SEARCH · PubMed Health

Results for “Histocompatibility”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 235 records · Page 13Linked to original sources

PubMed1982

Identification of an inherited form of Peyronie's disease with autosomal dominant inheritance and association with Dupuytren's contracture and histocompatibility B7 cross-reacting antigens.

Peyronie's disease is an inflammatory disorder with no confirmed etiology. We have documented the familial transmission of the disease as an autosomal dominant trait in 3 pedigrees. The occurrence of Dupuytren's contracture in 7 of 9 (78 per cent) affected individuals, which is a significant increase over the average 0 per cent reported in sporadic cases, suggests that both of these fibrosing disorders are pleiotropic effects of the same gene in these families. Similarly, the histocompatibility B7 cross-reacting antigens were present in 90 per cent of the patients with Peyronie's disease. Additional studies, including careful family histories and histocompatibility antigen typing, are necessary to elucidate the role of histocompatibility antigens as a relative risk factor.

Adult↗

PubMed1977

Influence of sex on histocompatibility matching in renal transplantation.

Histocompatibility matching for the HLA-A and HLA-B loci specificities influenced the survival of cadaver kidney transplants in male recipients but not in female recipients. The correlation between HLA matching and transplant survival for a three-year follow-up period was highly significant for 3455 male recipients but not significant for 2007 female recipients. Since this effect was not dependent on the sex of the donor, a sex-associated histocompatibility antigen could not have been responsible. The reason why histocompatibility matching influences one sex and not the other is not known. The observation may have improtant practical consequences and may help to explain difficulties in establishing a strong correlation between HLA matching and cadaver transplant outcome.

ABO Blood-Group System↗

PubMed1997

Triple immunosuppression protects murine intracerebral, hippocampal xenografts in adult rat hosts: effects on cellular infiltration, major histocompatibility complex antigen induction and blood-brain barrier leakage.

Recently we reported protection of intracerebral mouse to rat hippocampal xenografts upon treatment with a combination of cyclosporin A, prednisolone and azathioprine. These findings are now supported in an extended analysis of graft-infiltrating cells. Host T-cell and macrophage infiltration and the immunocytochemical level of cellular expression of major histocompatibility complex class I and II antigens, measured by densitometric analysis, were compared between recipient rats receiving cyclosporin A alone or cyclosporin A in combination with prednisolone and azathioprine. The combination therapy resulted in a much improved survival of the xenografted hippocampal tissue with preservation of organotypic granule and pyramidal cell layers. Graft infiltration by T-cells and macrophages was significantly lower and the level of major histocompatibility complex class I and II antigen expression by the infiltrating cells markedly reduced. Lower expression of donor-type major histocompatibility complex class I antigen was also found in the xenografts in the trimedicated recipients, together with reduced blood brain barrier leakage and astrogliosis at the host-graft interface. The results demonstrate the benefits of using combined immunosuppressive strategies for protection of histoincompatible brain xenografts in the central nervous system.

Animals↗

PubMed1997

Major histocompatibility complex as an antigen pump: self-declaration in somatic cell society.

Self-recognition by the immune system is a basic mechanism of vertebrates. Mechanisms of antigen presentation by somatic cells are based on the coupling of small peptides produced in cytoplasm and major histocompatibility complex major histocompatibility complex. The antigen pumps, including major histocompatibility complex, can present various internal molecules which are possible targets of autoimmunity, using a peptide binding mechanism. The antigen pump can transfer external signals by autoantibody and cellular immunity without a specific receptor system. This self-declaration mechanism continuously presents 'self' rather than 'non-self'. It is qualitatively impossible to differentiate self antigens from non-self antigens in this process at all. Somatic cell society is non-self for germ line DNA, since germ line DNA is symbiotic with somatic cell society. Consequently, non-self can be recognized through self-declaration.

Animals↗

PubMed1998

Delayed hypersensitivity to aminopenicillins is related to major histocompatibility complex genes.

