HIV感染的分子免疫发病机理

从细胞因子分布型失衡、活化诱导的T细胞凋亡、HIV基因产物的作用、抗原呈递细胞缺陷、粘附受体与趋化因子受体的作用等方面综述了HIV感染的分子免疫发病机理。     

白癜风发病机制的研究

白癜风是一种常见的皮肤色素脱失性疾病,其发病机制迄今尚未明确。该病发病机制复杂,涉及遗传、免疫、氧化应激、神经体液、黑素细胞凋亡和丢失、紫外线损伤机制等。     

免疫重建炎性综合征的研究进展

免疫重建炎性综合征是一种针对已存在的机会性感染或其他抗原的病理性炎症反应,常发生于HIV感染的患者经过抗逆转录病毒治疗后,目前发病机制尚不完全清楚,可能与机体免疫功能失调等多种因素有关.免疫重建炎性综合征的表现多种多样,主要介绍皮肤相关的一些临床表现、诊断、治疗和预防.尽管免疫重建炎性综合征最初研究仅涉及HIV阳性的人群,但研究发现还存在其他自身免疫炎症性疾病相关的免疫重建炎性综合征,因此,有必要进一步研究.     

尖锐湿疣患者淋巴细胞凋亡调控蛋白的表达

尖锐湿疣(CA)是由人乳头瘤病毒(HPV)感染引起的一种性病,CA的发生、发展和转归与患者机体免疫功能尤其是细胞免疫功能关系密切^[1],而患者机体免疫功能与淋巴细胞凋亡状况关系密切^[2]。我们用流式细胞计数法检测了CA患者外周血淋巴细胞(PBLC)凋亡调控蛋白(Fas、Fas-L、Bcl-2)的表达,旨在从凋亡角度探讨CA的免疫发病机制。     

梅毒及其与HIV合并感染的免疫机制研究

梅毒不同的临床表现多取决于细胞免疫的强度和持续时间,巨噬细胞、CD4+T淋巴细胞、CD8+T淋巴细胞、自然杀伤细胞均在梅毒感染的细胞免疫中起重要作用.而与HIV合并感染更是增加了其免疫机制的复杂性和临床表现的多形性.在与HIV合并感染的二期梅毒中,Th1、Th17型细胞免疫增强,而Th2型细胞免疫的改变目前尚不确切.梅毒与HIV合并感染时两者的免疫机制、病程以及疗效均可能发生影响,因此,有必要进行梅毒患者的HIV筛查和HIV感染者的梅毒筛查,以便获得及时有效的治疗.     

中药治疗银屑病实验研究进展

银屑病是一种慢性复发性炎症性皮肤病,大量研究表明它的发病与遗传、免疫、炎症、细胞增殖与凋亡、神经介质等多种因素相关。现有的中药治疗银屑病的实验研究主要是基于上述几个基本机制。     

活化诱导的细胞死亡与皮肤病

活化诱导的细胞死亡是机体通过一系列复杂的分子事件在细胞被活化的同时而启动的一种有序并适度的细胞凋亡机制 ,是维持生理状态稳定的一种重要调节方式。活化诱导的细胞死亡的缺陷与免疫和多种生理机能的紊乱密切相关 ,也是某些炎症性皮肤病、自身免疫性皮肤病乃至皮肤肿瘤等疾病发生机制中的重要环节     

凋亡物质清除障碍与系统性红斑狼疮

系统性红斑狼疮是常见的一种自身免疫性疾病。其发病机制和具体病因还不明确。研究表明,患者常有单核巨噬细胞清除能力下降、补体缺陷、脱氧核糖核酸酶Ⅰ的活性降低及Pentraxin家族改变等表现,这些因素导致的体内凋亡细胞物质的清除障碍,可能是系统性红斑狼疮的主要发病机制。     

活化诱导的细胞死亡与皮肤病

活化诱导的细胞死亡是机体通过一系列复杂的分子事件在细胞被活化的同时而启动的一种有序并适度的细胞凋亡机制，是维持生理状态稳定的一种重要调节方式。活化诱导的细胞死亡的缺陷与免疫和多种生理机能的紊乱密切相关，也是某些炎症性皮肤病、自身免疫性皮肤病乃至皮肤肿瘤等疾病发生机制中的重要环节。     

