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Query: UMLS:C0019693 (HIV)
 170,526 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The human thymus is a lymphoepithelial organ in which T cells develop during fetal life. After maturation and selection in the fetal thymic microenvironment, T cells emigrate to peripheral lymphoid tissues such as the spleen, gut, and lymph nodes, and establish the peripheral T cell repertoire. Although the thymus has enormous regenerative capacity during fetal development, the regenerative capacity of the human postnatal thymus decreases over time. With the advent of intensive chemotherapy regimens for a variety of cancer syndromes, and the discovery that infection with the Human Immunodeficiency Virus (HIV) leads to severe loss of CD4+ T cells, has come the need to understand the role of the human thymus in reconstitution of the immune system in adults. During a recent study of the thymus in HIV infection, we observed many CD8+ T cells in AIDS thymuses that had markers consistent with those of mature effector cytotoxic T cells usually found in peripheral immune tissues, and noted these CD8+ effector T cells were predominantly located in a thymic zone termed the thymic perivascular space. This article reviews our own work on the thymus in HIV-1 infection, and discusses the work of others that, taken together, suggest that the thymus contains peripheral immune cell components not only in the setting of HIV infection, but also in myasthenia gravis, as well as throughout normal life during the process of thymus involution. Thus, the human thymus can be thought of as a chimeric organ comprised of both central and peripheral lymphoid tissues. These observations have led us to postulate that the thymic epithelial atrophy and decrease in thymopoiesis that occurs in myasthenia gravis, HIV-1 infection, and thymic involution may in part derive from cytokines or other factors produced by peripheral immune cells within the thymic perivascular space.
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PMID:The human thymus. A chimeric organ comprised of central and peripheral lymphoid components. 984 26

The immune responses elicited after oral delivery of vaccinia virus (VV) recombinants are not well defined. In this study we show with mice, that after oral administration of a VV recombinant expressing the luciferase reporter gene, VV gene expression takes place for several days in gut-associated lymphoid (GALT) tissues as well as in the spleen. After 14 days, a significant mucosal IgA response against VV was detected in vaginal and intestinal washings, as well as a systemic specific IgG response, which was principally of the IgG2a subclass. Furthermore, orally immunized mice developed cellular immune responses to VV (CD8+ T cells and T helper activities) in mesenteric lymph nodes (MLN) and spleen. Oral immunization with a VV recombinant expressing, either the envelope protein of HIV or beta-galactosidase, induced a specific immune response, locally and systemically, against gp120 and beta-gal. The cytokine pattern found in supernatants of spleen and MLN cells after stimulation with VV antigens or gp120 was clearly of type 1 cytokines. These studies demonstrate that VV recombinants administered by the oral route generate mucosal and systemic immune responses against antigens of the virus vector and to the recombinant products. These observations are of significance in the use of poxvirus vectors as vaccines.
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PMID:Mucosal and systemic immune responses induced after oral delivery of vaccinia virus recombinants. 1019 17

Infantile acute gastroenteritis is still a frequent problem particularly in younger children, with high mortality rate in developing countries and high impact on health costs in industrialized countries. The increased knowledge on its pathophysiology has led to the definition of two distinct mechanisms of diarrhea: the secretory and the osmotic pathway. Investigation on the host-microorganism interaction revealed a complex scenario with sophisticated mechanisms developed by microorganisms during evolution to overcome the host defense system. The latter includes immune and non immune coordinated components, with a major role played by the GALT (gut associated lymphoreticular tissue). Knowledge of epidemiology and of the natural history of intestinal infections has led to rational diagnostic approach with substantial cut of medical costs. Novel therapeutic strategies have been made available with the use of probiotics and of passive immunotherapy together with a dramatic reduction of antibiotic treatment. HIV pandemy raises major problems which need rapid responses.
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PMID:[Acute infectious diarrhea in children]. 1023 81