BACKGROUND: Although in some cases delayed hypersensitivity may be observed, beta-lactam antibiotics frequently induce immediate allergic IgE-mediated reactions with the specificity localized in the acyl-side chain structure. Generally, delayed immunologic reactions are related to sensitized T lymphocytes and major histocompatibility complex restricted. OBJECTIVE: To investigate the prevalence of HLA class I and II antigens in patients with delayed hypersensitivity to aminopenicillins in order to evaluate a relationship between major histocompatibility complex immune response genes and aminopenicillins hypersensitivity. METHODS: We assessed 24 patients with history of delayed hypersensitivity to aminopenicillins using (1) skin test with penicilloyl polylysine, minor determinant mixture, benzylpenicillin, amoxicillin, and ampicillin; (2) patch tests with benzylpenicillin, amoxicillin, and ampicillin; (3) RAST for penicilloyls G and V; and (4) oral challenges with amoxicillin, ampicillin, and penicillin V in 18/24 patients. All patients were typed by microlymphotoxicity standard test for HLA class I and II antigens. Statistical analysis by chi2 test 2 x 2 contingency tables, according to Svejgaard, were used for comparison between patients and random Italian population (522 subjects). RESULTS: In the patients group we found higher prevalence of HLA A2 (12/24 = 50%, RR = 6.76 P < .001, EF = 0.425), DRw52 (20/24 = 83.3%, RR = 9.28, P < .001, EF = 0.74), and lower frequency of DR4 (3/24 = 12% ns). CONCLUSIONS: These data suggest that the immune mechanisms involved in adverse reactions to aminopenicillins in vivo are related to genetic markers of immune response and confirms that the presentation of penicillin-hapten determinants to lymphocyte is major histocompatibility complex restricted.

Adolescent↗

PubMed1972

Preparation of dialyzable histocompatibility antigen from BALB-c mice (cell-membrane fragments-proteolytic digestion-detergent solubilization).

Histocompatibility antigens solubilized from cell-membrane fragments of BALB/c mouse spleen and liver, by Triton X-100 and butyl alcohol, were subjected to digestion by proteolytic enzymes in an effort to obtain smaller molecular species that retained antigenic activity. Digestion with both trypsin and papain yielded two antigens of smaller molecular weights that retained the specificity of BALB/c histocompatibility antigen, as determined by the inhibition of allogeneic antibodies, agglutination of BALB/c erythrocytes, adsorption-hemagglutination versus the soluble histocompatibility antigen, and suppression of the ability of BALB/c spleen cells to produce hemolytic plaques to sheep erythrocytes. The two active products of trypsin digestion were, respectively, excluded by Sephadex G-50 but not by G-75, and excluded by G-25 but not by G-50. Papain digestion yielded one active antigen that was excluded by G-25 but not by G-50, and a smaller antigen that was excluded by G-10 but not by G-15 and, as determined by gel filtration, has a molecular weight slightly lower than vitamin B(12).

Alcohols↗

PubMed1983

Genetic mapping in the major histocompatibility complex by restriction enzyme site polymorphisms: most mouse class I genes map to the Tla complex.

From a genomic library constructed from sperm DNA of the inbred BALB/c mouse, we previously isolated 54 cosmid clones that contain 36 class I genes and can be divided by restriction map analyses into 13 gene clusters. We have isolated single- and low-copy DNA probes from each of these clusters to visualize restriction enzyme site polymorphisms in the DNAs from various congeneic and recombinant congeneic mice. These polymorphisms permit us to map each of the 13 cosmid clusters to a precise location in the major histocompatibility complex of the mouse. Thirty-one of 36 class I genes map into the Tla complex of the major histocompatibility complex whereas the remaining 5 genes map to the H-2 complex. Thus, all 36 class I genes are located in the major histocompatibility complex. Analysis of the number of restriction enzyme fragments visualized by the single- and low-copy DNA probes suggests that the class I genes in different inbred strains of mice probably undergo gene duplications and deletions, presumably by homologous but unequal crossing-over.

Animals↗

PubMed1989

Physical linkage of a guanine nucleotide-binding protein-related gene to the chicken major histocompatibility complex.

Several genes were found closely associated with major histocompatibility class I and class II beta-chain genes in chicken genomic DNA clusters by hybridizing tissue-specific cDNA probes to cosmid clones. A cDNA probe for one of these genes, probe C12.3 isolated from a chicken liver cDNA library, was used to clone the homologous sequence H12.3 from a human B-lymphoblastoid cell line cDNA library. C12.3 and H12.3 encode exactly the same 317-residue-long protein. The sequence of 12.3 shows significant homology with the two known guanine nucleotide-binding protein beta subunits (GP beta 1 and GP beta 2) and other proteins that all share the same segmented structure with seven internal homologous repeats about 45 residues in length. Unlike the chicken gene, the human H12.3 gene and its mouse counterpart are not located on the same chromosome as the major histocompatibility complex. A possible involvement of the C12.3 gene product in major histocompatibility complex-linked control of lymphocyte proliferation in chickens is discussed.

