英语翻译Another possible culprit contributing to HIV enteropathy
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英语翻译
Another possible culprit contributing to HIV enteropathy is local activation of the GI immune system.Infiltration of cytotoxic CB8 T cell,for example,has been observed to result in villous atrophy in individuals with celiac disease.Mitogenic T-cell stimulation is sufficient to cause enterocyte abnormalities in ex vivo tissue explants.Moreover,proinflammatory cytokines such as tumor necrosis factor(TNF),interferon(IL)-12,and IL-8 have been implicated in the of inflammatory bowel disease.In particular,high levels of TNF are thought to cause apoptosis of enterocytes,and treatment with anti-TNF antibodies is of great clinical benefit to individual with Crohn’s disease.With respect to HIV enteropathy,local immune activation likely plays a formative role,indeed,high levels of proinflammatory mediators such as the beta chemokines IL-6,IL-10,and IFN are found in the lamina propria of the colon of HIV-infected individuals.Moreover,the degree of inflammation within the GI tract correlates with viral replication.Although systemic immune activation is a hallmark of HIV-infection,its etiology has remained elusive.However,it has been reasonably postulated that local bacterial invasion across the damaged tight epithelial barrier may allow microbial products to stimulate the immune system locally,presumably,through receptors such as Toll-like receptors.Because HIV prefers to infect activated CD4 T cells,a crucial consequence of induction of local inflammation by any means that also involves CD4 T cells activation may serve to provide additional targets for the virus,thus augmenting its replication .
Another possible culprit contributing to HIV enteropathy is local activation of the GI immune system.Infiltration of cytotoxic CB8 T cell,for example,has been observed to result in villous atrophy in individuals with celiac disease.Mitogenic T-cell stimulation is sufficient to cause enterocyte abnormalities in ex vivo tissue explants.Moreover,proinflammatory cytokines such as tumor necrosis factor(TNF),interferon(IL)-12,and IL-8 have been implicated in the of inflammatory bowel disease.In particular,high levels of TNF are thought to cause apoptosis of enterocytes,and treatment with anti-TNF antibodies is of great clinical benefit to individual with Crohn’s disease.With respect to HIV enteropathy,local immune activation likely plays a formative role,indeed,high levels of proinflammatory mediators such as the beta chemokines IL-6,IL-10,and IFN are found in the lamina propria of the colon of HIV-infected individuals.Moreover,the degree of inflammation within the GI tract correlates with viral replication.Although systemic immune activation is a hallmark of HIV-infection,its etiology has remained elusive.However,it has been reasonably postulated that local bacterial invasion across the damaged tight epithelial barrier may allow microbial products to stimulate the immune system locally,presumably,through receptors such as Toll-like receptors.Because HIV prefers to infect activated CD4 T cells,a crucial consequence of induction of local inflammation by any means that also involves CD4 T cells activation may serve to provide additional targets for the virus,thus augmenting its replication .
另一种可能造成艾滋病毒的罪魁祸首肠病是胃肠免疫系统的本地激活.CB8细胞毒性T细胞浸润,例如,已被观察到的结果,在个人与腹腔疾病绒毛萎缩.有丝分裂的T -细胞的刺激就足以在离体组织块肠异常.此外,如肿瘤坏死因子(TNF),干扰素素(IL)-12和IL - 8炎性细胞因子有牵连的炎性肠道疾病.特别是,高水平的TNF被认为是导致肠上皮细胞凋亡,并与抗TNF抗体治疗具有临床受益与克罗恩病的个体.关于艾滋病毒肠病,局部免疫激活可能发挥的作用形成的,事实上,如乙型趋化因子的IL - 6和IL - 10的炎症介质水平高,干扰素是在感染艾滋病毒的发现结肠固有层个人.此外,胃肠道内的炎症程度与病毒复制密切相关.虽然全身免疫激活是艾滋病毒感染的特点,其病因一直难以实现.然而,它一直在合理推测,当地上皮屏障受损的紧张可能使细菌入侵微生物产品,以刺激免疫系统在本地,想必通过诸如Toll样受体受体等.由于艾滋病毒感染喜欢的CD4 T细胞活化,有局部炎症任何方式诱导后果,也涉及到关键的CD4 T细胞的活化可能有助于提供额外的目标的病毒,从而充实其复制.
英语翻译Another possible culprit contributing to HIV enteropathy
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