Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Histocompatibility Antigens Class I”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

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

At least 19 recordsLinked to original sources
PubMed1989

[Modulation of the expression of histocompatibility antigens class I (HLA-A,B,C) in the human pancreas].

In this study the expression of HLA class I molecules was analysed on caudal portions of ten pancreata from cadaver donors by means of indirect immunoperoxidase and immunophosphatase techniques. In 7 out of ten pancreata the results showed that islets tissue was almost negative for the expression of HLA Class I antigens as opposed to exocrine tissue that appeared positive. Within exocrine tissue and large sized islets strongly positive interstitial cells were also detected. Double stainings showed that the strongly positive interstitial cells expressed also Leu M1 antigens. Preliminary studies on the remaining three pancreata demonstrate an increase of hematic interstitial cells together with a parallel increase of HLA class I antigens by endocrine parenchyma. The above data suggest that an increase of interstitial cells within pancreas may influence islets antigenicity.

Antigens, Differentiation, Myelomonocytic↗
PubMed1991

Soluble histocompatibility antigen class I in breast cancer patients in relation to tumor burden.

Serum beta-2 microglobulin (B-2M) levels were studied in 365 breast cancer patients and 210 age-matched controls. The patients were divided into three groups: Group A, new patients at diagnosis; Group B, patients at follow-up; and Group C, metastatic patients. The mean B-2M of all breast cancer patients plus or minus one standard deviation (3.5 +/- 1.2; range, 1.1 to 5.9) was significantly higher than normal controls (1.29 +/- 0.49; range, 0.3 to 2.3; P less than 0.005). When the three patient groups were compared with each other, the mean B-2M level of Group A (3.0 +/- 1.5; range, 0.9 to 6.9) was similar to that of Group C (4.22 +/- 1.1; range, 2.0 to 6.4). The mean B-2M of both Groups A and C was significantly higher than that of Group B (2.38 +/- 1.02, range, 0.4 to 5.4; P less than 0.001). In Group A the mean B-2M decreased significantly after a 12-month period and reached the mean level of Group B but not that of normal controls. When patients in Group B were analyzed by their stage of disease at diagnosis, there was no significant difference between Stages I and II. There was a significant difference in the mean B-2M levels between Stages I and III. In relapsing patients, mean B-2M levels increased. These findings suggest that serum B-2M levels may reflect tumor burden, and even in patients at follow-up, occult tumor cells may activate the immune system.

Adult↗
PubMedDate not supplied

[Analysis of distribution of histocompatibility antigens class I and II in children with rheumatoid arthritis].

The authors studied distribution of antigens HLA A, B, C in 115 children and of antigens HLA DR in 102 children of the Russian nationality with classic or diagnosed juvenile rheumatoid arthritis (JRA). A rise in the frequency of antigens B21, B27 and DR3 was noted as compared to the control values. Then distribution of HLA-antigens was analysed in separate groups of patients depending on the nature of the clinical course of JRA. It was characteristic of patients of patients depending on the nature of the clinical course of JRA. It was characteristic of patients with mono-oligoarthritis with an polyarticular form of JRA to exhibit a rise in the frequency of antigens B27 and DRW8, with uveitis--of antigens A2, B27 and DRW8, with a high degree of activity of the inflammatory process--B21, with an allergic variant--B21, with an articulovisceral form--B21, DR3 and DR4, with Still's disease--DR3, rheumatoid nodes--DR2 and DR3. Thus, specificity of associations was determined in most of the cases by the nature of JRA clinical course. The authors confirm the number of associations previously described in the literature abroad.

Adolescent↗
PubMed1994

Major histocompatibility antigen class II expressing resting porcine T lymphocytes are potent antigen-presenting cells in mixed leukocyte culture.