Amino Acid Sequence↗

PubMed1990

Specific binding of antigenic peptides to separate alpha and beta chains of class II molecules of the major histocompatibility complex.

Class II molecules of the major histocompatibility complex bind antigenic peptides and present them to T-helper cells. Class II molecules are heterodimers consisting of one alpha and one beta chain. Here we report that each isolated alpha and beta chain binds antigenic peptides and that this binding is specific. The specificity of peptide binding was investigated by employing the murine major histocompatibility complex haplotypes I-Ad and I-Ek and fluorescence-labeled peptides of chicken ovalbumin and pigeon cytochrome c, respectively, which are known to be specific for these haplotypes. The major histocompatibility complex molecules were incubated with these peptides and subjected to SDS/PAGE under nondenaturing conditions. The gels were then scanned for the fluorescent peptides and, after silver staining, for proteins. We found that the fluorescence-labeled peptide fragment of ovalbumin bound preferentially to the isolated alpha and beta chains of I-Ad, whereas the fluorescence-labeled peptide fragment of pigeon cytochrome c bound preferentially to the isolated alpha and beta chains of I-Ek. The alpha and beta chains of each haplotype bound their specific peptides about equally well, suggesting comparable affinities. Our results indicate that in vivo the kinetic pathway for the formation of antigenic peptide complexes with the alpha/beta heterodimers may involve the initial formation of complexes of the alpha and/or beta chains with the specific antigenic peptides.

Animals↗

PubMed1993

Interference with major histocompatibility complex class II-restricted antigen presentation in the brain by herpes simplex virus type 1: a possible mechanism of evasion of the immune response.

Host survival of herpes simplex virus type 1 (HSV-1) infection depends on the establishment of latent infections in both peripheral and central nervous systems. Strains of HSV-1 that are successful in escaping the immune response produce a lethal infection. We now report a possible mechanism of immune response evasion used by HSV-1. After intraocular inoculation of mice, HSV-1 strain F established a latent infection in the brain, whereas strain KOS did not. The immune response to HSV-1 infection (strains KOS and F) in the brain was characterized by induction of major histocompatibility complex class II expression and recruitment of CD4+ and CD8+ cells to highly restricted sites of intracerebral viral infection. Major histocompatibility complex class II antigen expression was primarily intracellular in strain KOS infection centers and at the cell surface in strain F infection centers. We propose that major histocompatibility complex class II-restricted viral-antigen presentation to T cells is interrupted during strain KOS infections, thereby allowing KOS infection to evade T-cell-mediated events that would normally protect the host from a lethal infection. Immunocompromised mice (athymic or irradiate mice) could not survive strain F infections; however, latent F infections were established in irradiated mice reconstituted with naive lymph node and spleen cells. These data suggest that class II-restricted presentation of viral antigens is required for the control of HSV-1 infections in the nervous system.

Animals↗

PubMed1994

Peptidase activities of proteasomes are differentially regulated by the major histocompatibility complex-encoded genes for LMP2 and LMP7.

Recent studies have implicated proteasomes in the generation of the antigenic peptides that are presented on major histocompatibility complex class I molecules to T lymphocytes. Interferon gamma modifies the subunit composition of proteasomes and causes changes in their peptidase activities that should favor the production of peptides with hydrophobic or basic carboxyl termini (i.e., the types found on major histocompatibility complex class I molecules). It has been proposed that these changes in peptidase activity are due to incorporation into proteasomes of the major histocompatibility complex-encoded subunits LMP2 and -7, which are induced by interferon gamma. Here we show by gene transfection into lymphoblasts or HeLa cells that LMP7 increases the capacity (Vmax) of 20S and 26S proteasomes to cleave peptides after hydrophobic and basic residues without affecting hydrolysis after acidic residues. These changes depended on the amount of LMP7 subunits incorporated into proteasomes. Transfection of LMP2 reduced cleavage of peptides after acidic residues, increased hydrolysis after basic residues, and did not affect the hydrophobic activity. Since the activity of the total proteasome population changed after incorporation of only small amounts of LMP2 or -7, these subunits must cause major alterations in peptidase activity. Thus, their expression can account for the changes in proteasome activity induced by inteferon gamma, and these findings lend further support to the proposed roles of LMPs in altering the nature of the peptides generated for antigen presentation.

Amino Acid Sequence↗

PubMed1970

Histocompatibility type and immune responsiveness in random bred Hartley strain guinea pigs.

