Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0021051 (immunodeficiency)
 71,517 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Microglia, the resident tissue macrophages of the central nervous system, have a highly differentiated morphology and do not express many of the antigens typically associated with other tissue macrophages. Activation of microglia is associated with a change in morphology and an increase in their repertoire of antigen expression. Microglia become activated in many neuropathological conditions including chronic neurodegenerative diseases and human immunodeficiency virus neuropathology, yet little is known of the mechanisms involved. Here we demonstrate for the first time that microglia can be activated and induced to divide and/or undergo apoptosis via a beta 2-integrin (complement receptor type 3, CR3, Mac-1 or CD11b/CD18) using an anti-CR3 monoclonal antibody (McAb5C6). This antibody, which has been shown to block myelomonocytic recruitment during central nervous system inflammation, is unique in that it can cross the intact blood-brain barrier to activate microglia. Since CR3 not only binds the iC3b component of the alternative complement cascade but also denatured proteins this suggests a potential route for microglia activation in neuropathological conditions.
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PMID:Mitosis and apoptosis of microglia in vivo induced by an anti-CR3 antibody which crosses the blood-brain barrier. 825 20

CD8+CD45RA+ T lymphocytes present two distinct subpopulations expressing the CD11a molecule (LFA-1 alpha chain) with different intensity. CD11adim cells represent the unprimed population within the CD8+CD45RA+ subset, whereas CD11abright cells are activated and may be considered as memory lymphocytes. The aim of this study was to analyze the expression of CD11a and CD18 within the CD8+CD45RA+ population in young HIV-infected individuals at different stages of disease as a marker of activation and of disease progression. Blood cells from 82 HIV-infected individuals and 23 age-matched healthy controls were stained with unconjugated CD11a, CD18, PE-goat F(ab')2 anti-mouse, FITC-CD45RA, and TRI-Color CD8. Quantitative analysis for three-color immunofluorescence was carried out by flow cytometry. HIV+ subjects were subdivided into three groups according to their CD4+ cell number (group A, CD4+ cells > 500/microliters [20 subjects], group B, CD4+ cells between 500 and 200/microliters [36 subjects], and group C, CD4+ lymphocytes < 200/microliters [26 subjects]). We found a significant increase of CD11abright in the CD8+CD45RA+ subpopulation throughout the progression of the disease. The CD11abright percentage of positivity (mean) within the CD8+CD45RA+ subpopulation was 31% in healthy donors, 51% in group A, 52% in group B, and 68% in group C. CD11abright expression was closely related to CD18bright (p < 0.001), but not to CD38. The relative increase of CD11a and CD18 expression in CD8+CD45RA+ T lymphocytes parallels the decrease of CD4+ cells and the progression of disease: an inverse correlation between the percentages of CD4+ cells/microliter and CD8+CD45RA+CD11abright cells (p < 0.001) and a direct correlation between the number of CD4+ lymphocytes per microliter and both the number of CD8+CD45RA+CD11adim cells (p < 0.001) and the number of CD8+CD45RA+CD11abright (p = 0.002) was observed. The relative increase of CD8+CD45RA+CD11abright cells may represent an additional marker for monitoring HIV-induced immunodeficiency.
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PMID:Expansion of CD11abright cells in CD8+CD45RA+ from HIV-infected patients: a new early marker for disease progression? 857 89

We previously showed that superoxide (O2-) significantly enhanced human immunodeficiency virus type 1 (HIV-1)-induced syncytia formation in co-cultured infected and uninfected human T cells. In this study, we describe a novel chemotactic response of uninfected CD4+ T cells by stimulating infected T cells with O2-. Syncytia formation was amplified only when persistently infected cells were stimulated by O2-. When the infected cells in lower well of microplate were cultured with uninfected cells in the upper well of a Boyden chamber with 8.0 microns pores, uninfected cell migration to the porous membrane was significantly amplified by stimulating infected cells with O2-. In contrast, similar functions were slight under the same assay conditions in the presence of known chemokines such as human RANTES and macrophage inflammatory protein 1 (MIP-1 alpha and beta), which all activate T lymphocytes. In addition, it is unlikely that the O2(-)-induced chemotactic response is due to soluble HIV-1 proteins from infected cells or to amplified expression levels of cell surface functional molecules such as CD4 and LFA-1 (CD11a and CD18) as well as HIV-1 Env gp120 on uninfected and/or infected cells. Thus, an unknown chemotactic factor could be generated from infected T cells by stimulation with O2- and it might contribute to viral transmission by activating cell-to-cell interactions.
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PMID:Stimulation of human immunodeficiency virus type 1 infected cells with superoxide enhances the chemotactic motile response of CD4+ human T cells: implication for virus transmission by cell-to-cell interaction. 865 92

