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)

In the recent studies conducted in patients with various types of primary immunodeficiency diseases, an increased frequency of HLA-A1 or HLA-A2 antigens was reported. In order to determine the frequency of the histocompatibility antigens in ataxia telangiectasia (A-T), HLA typing was carried out in 30 patients with A-T along with their 23 parents and 4 siblings. The results were compared with 138 healthy controls. That study showed no significant difference for the frequencies of 19 HLA antigens of the A and B loci between the controls and A-T patients or their parents-siblings.
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PMID:Histocompatibility (HLA) factors in ataxia telangiectasia. 65 94

Thirteen patients with primary immunodeficiency disorders and their twenty-five healthy first-degree relatives were tissue typed and their HLA make-up was compared with that of a normal control population. HLA-A2 occured in 92.3% of patients as opposed to 60.8% in the control group (P less than 0.02), HLA-A9 in 7.6% vs. 25% (P less than 0.02) and HLA-B8 in 0% vs. 21% (P less than 0.04). One of the patients with severe combined immunodeficiency showed one "extraneous" HLA specifity.
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PMID:HLA frequencies in primary immunodeficiency diseases (pidd). 83 47

HLA typing was performed on 384 individuals of an isolated population of 1,500 people with a familial aggregate of lymphoma and immunodeficiency cases. Eighty-five % of the total population were descendants of the founding couple. First cousin marriages were common. There was a three-fold or higher increase of the following haplotypes as compared to the frequencies in Sheffield: HLA-A28,Bw35, HLA-A28, B18, HLA-A10, B18, HLA-A2, B18,HLA-A11, Bw40 and HLA-A11, B7. The frequency of HLA-A1, B8 was low (5.4%). The most common genotype was HLA-A2, B12/A2, B12 followed by HLA-A2, B12/A28, Bw35. We found 20 HLA homozygous individuals, of these 15 were HLA-A2, b12/a2, b12. There were two possible HLA cross-overs which may be confirmed and three postulated cross-overs which can never be confirmed as one or both parents of the individuals in question are deceased. Some of the haplotypes could be traced back to the first, second and third generations, i.e. to the first half of the nineteenth century. No single haplotype or antigen was shared by the patients.
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PMID:HLA haplotypes in a genetic isolate in Newfoundland. A population showing 8% homozygosity and a familial aggregate of lymphoma and immunodeficiency cases. 97 11

Earlier findings indicate that peptides can affect the expression of major histocompatibility complex (MHC) class I molecules on the surface of cells with defective peptide loading mechanism. We have used peptide induced increase of class I antigen expression to assess peptide interaction with MHC class I molecules. A panel of 41 overlapping synthetic peptides derived from the human immunodeficiency virus-1 (HIV-1) gag protein and 33 nonoverlapping peptides from Epstein-Barr virus (EBV) proteins EBNA-1, 2, 3, 4, 5, 6, LMP, BZLF2, BILF2, BSLF2, BALF4 and BcLF1 was assessed for the ability to enhance the expression of HLA-A2.1, H-2Db, Kb and Dd on the murine RMA-S and human 721.174/T2 (.174/T2) lines by indirect immunofluorescence. Considering doubling of the fluorescence intensity in the peptide-treated samples as positivity, 6 of 39 HIV and 1 of 32 EBV peptides were found to bind to A2.1, 6 of 39 HIV gag and 7 of 16 EBV peptides to Db, 8 of 39 HIV gag and 5 of 16 EBV peptides to Kb and 2 of 39 HIV gag and 1 of 17 EBV peptides to Dd. The sensitivity of the method is comparable to the in vitro class I assembly assay with conformation-dependent monoclonal antibody and is more discriminating than the solid-phase assay. Due to its simplicity this method can also serve for testing large peptide panels for binding capacity to various class I molecules. Moreover, the method provides information about the relevance of in vitro tests for class I assembly in living cells.
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PMID:Assessment of major histocompatibility complex class I interaction with Epstein-Barr virus and human immunodeficiency virus peptides by elevation of membrane H-2 and HLA in peptide loading-deficient cells. 132 2

Cytotoxic T lymphocytes (CTL) are present at high activities in adult patients infected with the human immunodeficiency virus (HIV). In this report, CTL effectors were identified in peripheral blood mononuclear cells (PBMC) of children born to HIV-1-infected mothers. These CTL killed HLA-matched HIV-1-infected H9 target cells or doubly transfected P815-A2-env, gag or nef mouse tumor cells, which expressed the viral antigens in association with HLA-A1/A3 or HLA-A2, respectively. HIV-1-specific CTL were detected early after birth (less than 2 months) and remained present during the asymptomatic phase of the infection. As in HIV-1-infected adults, HIV-specific CTL declined with disease progression. Surprisingly, HIV-1-specific CTL were detected in the PBMC of three children who subsequently became seronegative.
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PMID:Cytotoxic T lymphocyte responses in the peripheral blood of children born to human immunodeficiency virus-1-infected mothers. 138 9