Outbred Hartley strain guinea pigs capable of responding immunologically to 2,4-dinitrophenylated poly-L-lysine were shown to display a histocompatibility specificity in common with inbred strain 2 guinea pigs. This histocompatibility specificity was not detected in guinea pigs unable to respond immunologically to DNP-PLL. The result suggests that the poly-L-lysine specific immune response gene is very closely linked or even identical with a gene determining a major histocompatibility antigen in guinea pigs.

Animals↗

PubMed1978

Primary in vitro cell-mediated lympholysis reaction of NZB mice against unmodified targets syngeneic at the major histocompatibility complex.

T-cell cytotoxicity of NZV mice was tested after in vitro sensitization against a group of H-2 identical strains (BALB/c, B10.D2, DBA/2, HW19). A highly significant and unexpected unidirectional cell-mediated lympholysis (CML) reaction by the sensitized NZB effector cells on these targets was found. After sensitization in vitro with stimulator cells of one H-2d strain, NZB effector cells (H-2d) lysed all other H-2d targets and to a lesser degree, some non-H-2d targets (C57BL/10, DBA/1, B10.Q, CBA, B10.S, A.SW). NZB targets were not lysed. Differences in the major histocompatibility region between NZB and other H-2d strains could be excluded as a possible explanation for the observed reaction of NZB (H-2d) against other H-2d strains. These results consequently represent the first description of a primary in vitro CML directed against determinants not coded for in the major histocompatibility complex. The responsible effector cells are demonstrated to be T cells. The CML of NZB against H-2 identiical targets appears best explained by a reaction against minor histocompatibility antigens. This, and the observed cross-reactions, would indicate that the cytotoxic T-cell system in NZB mice is not subjected to restrictions found in all normal mouse strains tested until now under similar conditions. It is suggested that this hyperreactivity is related to the autoimmune responsiveness of the NZB strain.

Animals↗

PubMed1980

Systemic immune unresponsiveness induced in adult mice by anterior chamber presentation of minor histocompatibility antigens.

The ability to introduce carefully controlled numbers of viable cells into the anterior chamber of mouse eyes made it possible to examine the interrelationship between presentation of antigens into the anteior chamber and into conventional body sites and their synergistic/antagonistic effects on the immune system. P815 mastocytoma (DBA/2; H-2d) cells are syngeneic with BALB/c hosts at the major histocompatibility locus, but differ at multiple minor histocompatibility loci. When P815 cells were injected subcutaneously, they were rejected by BALB/c recipients who became specifically immune. By contrast, when P815 cells were injected intracamerally, they grew progressively into massive intraocular tumors; moreover, these BALB/c hosts proved subsequently unable to reject subcutaneously injected P815 cells, and, more impressively, failed to reject DBA/2 skin allografts placed orthotopically. Minor histocompatibility antigens, presented first through the anterior chamber of mouse eyes, elicit a suppressive rather than an aggressive host immune response that protects cells that bear these antigens from a destructive alloimmune reaction at both intracameral and systemic sites.

Animals↗

PubMed1981

Induction of lymphoid cell chimerism in noninbred, histocompatible rabbits. A new model for studying allotype suppression in the rabbit.

Noninbred rabbits, matched with regard to the major histocompatibility complex (RLA-A and RLA-D loci) but mismatched for Ig allotypes, served as donors (adult) and recipients (newborn) of lymphoid cells. Lasting chimerism regularly followed the transfer of 1 x 10(8)-3 x 10(8) spleen, lymph node, or bone marrow cells, as indicated by the continued production of Ig with allotypic determinants of both donor and recipient. Typically, Ig of donor allotype accounted for 25-50% of total allotypic Ig at 4 wk of age and the amount of donor Ig produced remained stable for up to 20 mo. Total allotypic Ig levels remained normal in the chimeric rabbits. "Chimeric drift" or a gradual diminution of donor products over a period of several months, occurred in some individuals. Transfer of lymphoid cells from allotype-suppressed adult donors to newborns of appropriate allotypes did not result in specific suppression of the target allotype in the recipients. Other experiments showed that lymphoid cells from suppressed donors adoptively transferred to histocompatible recipients continued to synthesize Ig of the nonsuppressed type only. The suitability of using an outbred population of histocompatible but allotype-mismatched rabbits for analyzing allotype suppression and other immunoregulatory phenomena is demonstrated by the results presented here.

Animals↗

PubMed1999

Immunoglobulin E-independent major histocompatibility complex-restricted T cell peptide epitope-induced late asthmatic reactions.