RANTES, a beta-chemokine, can suppress human immunodeficiency virus (HIV) as well as simian immunodeficiency virus (SIV) infections in T-lymphocyte cultures in vitro. However, the association of RANTES levels in peripheral blood with viral loads and disease outcome in HIV infection has been inconclusive. SIV-infected rhesus macaques were evaluated to determine whether RANTES gene expression correlated with suppression of viral infection in intestinal lymphoid tissues. Intestinal tissues were obtained from rhesus macaques infected with either pathogenic or nonpathogenic SIVmac variants at various stages of infection (primary acute, asymptomatic, and terminal). We examined the level of SIV infection (in situ hybridization), RANTES expression (quantitative competitive RT-PCR), and T-cell counts (immunohistochemistry). The most pronounced increase in RANTES gene expression in intestinal tissues was observed in primary SIV infection, which correlated with the pathogenicity of the infecting virus and not the tissue viral loads. Our results demonstrated that in contrast to the occurrence of viral suppression by RANTES in vitro, there was no direct correlation between high RANTES gene expression and suppression of viral loads in intestinal lymphoid tissues. Thus RANTES expression in the gut lymphoid tissue may not be a correlate for viral suppression. However, RANTES gene expression in primary SIV infection may be part of early host immune response to viral infection.
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PMID:Alterations in RANTES gene expression and T-cell prevalence in intestinal mucosa during pathogenic or nonpathogenic simian immunodeficiency virus infection. 1036 94

CD4 and CD8 lymphocyte numbers in the gut lamina propria are grossly altered in HIV-1 infection, out of proportion to alterations in the circulation. Such alterations in lymphocyte counts in the tissues may be due to altered leucocyte migration from the blood. One factor affecting leucocyte migration is adhesion molecule expression. Levels of adhesion molecule expression on peripheral CD4 and CD8 lymphocytes, monocytes and neutrophils from HIV-1-infected (AIDS and non-AIDS) and low-risk control individuals were compared. CD11a, CD62L, CD44, CD49d and beta7 integrin expression were examined by FACS analysis of fresh whole blood. Significant alterations in adhesion molecule expression were detected in HIV infection. The most striking alterations were observed in the CD8 lymphocyte population. CD11a expression was increased and CD62L and CD44 decreased. The CD4 lymphocyte population followed a similar, though less striking, pattern of alteration in adhesion molecule expression. Neutrophils displayed significantly reduced expression of both CD11a and CD62L, but only after onset of AIDS. Monocytes from infected individuals without AIDS displayed a different pattern of altered adhesion molecule expression compared with individuals with AIDS. These findings suggest that in HIV infection, leucocyte functions, such as migration, which require adhesion molecules are abnormal.
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PMID:Alterations in blood leucocyte adhesion molecule profiles in HIV-1 infection. 1044 67

Oral manifestations of gastro-intestinal disease are commonly under-diagnosed. This paper is the third in the series entitled 'Recognizing and Caring for the Medically Compromised Child' and seeks to facilitate the process of diagnosis and management of disorders affecting the gastro-intestinal tract in terms of both oral and gut signs and symptoms. This paper concludes with a section devoted to the recognition of HIV disease in paediatric patients, both orally and generally, and its implications for management within the dental surgery.
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PMID:Recognizing and caring for the medically compromised child: 3. Disorders affecting the gastro-intestinal tract and human immunodeficiency virus infection. 1047 8

Taking advantage of the ability of pentameric cholera toxin B subunit (CTB) to bind selectively to GM1, we developed recently a CTB-mediated GM1 lipid vesicle delivery system to target drugs and proteins to mucosal tissues [1]. In this report, we present the use of such a strategy to deliver an HIV envelope protein (HIV-env) to mucosal tissues via intranasal route. Intranasal administration of a recombinant HIV envelope protein formulated in CTB-associated GM1 lipid vesicles enhanced mucosal IgA antibody responses detected in the nasal and gut tissues, compared to that of control animals immunized with antigen formulated in GM1-free vesicles with CTB or formulated in alum-associated vesicles with CTB. We found a nearly 2- to 3-fold enhancement in IgA antibody titers detected both in nasal and gut tissues using the CTB-GM1 lipid vesicle delivery system, compared to using the GM1-free lipid vesicle system. Intranasal administration of HIV-env formulated in the CTB-associated GM1 vesicles also induced a significant level of serum IgG and cellular immune responses against HIV-env. IgG isotype analysis indicates that CTB in GM1 vesicle delivery system enhanced both IgG1 and IgG2a while CTB in alum formulation enhanced only IgG1. However, IgA and IgG antibody responses against CTB were similar for GM1 vesicles regardless of whether HIV-env was present in the vaccine formulation. Collectively, these data indicate that delivery of HIV-env to mucosal epithelial cells with CTB-associated GM1 lipid vesicles enhanced mucosal and systemic immune responses against the HIV-envelope protein. It is possible that both the CTB-mediated targeted delivery of antigen-loaded GM1 lipid vesicles and mucosal adjuvanticity of CTB may be involved in enhancing the immune responses.
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PMID:Formulation of HIV-envelope protein with lipid vesicles expressing ganglioside GM1 associated to cholera toxin B enhances mucosal immune responses. 1054 18

