transfer of Ia-reactive T-cell clones. II. LTR by epidermal invasion of cytotoxic lymphokine-producing autoreactive T cells.

细胞毒性T细胞 淋巴因子 生物 克隆(Java方法) 抗原 免疫学 单克隆抗体 淋巴毒素 T淋巴细胞 分子生物学 过继性细胞移植 T细胞 免疫系统 抗体 体外 基因 遗传学
作者
Tetsuo Shiohara,N. Moriya,Tomoko Mochizuki,Masaji Nagashima
出处
期刊:Journal of Investigative Dermatology [Elsevier BV]
卷期号:89 (1): 8-14 被引量:19
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摘要

Recent studies have suggested that T lymphocytes with helper phenotype may play an important role in the pathogenesis of lichenoid tissue reactions (LTR). In order to elucidate whether murine self-Ia-specific autoreactive T cells with helper phenotype can induce LTR in naive syngeneic hosts, two clones of autoreactive cloned T cells with both helper and cytotoxic activities, capable of producing the cytotoxic lymphokines gamma interferon and lymphotoxin in response to self-Ia antigens, were examined for their ability to induce LTR. One clone, BB5, when injected into footpads of syngeneic hosts, induced prominent epidermotropic cellular infiltrates that led to basal vacuolar degeneration and Civatte body formation; the other clone, C10, did not. No difference between BB5 and C10 was detected with respect to their ability to induce delayed-type hypersensitivity reactions. Immunohistochemical studies using anti-Lyt monoclonal antibodies showed that BB5-induced LTR was induced by the epidermal invasion of the injected BB5 cells themselves. We further observed that the infusion of BB5 cells not only resulted in Ia antigen expression on keratinocytes, but was also accompanied by a morphologic change in Langerhans cells at 24 h, when the epidermal invasion had not yet developed. However, similar observations were also observed with C10 cells, indicating that Ia expression on keratinocytes may not be a prerequisite for the induction of LTR.

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