Intradermal administration of short overlapping peptides derived from chain 1 of the cat allergen Fel d 1 (FC1P) that did not cross-link IgE, elicited isolated late asthmatic reactions with no visible early or late cutaneous response in 9/40 cat-allergic asthmatics. Four of the nine were human histocompatibility leukocyte antigen DR13-positive, as compared with only 1/31 nonreactors. The other five reactors expressed either DR1 or DR4. To confirm major histocompatibility complex restriction, fibroblast cell lines transfected with HLA-DR molecules were used to present FC1Ps to cat allergen-specific T cell lines derived from subjects before peptide injection. FC1P3 (peptide 28-44 of Fel d 1 chain 1) was recognized in the context of DR13 alleles (DRB1*1301, 1302) and induced specific T cell proliferation and IL-5 production. T cells from a DR1(+) responder proliferated and produced IL-5 in the presence of FC1P3 and DR1 (DRB1*0101) fibroblast cell lines, whereas T cells from a DR4(+) subject recognized FC1P2 (peptide 22-37) when presented by DRB1*0405. We conclude that short, allergen-derived peptides can directly initiate a major histocompatibility complex-restricted, T cell-dependent late asthmatic reaction, without the requirement for an early IgE/mast cell-dependent response, in sensitized asthmatic subjects.

Adult↗

PubMed1999

The transmembrane sequence of human histocompatibility leukocyte antigen (HLA)-C as a determinant in inhibition of a subset of natural killer cells.

Molecular interactions with the extracellular domains of class I major histocompatibility complex proteins are major determinants of immune recognition that have been extensively studied both physically and biochemically. However, no immunological function has yet been placed on the transmembrane or cytoplasmic amino acid sequences of these proteins despite strict conservation of unique features within each class I major histocompatibility complex locus. Here we report that lysis by a subset of natural killer (NK) cells inhibited by target cell expression of human histocompatibility leukocyte antigen (HLA)-Cw6 or -Cw7 was not inhibited by expression of chimeric proteins consisting of the extracellular domains of HLA-C and the COOH-terminal portion of HLA-G. Assays using transfectants expressing a variety of HLA-Cw6 mutants identified the transmembrane sequence and, in particular, cysteine at position 309 as necessary for inhibition of 68% (25/37) of NK cell lines and 23% (33/145) of NK clones tested. Moreover, these NK clones inhibited by target cell expression of HLA-Cw6 and dependent upon the transmembrane sequence were found not to express or to only dimly express NK inhibitory receptors (NKIR1) that are EB6/HP3E4-positive. Furthermore, assays using monoclonal antibody blocking suggest that an NK receptor other than NKIR1 or CD94 is responsible for recognition dependent upon the transmembrane sequence of HLA-Cw6.

Amino Acid Sequence↗

PubMed2001

The immunogenicity of a new human minor histocompatibility antigen results from differential antigen processing.

Minor histocompatibility antigens (mHAgs) present a significant impediment to organ and bone marrow transplantation between HLA-identical donor and recipient pairs. Here we report the identification of a new HLA-A*0201-restricted mHAg, HA-8. Designation of this mHAg as HA-8 is based on the nomenclature of Goulmy (Goulmy, E. 1996. Curr. Opin. Immunol. 8:75-81). This peptide, RTLDKVLEV, is derived from KIAA0020, a gene of unknown function located on chromosome 9. Polymorphic alleles of KIAA0020 encode the alternative sequences PTLDKVLEV and PTLDKVLEL. Genotypic analysis demonstrated that the HA-8-specific cytotoxic T lymphocyte (CTL) clone SKH-13 recognized only cells that expressed the allele encoding R at P1. However, when PTLDKVLEV was pulsed onto cells, or when a minigene encoding this sequence was used to artificially translocate this peptide into the endoplasmic reticulum, it was recognized by CTLs nearly as well as RTLDKVLEV. This indicates that the failure of CTLs to recognize cells expressing the PTLDKVLEV-encoding allele of KIAA0020 is due to a failure of this peptide to be appropriately proteolyzed or transported. Consistent with the latter possibility, PTLDKVLEV and its longer precursors were transported poorly compared with RTLDKVLEV by transporter associated with antigen processing (TAP). These studies identify a new human mHAg and provide the first evidence that minor histocompatibility differences can result from the altered processing of potential antigens rather than differences in interaction with the relevant major histocompatibility complex molecule or T cell receptor.

Alleles↗