In this report, we described induction of HIV envelope (env)-specific systemic and mucosal immune responses by oral vaccination of BALB/c mice with env-encoded plasmid DNA encapsulated in poly(dl-lactide-co-glycolide) (PLG) microparticles. We demonstrated that intragastric administration of the encapsulated plasmid DNA resulted in transduced expression of the env glycoprotein in the intestinal epithelium. Mice immunized orally exhibited env-specific type 1 and cytotoxic T lymphocyte (CTL) responses in spleen and the inductive (Peyer's patches) and effector (lamina propria) mucosal tissues of gut. Oral administration of PLG-encapsulated plasmid DNA encoding gp160 also induced env-specific serum antibodies, and an increased level of IgA directed to gp160 was detected in fecal washes of the immunized mice. In contrast, intramuscular (i.m.) administration of naked or PLG-encapsulated DNA vaccine induced only systemic cellular and humoral responses to the env glycoprotein. Using an HIV env-expressing recombinant vaccinia viral intrarectal murine challenge system, we observed higher resistance to mucosal viral transmission in mice immunized orally than in animals injected i.m. with PLG-encapsulated plasmid DNA encoding gp160. Results of these studies demonstrate the feasibility of using orally delivered PLG microparticles containing plasmid DNA-encoded HIV gp160 for induction of env-specific systemic and mucosal immune responses and protection against recombinant HIV env vaccinia virus challenge.
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PMID:Oral DNA vaccination promotes mucosal and systemic immune responses to HIV envelope glycoprotein. 1064 78

Acute HIV-1 infection depletes CD4(+) T cells in gut-associated lymphoid tissue (GALT). The failure of containment of local viral replication, and consequent CD4(+) T cell depletion, might be due to delayed mobilization of effector CD8(+) T cells or absence of functioning HIV-1-specific CD8(+) T cell effectors within GALT. No studies have addressed human intestinal HIV-1-specific CD8(+) T cell functions. We sought to determine whether functional HIV-1-specific CTL were present in GALT and whether the repertoire differed from HIV-1-specific CTL isolated from peripheral blood mononuclear cells. From three HIV-1-infected subjects, we isolated HIV-1-specific CD8(+) T cells expressing the mucosal lymphocyte integrin CD103 from GALT. These antigen-specific effector cells could be expanded in vitro and lysed target cells in an MHC class I-restricted manner. HIV-1-specific CTL could be isolated from both duodenal and rectal GALT sites, indicating that CD8(+) effectors were widespread through GALT tissue. The breadth and antigenic specificities of GALT CTL appeared to differ from those in peripheral blood in some cases. In summary, we found HIV-1-specific CD8(+) effector T cells in GALT, despite HIV-1-induced CD4(+) T cell lymphopenia. This suggests that HIV-1-specific CTL in gut tissue can be maintained with limited CD4(+) T cell help.
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PMID:Characterization of HIV-1-specific cytotoxic T lymphocytes expressing the mucosal lymphocyte integrin CD103 in rectal and duodenal lymphoid tissue of HIV-1-infected subjects. 1079 91

These antibodies are specific for antigens in the cytoplasm of neutrophils. The main antigenic targets are proteinase 3(PR3) and myeloperoxydase (MPO) but other targets have been described without determinant conclusions for clinical practice. Staining patterns can be distinguished by an indirect immunofluorescence test (IFI), in which ethanol fixed neutrophils from healthy donors are incubated with patient's sera. Two patterns are distinguished: cytoplasmic pattern (c-ANCA) and perinuclear pattern (p-ANCA). When ANCA are detected by IFI, from a practical point of view, anti -MPO and anti-PR3 antibodies are tested. ANCA have been strongly associated with a spectrum of necrotizing small vessel vasculitides that includes Wegener's granulomatosis, microscopic polyangiitis, Churg and Strauss syndrome, pauci-immune focal necrotizing and crescentic glomerulonephritis. ANCA are a diagnosic marker and useful for the follow-up of the patients. ANCA can be observed in other pathologies: rhumatismal autoimmune diseases, inflammatory gut diseases, after drugs (hydralazine, minocycline, propylthiouracil), after silical exposition, infections (cystic fibrosis, endocarditis, HIV infection). The specificity is different and rarely anti-MPO. The ANCA role for the development of vasculitis is not completely elucidated. Some arguments are against a primary role of ANCA in the development of vasculitis. Certainly, amplification role for neutrophil activation is demonstrated but the primary event responsible of neutrophil activation is not yet defined.
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PMID:[Antineutrophil cytoplasm antibodies (ANCA): description and immunopathological role]. 1089 69


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