The two subunits of the human class I histocompatibility antigen (HLA)-A2 have been expressed at high levels (20-30 mg/liter) as insoluble aggregates in bacterial cells. The aggregates were dissolved in 8 M urea and then refolded to form an HLA-A2-peptide complex by removal of urea in the presence of an antigenic peptide. Two peptides from the matrix protein and nucleoprotein of influenza virus are known to bind to HLA-A2, and both support the refolding of the recombinant HLA-A2 molecule. An additional peptide, a nonamer from the gp120 envelope protein of human immunodeficiency virus type 1, also supported refolding. Yields of purified recombinant HLA-A2 are 10-15%. In the absence of an HLA-A2-restricted peptide, a stable HLA-A2 complex was not formed. Monoclonal antibodies known to bind to native HLA-A2 also bound to the recombinant HLA-A2-peptide complex. Three purified HLA-A2-peptide complexes refolded from bacterially produced protein aggregates crystallize under the identical conditions as HLA-A2 purified from human lymphoblastoid cells. Crystals of the recombinant HLA-A2 molecule in complex with the influenza matrix nonamer peptide, Mp(58-66), diffract to greater than 1.5-A resolution.
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PMID:HLA-A2-peptide complexes: refolding and crystallization of molecules expressed in Escherichia coli and complexed with single antigenic peptides. 156 34

The sequences of a set of 63 peptides of demonstrated T immunogenicity have been analyzed and compared with two different randomly generated sets of sequences. This study indicates a statistically significant tendency of T immunogenic peptides to be constituted of clusters of rare tetrapeptides, as evaluated from the available sequence data banks. This result has been used to locate potential T epitopes in the human immunodeficiency virus (HIV) gag protein. Four peptides corresponding to the best candidate T epitopes (chosen in regions of conserved sequence among different virus isolates) have been synthesized and found to be recognized by a HIV-1-specific, HLA-A2-restricted human cytotoxic T cell line.
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PMID:T-immunogenic peptides are constituted of rare sequence patterns. Use in the identification of T epitopes in the human immunodeficiency virus gag protein. 246 6

The human immunodeficiency virus type 1 (HIV-1) induces a strong cytotoxic T lymphocyte (CTL) response in humans following infection. HIV-specific CTL can be detected directly in the blood and lungs of infected patients, and can be expanded in vitro by stimulation with autologous HIV-infected lymphoblasts. Furthermore, CTL specific for HIV envelope glycoprotein gp160 have been obtained in mice by immunization with recombinant vaccinia virus (VV) that carry the HIV env gene. In this study, we show that mice also produce strong CTL responses to gag and nef proteins following immunization with VV recombinants, thus providing a convenient model system to study T lymphocyte immunity to defined HIV antigens. To determine the specificity of circulating HIV-immune CTL in humans, a panel of doubly transfected mouse P815 tumor cells was produced which express the human HLA-A2 or HLA-A3 transplantation antigen gene and one HIV-1 gene (env, gag or nef). Using these cells as targets to CTL, we show that HIV-infected humans carry co-existing CTL sub-populations of different specificities. Each subpopulation appears to vary in intensity among different individuals. Surprisingly, CTL specific for regulatory, non-structural nef protein appear to be a major constituent of the human immune response to HIV.
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PMID:Multiple subsets of HIV-specific cytotoxic T lymphocytes in humans and in mice. 267 60

Noncytopathic infection of human T-lymphoid cell line CR-10 with human immunodeficiency virus (HIV) (CEM-N1T isolate) resulted in a gradual loss of cell surface receptors for OKT4/OKT4A (HIV receptor), OKT8, OKT3, and OKT11 but not for OKT9 (transferrin receptor) within 10 days after infection. Surface receptor decline was accompanied by a rapid increase in HIV antigens and mRNA expression. Multireceptor downregulation was also observed in three T-lymphoid cell lines (MT-4, CEM, and HBD-1) cytopathically infected with the HIV/N1T virus and in HUT-78 cells infected with the HIV/SF-2 isolate. HIV-infected and uninfected CR-10 cells contained similar levels of mRNAs coding for T3, T8, T9, T11, HLA-A2, and HLA-B7 proteins. By densitometry, fully infected CR-10 cells showed approximately 75% reduction in T4 and tubulin (beta chain) mRNA levels when compared with uninfected CR-10 cells. No such reduction was detected in HIV-infected MT-4 and HBD-1 cells. A T-cell receptor gene (beta chain) rearrangement study revealed that no distinct CR-10 subpopulation was selected out upon infection with HIV. Our results suggest that the reduction in cell surface receptors observed between 1 and 2 weeks postinfection cannot be directly attributed to similar reductions in mRNA levels coding for these receptor proteins. We conclude that HIV infection induces posttranscriptional downregulation of several T-cell surface receptors.
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PMID:Downregulation of cell surface molecules during noncytopathic infection of T cells with human immunodeficiency virus. 350 Mar 27

We prepared and crystallized five complexes of the human histocompatibility molecule HLA-A2 with peptides derived from human immunodeficiency virus type 1, human T lymphotropic virus type 1, influenza A virus and hepatitis B virus proteins. Each HLA-A2 complex was refolded in vitro from insoluble proteins produced in bacteria; to crystallize, two of the complexes required seeding with microcrystals of another complex. Maintained at -160 degrees C, single co-crystals of each of the five peptide-HLA-A2 complexes yielded complete X-ray diffraction data sets to a resolution of approximately 2.5 A. After a sufficient number of diffraction peaks were acquired during data collection, the direct analysis of integrated intensities established the point group of the co-crystal, thus allowing an efficient data collection strategy to be designed. The subsequent examination of systematic absences revealed that the five peptide-HLA-A2 co-crystals formed in space groups P1, P2(1), or P2(1)2(1)2(1). Molecular replacement structure solutions yielded unambiguous protein electron density maps, thus confirming the space group determinations. The system of obtaining HLA-A2 co-crystal structures described here is applicable to other crystallographic problems where structures of several related molecules from uncharacterized single crystals are required.
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PMID:Five viral peptide-HLA-A2 co-crystals. Simultaneous space group determination and X-ray data collection. 751 39


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