Engagement of monocytic cell membrane proteins was shown to enhance human immunodeficiency virus type 1 (HIV-1) replication in monocytic cells. Cross-linking of CD18, CD11a, or CD45 by immobilized antibodies produced up to an 11-fold enhancement of HIV-1 release in the OM10.1 monocytic cell line in a tumor necrosis factor-alpha (TNF-alpha)-dependent manner. In addition, adhesion of OM10.1 cells to immobilized intercellular adhesion molecule-1 (ligand for CD18/CD11a) induced similar TNF-alpha-dependent enhancement of HIV-1 replication. After phenotypic differentiation of OM10.1 cells, engagement of cell membrane proteins CD18, CD11a, CD44, CD45, or CD58 by soluble antibodies enhanced HIV-1 replication in a TNF-alpha-dependent manner. These data suggest that cross-linkage of monocytic cell membrane proteins during cell-cell interaction and specifically during antigen presentation to CD4 T cells may enhance HIV-1 replication, facilitating infection of adjacent cells.
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PMID:Engagement of adhesion molecules (CD18, CD11a, CD45, CD44, and CD58) enhances human immunodeficiency virus type 1 replication in monocytic cells through a tumor necrosis factor-modulated pathway. 865 13

The syndrome of leukocyte adhesion deficiency (LAD) is a rare congenital immunodeficiency which is usually manifested from birth by serious infections of the skin and mucosal membranes. The molecular basis of the disease is heterogeneous: quantitative or qualitative disorders of the beta 2 integrin sub-unit are involved which lead to the absence or substantially reduced expression of adhesive molecules of the CD11/CD18 complex on leukocytes. The authors describe the case of a boy who suffered from this syndrome. The diagnosis was established at the age of four years, based on the typical clinical picture and confirmed by examination of integrins on lymphocytes and granulocytes which were zero. During the mother's subsequent pregnancy prenatal diagnosis was made by puncture of the umbilical cord during the 22nd week of gestation. Affection of the foetus by this syndrome was ruled out by examination of integrin expression on foetal leukocytes, a normal finding was confirmed also after delivery. During delivery umbilical blood was collected which was frozen and later used for therapeutic transplantation to the sibling suffering from LAD. This is the first case of this syndrome in the Czech Republic and first prenatal diagnosis which led to aimed collection of umbilical blood used for treatment of this rare immunodeficiency.
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PMID:[The first case of leukocyte integrin deficiency syndrome in the Czech Republic and successful prenatal diagnosis in the affected family]. 868 57

Cultured Langerhans' cells (CLC) exhibit enhanced antigen-presenting function compared to freshly isolated LC (FLC), but they are commonly believed to be inefficient at processing intact proteins. In this study, FLC and CLC from normal, human immunodeficiency virus (HIV) seronegative volunteers were compared for their ability to present the HIV-1 envelope glycoprotein gp120 or reverse transcriptase (p66) antigens to autologous, specific CD4+ T cell lines. Epidermal cell suspensions enriched for LC were prepared from suction blister roofs. FLC stimulated T cells at lower antigen concentrations compared to unfractionated peripheral blood mononuclear cells (PBMC). CLC were more potent on a per cell basis than FLC, PBMC or adherent monocytes at presenting native gp120, native p66 or immunogenic peptides. CLC were also more efficient than FLC or PBMC in terms of the amount of antigen required for T-cell activation. Chloroquine and leupeptin inhibited presentation of intact p66, but not of an immunodominant peptide, by FLC or CLC, thus indicating that both cells utilize antigen-processing mechanisms that are based on intracellular acidification and protease activity. Incubation of CLC with monoclonal antibodies against HLA-DR, CD11b, CD18, CD50, CD54, CD58 or CD80, but not anti-major histocompatibility complex class I (MHC-I), inhibited antigen-specific T-cell proliferation to varying degrees. We conclude that human CLC retain the ability to process and present protein antigens potently to CD4+ T cells. Thus, CLC have the capacity to participate actively in the generation and maintenance of T-helper cell immunity to viral antigens during HIV-1 infection.
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PMID:Cultured human Langerhans' cells are superior to fresh cells at presenting native HIV-1 protein antigens to specific CD4+ T-cell lines. 869 96

