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)

A brief commentary on leukocyte adhesion molecules, including integrin family, immunoglobulin superfamily and selectin or LEC-CAM family is made. A recent concept on the molecular mechanisms of the leukocyte adhesion to cell surface is also described. An immunodeficiency disease called "leukocyte adhesion deficiency (LAD)" that is defective in expression of leukocyte adhesion molecules of integrin family, LFA-1, Mac-1 and p150, 95, is discussed with special reference to its clinical features, laboratory findings, neutrophil functions, lymphocyte functions and molecular defects. Some abnormal expression of a Fc-gamma receptor in neutrophils and new data concerning the molecular defects found in Japanese patients are also included.
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PMID:[Leukocyte adhesion molecules and their abnormality]. 137 66

UCD line 140 chickens have been previously reported to develop a syndrome of spontaneous 7s immunoglobulin deficiency and the presence of autoantibodies. Earlier studies demonstrated that these inbred birds have normal peripheral blood T and B cell numbers; they also respond normally to allogeneic stimulation. Although the 7s immunodeficiency does not manifest itself until several months of age, line 140 birds have a premature degeneration of bursa. Because of the recent development of monoclonal reagents specific for bursal elements, including surface epithelium, basement membrane associated epithelium, follicle associated epithelium, and lymphoid subpopulations, we have examined line 140 and control birds for the expression of bursal epithelial cell antigens. Line 140 birds, in contrast to control chickens, have a dramatic early alteration in the expression of an epithelial cell marker in the bursa, thymus, and intestine. Moreover, to further address this issue, we transplanted bursa from 10-day embryos onto the chorioallantoic membrane, a privileged site. Bursae from control birds became abnormal when transplanted onto line 140 CAM; they remained normal when transplanted among several control chicken lines. In contrast, line 140 bursa remained abnormal independent of the transplant procedure. Due to the marked bursal abnormality observed specific to the dysgammaglobulinemia chicken line, we propose that the microenvironmental features of line 140 bursa may predispose these birds to the development of humoral immunodeficiency and autoantibodies.
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PMID:Abnormalities associated with the bursal microenvironment in spontaneous dysgammaglobulinemia of UCD line 140 chickens. 200 41

On the basis of reports demonstrating possible roles for leukocyte function-associated antigen 1 (LFA-1) and intercellular adhesion molecule 1 (ICAM-1), the ligand for LFA-1, in human immunodeficiency virus type 1 (HIV-1) infection, we have explored the involvement of the ICAM-1 molecule by using selected synthetic peptides derived from the protein sequence. Replication was assessed in MT-2 cells, highly susceptible to HIV infection, in the presence of four synthetic peptides derived from the ICAM-1 amino acid sequence. This cell type was chosen for the ability to form marked syncytia on infection with cell-free virus. Under the conditions used, minimal or no cytotoxicity was observed with the peptides up to concentrations of 50 micrograms/ml. A peptide corresponding to a unique region of ICAM-1, JF9 [ICAM-1(367-394, A-378)], had little effect on virus replication despite its ability to inhibit cell-cell adhesion. In contrast, an N-terminal peptide, JF7B [ICAM-1(1-23)], consistently inhibited virus replication in MT-2 cells in a dose-dependent manner, as measured by cell-free reverse transcriptase (RT) activity (up to 70% inhibition), soluble virus antigen production (up to 60% inhibition), and syncytium formation (virtually complete inhibition up to 6 days post infection). Testing of W-CAM-1 antibody, and anti-ICAM-1 antibody that inhibits cell-cell adhesion, revealed no significant inhibitory effects on RT activity, virus antigen production, and syncytium formation in HIV-1-infected MT-2 cells at a level that markedly inhibited cell-cell adhesion (10 micrograms/ml).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Synthetic peptide analogs of intercellular adhesion molecule 1 (ICAM-1) inhibit HIV-1 replication in MT-2 cells. 810 34