白癜风发病机制研究进展

白癜风是一种常见的皮肤色素脱失性疾病,导致皮损中黑素细胞损伤的分子机制迄今尚未明确。该病发病机制复杂,涉及遗传、免疫-炎症、氧化应激、功能性黑素细胞凋亡和(或)丢失、神经体液等假说。目前比较推崇的观点是氧化应激在遗传易感个体可能为始动因素,而固有免疫所致炎症的作用也不容忽视,这两者均可直接抑制或损害黑素细胞,并通过激发链式适应性免疫反应来清除黑素细胞,诱发白斑。     

From human immunodeficiency virus (HIV) infection of the brain to dementia.

Human immunodeficiency virus (HIV) can cause both primary and secondary brain diseases. Numerous neuropathological studies have shown that up to 90% of patients with acquired immune deficiency syndrome (AIDS) have lesions in the nervous system. In this review, we discuss the entry of HIV into the brain, the general features of HIV associated neuropathology, the role of different brain cells in HIV mediated neuronal damage, and the putative molecular mechanisms involved. We conclude by correlating which factors might be important in the development of HIV associated dementia.     

The immunopathogenesis of AIDS

In summary, the understanding of the pathogenesis of immune dysfunction in HIV infection is incomplete. New mechanisms by which HIV disrupts the immune system through alterations in basic biochemical events in CD4 T cells are continually being discovered. In a positive light, because of the complexity involved in HIV-mediated induction of immune suppression, logic suggests there is potential for reversing some of these processes.     

Histopathologic features seen in cutaneous photoeruptions in HIV-positive patients

Background There have been scattered reports of HIV+ patients with increased reactions to light as well as anecdotal reports of HIV+ patients with increased morbidity secondary to radiation therapy. Methods As a part of a military study of HIV+ patients, we followed 987 patients for cutaneous disease for 4 years. All patients were questioned on a periodic basis about increased sensitivity to light. These patients received a physical examination at each protocol visit, and they were given the opportunity to receive all their dermatologic care within the HIV clinic. Fourteen of the patients with photo-induced eruptions were evaluated clinically at the time of the eruption, and 11 of these were biopsied. Results Thirty-three of the patients reported photo-induced reactions unrelated to oral medications. Although sensitivity to light often began in the early stages of HIV disease, reactions became more severe and more chronic with disease progression. Histologic features varied from few to numerous apoptotic/necrotic keratinocytes within the mid to upper levels of the epidermis associated with a perivascular inflammatory infiltrate, to apoptotic/necrotic keratinocytes throughout an acanthotic epidermis with a liehenoid/interface infiltrate. Conclusions Although the pathogenesis of these light reactions is not known, these reactions may be related to depletion of endogenous scavengers which results in increased oxidative stress and is modulated by the pattern of immune dysregulation and metabolic dysregulation induced by HIV disease.     

Unraveling the paradoxes of HIV-associated psoriasis: a review of T-cell subsets and cytokine profiles

HIV-associated psoriasis appears paradoxical, being a T-cell mediated disease in the face of decreasing T-cell counts. Furthermore, psoriasis is generally mediated by type-1 cytokines, whereas in HIV, type-2 cytokines tend to predominate. How can one have psoriasis in the essentially Th2 environment of HIV? The details and pertinent research regarding T cell subsets and cytokine profiles in psoriasis, HIV, and HIV-associated psoriasis were reviewed. It appears that both in the presence and absence of HIV infection, psoriasis is largely mediated by memory CD8 T cells, and that IFN-gamma secreted by these cells and others is of key importance. Studying psoriasis in a model such as HIV in which certain elements of the immune system are stripped away or altered may help us better understand the pathogenic mechanisms and potential treatment targets for psoriasis vulgaris.     

