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首页> 外文期刊>Clinical and Experimental Immunology: An Official Journal of the British Society for Immunology >The skin homing receptor cutaneous leucocyte-associated antigen (CLA) is up-regulated by Leishmania antigens in T lymphocytes during active cutaneous leishmaniasis.
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The skin homing receptor cutaneous leucocyte-associated antigen (CLA) is up-regulated by Leishmania antigens in T lymphocytes during active cutaneous leishmaniasis.

机译：在活动性皮肤利什曼病期间，T淋巴细胞中的利什曼原虫抗原上调了皮肤归巢受体皮肤白细胞相关抗原（CLA）。

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摘要

The cutaneous leucocyte-associated antigen receptor (CLA) can direct Leishmania-specific T lymphocytes towards inflamed skin lesions. Homing receptors [CLA, lymphocyte-associated antigen 1 (LFA-1) or CD62L] were analysed in lymphocytes from blood and cutaneous leishmaniasis (CL) lesions. CL patients with active lesions (A-CL) presented lower levels of T lymphocytes expressing the CLA(+) phenotype (T CD4(+) = 10.4% +/- 7.5% and T CD8(+) = 5.8% +/- 3.4%) than did healthy subjects (HS) (T CD4(+) = 19.3% +/- 13.1% and T CD8(+) = 21.6% +/- 8.8%), notably in T CD8(+) (P < 0.001). In clinically cured patients these percentages returned to levels observed in HS. Leishmanial antigens up-regulated CLA in T cells (CLA(+) in T CD4(+) = 33.3% +/- 14.1%; CLA(+) in T CD8(+) = 22.4% +/- 9.4%) from A-CL but not from HS. An enrichment of CLA(+) cells was observed in lesions (CLA(+) in T CD4(+) = 45.9% +/- 22.5%; CLA(+) in T CD8(+) = 46.4% +/- 16.1%) in comparison with blood (CLA(+) in T CD4(+) = 10.4% +/- 7.5%; CLA(+) in T CD8(+) = 5.8% +/- 3.4%). Conversely, LFA-1 was highly expressed in CD8(+) T cells and augmented in CD4(+) T from peripheral blood of A-CL patients. In contrast, CD62L was not affected. These results suggest that Leishmania antigens can modulate molecules responsible for migration to skin lesions, potentially influencing the cell composition of inflammatory infiltrate of leishmaniasis or even the severity of the disease.
机译：皮肤白细胞相关抗原受体（CLA）可以将利什曼原虫特异性T淋巴细胞导向发炎的皮肤病变。在血液和皮肤利什曼病（CL）病变的淋巴细胞中分析了归巢受体[CLA，淋巴细胞相关抗原1（LFA-1）或CD62L]。具有活动性病变（A-CL）的CL患者表现出较低水平的T淋巴细胞表达CLA（+）表型（T CD4（+）= 10.4％+/- 7.5％和T CD8（+）= 5.8％+/- 3.4 ％）高于健康受试者（HS）（T CD4（+）= 19.3％+/- 13.1％和T CD8（+）= 21.6％+/- 8.8％），尤其是T CD8（+）（P <0.001 ）。在临床治愈的患者中，这些百分比恢复到HS中观察到的水平。利什曼原虫抗原上调了T细胞中的CLA（T CD4（+）中的CLA（+）= 33.3％+/- 14.1％; T CD8（+）中的CLA（+）= 22.4％+/- 9.4％） -CL，但不是来自HS。在病变中观察到CLA（+）细胞富集（T CD4（+）中的CLA（+）= 45.9％+/- 22.5％; T CD8（+）中的CLA（+）= 46.4％+/- 16.1％ ）与血液相比（T CD4（+）中的CLA（+）= 10.4％+/- 7.5％; T CD8（+）中的CLA（+）= 5.8％+/- 3.4％）。相反，从A-CL患者的外周血中，LFA-1在CD8（+）T细胞中高表达，并在CD4（+）T中增加。相反，CD62L不受影响。这些结果表明，利什曼原虫抗原可调节负责迁移至皮肤病变的分子，从而潜在地影响利什曼原虫病的炎性浸润的细胞组成，甚至影响疾病的严重性。

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