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人类免疫缺陷病毒感染中的肠道免疫异常。

Enteric immunologic abnormalities in human immunodeficiency virus infection.

作者信息

Ullrich R, Zeitz M, Riecken E O

机构信息

Department of Gastroenterology, Medical Clinic, Free University of Berlin, Germany.

出版信息

Semin Liver Dis. 1992 May;12(2):167-74. doi: 10.1055/s-2007-1007388.

Abstract

The intestinal mucosa is an important portal of entry of HIV, and HIV-infected mononuclear cells are found in the intestinal lamina propria of 30 to 50% of HIV-infected patients even at early stages of the disease. HIV infection of epithelial cells has not consistently been detected and is still controversial. Intestinal T cells are phenotypically and functionally distinct from circulating T cells, especially in their state of activation and differentiation, which both affect the replication and cytopathicity of HIV. An increase in CD8+ cells and variable decreases in CD4+ cells have been found in the intestinal lamina propria by immunohistologic studies, resulting in a decreased CD4 to CD8 ratio; in addition, CD25 expression is reduced. Changes in intraepithelial lymphocytes are unclear. B-cell differentiation seems to be disturbed because IgA plasma cells and IgA2 secretion are reduced. Depletion or functional impairment of activated mucosal lamina propria lymphocytes by HIV infection could explain the breakdown of the mucosal immune barrier leading to opportunistic diseases; in addition, due to the interrelationship between mucosal immune system and epithelium, these changes might be responsible for the partial bowel atrophy and maturational defects in enterocytes of HIV-infected patients.

摘要

肠道黏膜是HIV重要的进入门户,即使在疾病早期,30%至50%的HIV感染患者的肠道固有层中也能发现被HIV感染的单核细胞。上皮细胞的HIV感染尚未得到一致检测,仍存在争议。肠道T细胞在表型和功能上与循环T细胞不同,尤其是在其激活和分化状态方面,这两者都会影响HIV的复制和细胞病变效应。免疫组织学研究发现,肠道固有层中CD8 +细胞增加,CD4 +细胞可变减少,导致CD4与CD8比值降低;此外,CD25表达降低。上皮内淋巴细胞的变化尚不清楚。B细胞分化似乎受到干扰,因为IgA浆细胞和IgA2分泌减少。HIV感染导致活化的黏膜固有层淋巴细胞耗竭或功能受损,这可以解释黏膜免疫屏障的破坏导致机会性疾病;此外,由于黏膜免疫系统与上皮之间的相互关系,这些变化可能是HIV感染患者部分肠萎缩和肠上皮细胞成熟缺陷的原因。

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