Apoptosis in dendritic cell biology

Apoptosis or programmed cell death regulates many aspects in immunological homeostasis and, thus, controls the initiation, magnitude, duration, and termination of immune responses. Recent studies on dendritic cells (DC), including Langerhans cells (LC), have reinforced this concept by documenting that these antigen presenting cells express surface receptors and ligands that are known to mediate apoptotic cell death and that they are highly susceptible to apoptotic signals. In this review article, four major topics concerning apoptosis in the biology of DC will be overviewed: (a) molecular mechanisms of apoptosis; (b) DC apoptosis induced by various stimuli; (c) regulation of DC apoptosis; and (d) cross-priming and cross-tolerance induced by DC ingesting apoptotic bodies.     

Cutaneous extranodal NK/T‐cell lymphoma mimicking cellulitis an HIV positive patient without lymphopenia

We present the case of a 28‐year‐old male with a history of human immunodeficiency virus (HIV) with a 1‐month history of a steadily enlarging, firm painful lesion on the right posterior shoulder. The patient was initially treated for cellulitis given his clinical picture. Histopathologic examination revealed an angiocentric and dermal proliferation of markedly atypical lymphoid cells with numerous mitoses and apoptotic bodies along with broad zones of necrosis. Biopsy revealed the presentation to be consistent with NK/T‐cell lymphoma. The cutaneous lesions from NK/T‐cell lymphoma can often be initially mistaken for cellulitis, therefore this malignancy should be included on the differential in a patient HIV/acquired immune deficiency syndrome (AIDS).     

The biology of HIV infection

This article reviews the cell and molecular biology of human immunodeficiency virus (HIV), emphasizing the features that lead to opportunistic infection by organisms such as mycobacteria. Mycobacteria, especially M. avium complex and M. tuberculosis infections, are closely associated with HIV disease. HIV is a very small retrovirus and its high mutation rate leads to extremely variable viral populations, both within and between individuals. It is coated with glycoprotein 120 (gp120), which it uses to bind to and infect a range of CD4+ leukocytes, depending on the co-receptor specificity. T cell-tropic HIV strains tend to use the CXCR-4 chemokine receptor, while macrophage-tropic strains tend to use the CCR-5 chemokine receptor. Immunosuppression is induced in a number of ways. As well as frank depletion of virus-infected T cells, antigen-specific T cell clones can be selectively deleted by mechanisms such as defective antigen presentation by HIV-infected macrophages (activation-induced cell death). Changes in cytokine production in HIV infection are also proposed. All this leads to falling T cell counts, B cell dysregulation and macrophage dysfunction. Opportunistic infections exploit this immunosuppressed environment. Certain infections are prevalent, reflecting factors such as environmental exposure to pathogens, poor mucosal defences and subcellular interactions between HIV and, e.g. viral or mycobacterial infections. Opportunistic infection exacerbates immune destruction by HIV, producing a vicious cycle that is ultimately fatal.     

中药单体成分抗白念珠菌实验的研究进展

 近年来随着激素、生物制剂的广泛使用以及HIV、癌症发病率的升高,免疫低下人群逐渐增多,条件致病菌白念珠菌的感染逐年增多,其对抗真菌药物的耐药作用也日渐突出。中药单体成分具有良好的抗真菌作用,毒副作用小,可与抗真菌药物协同作用,降低真菌耐药性,越来越引起重视。本文就中药单体成分小檗碱、黄芩苷、苦参碱等抗白念珠菌的相关实验研究进展作一综述。      

Apoptosis in HIV-1 infection

Apoptosis is a key event in biologic homeostasis with particular importance to the immune system. It is an active energy-dependent process that is tightly regulated and controlled by a variety of signal transduction pathways. Apoptosis modulation plays a part in the pathogenesis of many human diseases, including HIV infection. Although multiple mechanisms may contribute to the decline in CD4 T-lymphocyte numbers observed, apoptosis is a significant factor. Alterations in levels of apoptosis are observed in both directly infected and uninfected bystander cells and a variety of pathways of apoptosis induction have been implicated. Apoptosis induction is related to death receptor and mitochondrial-induced pathways in specific circumstances. These events have been linked to individual HIV proteins and have been demonstrated to be altered by antiretroviral therapy.