Impaired polymorphonuclear neutrophil (PMN) function may contribute to the onset of certain bacterial and fungal infections and to tissue damage in human immunodeficiency virus (HIV)-infected patients. Published data on PMN function in HIV infection are controversial, possibly because most studies have involved PMNs isolated from the normal blood environment by various procedures that may modify PMN responses. We therefore used flow cytometry to study the expression of adhesion molecules at the PMN surface, actin polymerization, and the oxidative burst of whole-blood PMNs in 42 HIV-infected patients at different stages of the disease. These PMNs were activated in vivo, as shown by increased expression of the adhesion molecule CD11b/CD18, reduced L-selectin antigen expression, increased actin polymerization, and increased H2O2 production. The alterations were present in asymptomatic patients with CD4+ cell counts above 500/microliters and did not increase with progression of the disease. This PMN activation could contribute to the oxidative stress described in HIV infection. Stimulation by bacterial N-formyl peptides showed dysregulation of L-selectin shedding and decreased H2O2 production after cx vivo priming with tumor necrosis factor-alpha or interleukin-8. These latter impairments, which correlated with the decrease in CD4+ lymphocyte numbers, could contribute to the increased susceptibility of HIV-infected patients to bacterial infections.
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PMID:Impairment of polymorphonuclear neutrophil function in HIV-infected patients. 869 65

Langerhans' cells (LC) are epidermal bone-marrow-derived dendritic cells. They represent in mankind 1 to 6% of the epidermal cells from which they can be distinguished by specific phenotype (membrane receptors and antigens related to the immune function) and by ultrastructural specific organelles: the Birbeck granules. In dogs and cats, such cells were recently described; they display a phenotype very similar to that of human LC (CD1, CD8, CD11/18, CD45 and MHC II positive for canine LC, and CD18, CD4, panleukocyte antigen and MHC II positive for feline ones) and in both species, Birbeck granules are observed. Furthermore occurs in dog a benign self-healing LC tumor: the canine cutaneous histiocytoma (CCH). This tumor exhibits numerous comparison points with a human LC disorder named Hashimoto-Pritzker disease, and thus may constitute an interesting model to explore causes of such a proliferation and mechanisms of tumor rejection. In 1986, Pedersen isolated in cats a new retrovirus very similar to the human immunodeficiency virus (HIV), the feline immunodeficiency virus (FIV). Since human LC may be infected by HIV, feline LC may represent a good candidate for an FIV model for exploring the infection of human LC by the HIV and for shedding light on the role of human LC located in the mucous membranes in the initial viral inoculation process.
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PMID:[Dendritic cells in dogs and cats: models of study in human pathology]. 878 98

A 6-year-old boy with the severe form of the leukocyte adhesion deficiency syndrome (LAD) received a transplant of cord blood (CBT) from his HLA-identical brother. The donor was proved healthy by successful prenatal diagnosis. CBT was performed after conditioning with etoposide, busulfan and cyclophosphamide. After hematopoietic recovery complete chimerism was proved as well as the normal expression of CD11x/CD18 complex on circulating leukocytes. The only post-transplant complication was a mild pneumonitis resolving on the corticosteroid therapy. Thirteen months after CBT the boy is in good health and shows no signs of immunodeficiency. As far as we know this is the first report of successful CBT in a patient with LAD syndrome.
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PMID:Successful HLA-identical sibling cord blood transplantation in a 6-year-old boy with leukocyte adhesion deficiency syndrome. 883 30

The genes responsible for many X-linked and autosomal recessive primary immunodeficiency diseases have been identified during the past two years. Now we can diagnose more than a dozen primary immunodeficiency diseases by genetic methods as well as immunological ones. We describe here two patients with leukocyte adhesion deficiency (LAD) and with X-linked agammaglobulinemia (XLA) the diagnoses of which were confirmed by genetic analysis. A patient with LAD showed a missense mutation of the CD18 gene from C to T at nucleotide position 605 resulting in a proline178-->leucine substitution. The mutation of the other allele has not yet been analyzed, because few CD18 mRNAs were translated from the mutated DNA. Another patient with XLA had a missense mutation of Btk gene at position 1204 of C to T resulting in a change of leucine358-->phenylalanine. In view of the mutation of the Sac I restriction site from GAGCTC to GAGTTC we can easily differentiate patients and the carrier from normal persons by the amplification of genomic Btk DNA. Through these studies unknown functions of these genes will be clarified in the near future.
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PMID:[Identification of mutations that were responsible for primary immunodeficiency diseases]. 885 Nov 94


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