Oral mucosal immunity and HIV infection: current status
Oral mucosal immunity and HIV infection: current status
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DOI：
10.1034/j.1601-0825.2002.00013.x
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发表时间：
2002-01-01
期刊：
影响因子：
3.8
通讯作者：
Sweet, SP
中科院分区：
文献类型：
--
作者：
Challacombe, SJ;Sweet, SP
有一个悖论，深刻的HIV诱导的免疫缺陷是目前全身，而大多数感染与HIV疾病的存在或启动在粘膜表面。因此，有必要了解特异性和非特异性的粘膜保护机制，对艾滋病毒及其共病原体。大多数HIV感染是由于病毒穿过粘膜而发生的。粘膜表面对HIV感染的抵抗可能与某些个体中HIV特异性CD 8（+）T细胞应答有关，可能是保护性疫苗设计的基础。然而，粘膜中的T细胞、巨噬细胞和树突状细胞可能是HIV进入的门户。HIV的转胞吞作用可以从粘膜表面发生到粘膜下表面，反之亦然，并且可以被粘膜免疫球蛋白和上皮细胞内的中和伊加抑制。HIV引起的口腔上皮细胞的改变，连同粘膜CD 4（+）T细胞的损伤和随之而来的细胞因子分泌的改变，可能有助于继发性感染。它也似乎是艾滋病毒感染与唾液伊加水平下降，虽然在唾液和血清中的伊加浓度之间的二分法已被报道。然而，粘蛋白抗体反应似乎得以维持。粘膜免疫抗HIV的可能性受到了相当大的关注，有证据表明分泌型伊加抗体对不同的HIV毒株具有中和作用。除了特异性免疫因子外，先天性非特异性因子可能在保护粘膜表面方面具有重要意义，包括乳铁蛋白、分泌性白细胞蛋白酶抑制剂、粘蛋白、富含脯氨酸的蛋白质和半胱氨酸蛋白酶抑制剂。这些化合物可能是外用制剂中有用的候选杀病毒剂。因此，体液，细胞和先天免疫机制，以及淋巴细胞-上皮细胞的相互作用，可能都是受损的粘膜表面作为HIV感染的结果，并可能有助于粘膜感染过程的易感性。
There is a paradox that profound HIV-induced immunodeficiency is present systemically, whereas the majority of infections associated with HIV disease are present or initiated at mucosal surfaces. There is therefore a need to understand both specific and non-specific mechanisms of mucosal protection against HIV and its copathogens. The majority of HIV infections occur as a result of the passage of virus across mucosal membranes. Resistance to HIV infection at mucosal surfaces may be related to HIV-specific CD8(+) T cell responses in some individuals and may be the basis for protective vaccine design. However, T-cells, macrophages and dendritic cells in mucosa may be a portal of entry for HIV. Transcytosis of HIV can occur from the mucosal to the submucosal surface and vice versa, and may be inhibited by mucosal immunoglobulins and neutralizing IgA within epithelial cells. HIV-induced alterations to oral epithelial cells, together with impairment of mucosal CD4(+) T-cells and consequent altered cytokine secretion, may contribute to secondary infections. It also appears that HIV infection is associated with decreased salivary IgA levels, although a dichotomy between IgA concentrations in saliva and serum has been reported. Mucosal antibody responses, however, seem to be maintained. Considerable attention has been given to the possibility of mucosal immunization against HIV and there is evidence that secretory IgA antibody is neutralizing to different HIV strains. In addition to specific immune factors, it is likely that innate nonspecific factors may be significant in protecting mucosal surfaces, including lactoferrin, secretory leukocyte protease inhibitor, mucins, proline rich proteins and cystatins. These may be useful candidate virucides in topical preparations. Thus humoral, cellular and innate immune mechanisms, as well as lymphocyte-epithelial interactions, may all be impaired at mucosal surfaces as a result of HIV infection and may contribute to the susceptibility of mucosa to infective processes.