In vasculitis of small muscular arteries, activation of vessel-infiltrating CD8 T cells seems to be antigen-independent
In vasculitis of small muscular arteries, activation of vessel-infiltrating CD8 T cells seems to be antigen-independent
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DOI：
10.1007/s00428-017-2264-2
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发表时间：
2018-02-01
期刊：
影响因子：
3.5
通讯作者：
Kanno, Hiroyuki
中科院分区：
文献类型：
--
作者：
Kobayashi, Mikiko;Ogawa, Eisaku;Kanno, Hiroyuki
结节性多动脉炎（PAN）和局限性PAN的病因仍然是未知的，虽然T细胞介导的免疫机制已被认为。CD 8 T细胞不仅参与抗原依赖性适应性免疫系统，还参与抗原非依赖性先天免疫系统。非抗原活化的CD 8 T细胞表达独特的表型：颗粒酶B（GrB）阳性/CD 25阴性/程序性死亡-1（PD-1）阴性。本研究的目的是评估T细胞，特别是先天性CD 8 T细胞，在血管炎的发展中的参与。本文收集了28例皮肤小肌性血管炎（CVSMA）的皮肤活检标本。该系列包括21例皮肤动脉炎，3例PAN，4例类风湿性血管炎。排除了抗神经元胞浆抗体相关性血管炎病例。免疫组化法检测血管炎病灶中浸润淋巴细胞的表型。在大多数CVSMA病例中，浸润内膜的CD 8 T细胞数量高于CD 4 T细胞，并观察到大量GrB阳性细胞（代表活化的CD 8 T细胞）。然而，GrB/CD 25双阳性细胞，对应于抗原活化的T细胞，在少数病例中非常少。未检测到PD-1阳性细胞，PD-1也在抗原活化的CD 8 T细胞上表达。我们得出结论，T细胞介导的免疫机制，涉及细胞毒性CD 8 T细胞，可能在CVSMA的发展中发挥作用。活化的CD 8 T细胞中CD 25的低表达表明活化是抗原非依赖性的。
The etiology of polyarteritis nodosa (PAN) and localized PAN is still unknown, although a T cell-mediated immune mechanism has been considered. CD8 T cells participate not only in the antigen-dependent adaptive immune system, but also in the antigen-independent innate immune system. Non-antigen-activated CD8 T cells express a unique phenotype: granzyme B (GrB) positive /CD25 negative /programmed death-1 (PD-1) negative. The aims of this study were to assess the participation of T cells, especially innate CD8 T cells, in the development of vasculitis. Twenty-eight consecutive cases of skin biopsy specimens with cutaneous vasculitis of small muscular arteries (CVSMA) were retrieved. The series comprises of 21 cases of cutaneous arteritis, three cases of PAN, and four cases of rheumatoid vasculitis. Cases of antineutrophil cytoplasmic antibody-associated vasculitis were excluded. The phenotypes of infiltrating lymphocytes in vasculitis lesions were evaluated by immunohistochemistry. In most cases of CVSMA, the number of CD8 T cells infiltrating the intima was higher than that of CD4 T cells, and significant numbers of GrB-positive cells, which represent activated CD8 T cells, were observed. However, GrB/CD25-double-positive cells, which correspond to antigen-activated T cells, were very few in a small number of cases. Cells positive for PD-1, which is also expressed on antigen-activated CD8 T cells, were not detected. We conclude that a T cell-mediated immune mechanism, involving cytotoxic CD8 T cells, may play a role in the development of CVSMA. Low expression of CD25 in activated CD8 T cells suggests that activation was antigen-independent.