Didanosine (ddI) that inhibits the reverse transcriptase of human immunodeficiency virus (HIV) causes steatosis and fulminant hepatitis in some patients with HIV. We studied hepatic histopathologic changes with particular attention to ddI-induced Mallory body formation. Three liver biopsies were performed on three patients with HIV who were treated with ddI; an autopsy was performed on a patient with HIV who was also treated with ddI. All hepatic specimens were studied with a routine liver immunohistochemical panel including antibodies to ubiquitin and cytokeratin (CAM 5.2). Morphologically, all hepatic specimens showed focal to diffuse steatosis with a predominance of macrovesicular fatty change. Fibrosis was minimal in three cases. No secondary bacterial and fungal infections were noted. Single or clusters of "empty cells" were present, and some contained Mallory bodies validated by ubiquitin stain. Empty cells are hepatocytes that fail to stain positive for cytokeratin. The Mallory bodies were different from the others because they were randomly distributed and occurred in noncirrhotic hepatic tissue. In the autopsy specimen, the Mallory bodies had a centrilobular location with central fibrosis (central sclerosing hyaline necrosis).
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PMID:2',3'-Dideoxyinosine-induced Mallory bodies in patients with HIV. 929 55

There is growing literature on the subject of aneurysmal degeneration of arteries in patients who are infected with HIV. A patient recently seen at our medical center with an aneurysm of the carotid artery stimulated our interest in reviewing the mechanisms by which HIV may initiate or predispose to these pathologies. There are at least three major possibilities: (1) immunodeficiency allows bacteria that are known to cause mycotic aneurysms to proliferate without immune restraint; (2) one or more of the HIV envelope proteins sufficiently resemble one or more artery-specific-antigenic proteins (ASAPs) that may trigger an autoimmune response (molecular mimicry); and (3) the HIV virus itself infects arterial-resident cells that maintain the integrity of the load-bearing matrix. The computational searches reported here suggest that the ASAP, matrix cell adhesion molecule-1 (Mat-CAM-1), has a high degree of similarity to known ligands for HIV envelope proteins gp41 and gp120. No similarities of Mat-CAM-1 to the HIV envelope glycoproteins were detected. Accordingly, among the possibilities for explaining the HIV/aneurysm connection, direct infection of aortic fibroblasts by the HIV virus is more likely to be the pathogenetic mechanism than the process of molecular mimicry.
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PMID:Arterial aneurysms in HIV patients: molecular mimicry versus direct infection? 1718 60

Results from Merck's phase II adenovirus type 5 (Ad5) gag/pol/nef test-of-concept trial showed that the vaccine lacked efficacy against human immunodeficiency virus (HIV) infection in a high-risk population. Among the many questions to be explored following this outcome are whether (i) the Ad5 vaccine induced the quality of T-cell responses necessary for efficacy and (ii) the lack of efficacy in the Ad5 vaccine can be generalized to other vector approaches intended to induce HIV type 1 (HIV-1)-specific T-cell responses. Here we present a comprehensive evaluation of the T-cell response profiles from cohorts of clinical trial subjects who received the HIV CAM-1 gag insert delivered by either a regimen with DNA priming followed by Ad5 boosting (n = 50) or a homologous Ad5/Ad5 prime-boost regimen (n = 70). The samples were tested using a statistically qualified nine-color intracellular cytokine staining assay measuring interleukin-2 (IL-2), tumor necrosis factor alpha, macrophage inflammatory protein 1beta, and gamma interferon production and expression of CD107a. Both vaccine regimens induced CD4(+) and CD8(+) HIV gag-specific T-cell responses which variably expressed several intracellular markers. Several trends were observed in which the frequencies of HIV-1-specific CD4(+) T cells and IL-2 production from antigen-specific CD8(+) T cells in the DNA/Ad5 cohort were more pronounced than in the Ad5/Ad5 cohort. Implications of these results for future vaccine development will be discussed.
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PMID:DNA gag/adenovirus type 5 (Ad5) gag and Ad5 gag/Ad5 gag vaccines induce distinct T-cell response profiles. 1852 23