The immune system of swine is unique in that the expression of CD4 and CD8 antigens defines four subpopulations of extrathymic resting T lymphocytes in blood as well as in lymphoid tissues. Recently, we documented an additional peculiarity of the porcine T lymphocyte population: a substantial proportion of resting T lymphocytes show constitutive surface expression of MHC II antigens (Saalmüller et al. 1991, Immunobiol. 183, 102). These cells belong predominantly either to the CD4-CD8+ or to the CD4+CD8+ T lymphocyte subpopulations. This report describes the antigen-presenting cell function of MHC II+ T lymphocytes in mixed leukocyte cultures. Experiments employing highly purified T lymphocytes as alloantigen-presenting stimulator cells resulted in a high proliferative and cytolytic alloantigen-specific T lymphocyte response. After separation of T lymphocyte stimulators into MHC II- and MHC II+ fractions, alloantigen-presenting cell function could be assigned to the MHC II+ T lymphocyte subset. Although the mechanisms involved in the response to alloantigen are not completely understood and may be different from conventional antigen presentation, this is the first report where naive resting MHC II+CD8+ T lymphocytes can be defined as antigen-presenting cells, presenting alloantigen to cells of their own lineage.

Animals↗
PubMedDate not supplied

Effects of placental extracts on the immune response to histocompatibility antigens: class deviation of alloantibody response and allograft enhancement.

Placental extracts obtained from CBA (H-2k) mice during syngeneic (CBA female X CBA male) pregnancy were evaluated for their capacity to deviate the immune reaction of CBA mice toward A/J(H-2a) immunizing spleen cells, as tested by alloantibody subclass formation and Sa 1 allograft accelerated rejection-or enhancement. The immunomodulatory activity appeared to be located in the soluble and in the insoluble extracts of placenta. The sodium deoxycholate (SDO) solubilized proteinic material, fractionated on Concanavalin A [Con A] and injected to CBA mice simultaneously with A/J spleen cells caused a suppression of the hemagglutinating titer and C-mediated cytotoxicity (IgG2). However, it also favoured antibody-mediated mast cell degranulation (IgG1) and Sa 1 allograft enhancement. The presence and role of IgG1 antibodies in both tumor enhancement and gestation has been described. It is concluded that placenta contains Con A-binding glycoproteins which are located in the membranes and released in soluble form. They exert their immunomodulatory effect in a way which might help the successful outcome of pregnancy as it helps to enhance the development of allografted sarcoma.

Animals↗
PubMed1987

Biosynthesis and processing of class II histocompatibility antigens.

The class II major histocompatibility antigens at the cell surface exist as heterodimers of alpha and beta subunits. During biosynthesis, these subunits are associated with a third chain, the invariant (I) or I chain. Association with the I chain occurs early in biosynthesis in the rough endoplasmic reticulum and persists during transport through the Golgi apparatus. One of the two alpha subunit N-linked oligosaccharides and the single beta subunit N-linked oligosaccharide are converted to the complex form during Golgi transit. In the human system, both I chain N-linked oligosaccharides can also be processed to the complex form, and at least two O-linked oligosaccharides can be added to the I chain. At some point during transit to the cell surface, class II antigens associate with a proteoglycan bearing chondroitin sulfate side chains. Complexes containing alpha, beta and I chain subunits and the associated proteoglycan accumulate in human B-cell lines treated with the ionophore monensin, an inhibitor of Golgi transport, suggesting that this may be a biosynthetic intermediate in class II antigen transport and assembly. Prior to cell surface expression of class II antigens, the exocytic pathway which they follow intersects the endocytic route, followed by certain ligands internalized by receptor-mediated endocytosis. The I chain appears to dissociate from mature class II alpha, beta dimers prior to their cell surface expression but following the intersection of the exocytic and endocytic pathways.

Animals↗
PubMed1992

Quantitative regional variation in the expression of major histocompatibility class II antigens in enterocytes of the mouse small intestine.

The qualitative and quantitative expression of major histocompatibility class II antigens was investigated in the absorptive epithelium of the duodenum, jejunum, and ileum from mice of C3H/He (H-2k haplotype) and C57BL/6 (H-2b haplotype) strains by peroxidase-antiperoxidase labelling and image analysis. Immunohistochemical labelling revealed that the expression of class II antigens was greatest in the ileum and decreased proximally towards the duodenum. The villus epithelium of the duodenum showed a granular staining pattern in the apices of some cells. In the jejunum, an increased expression was demonstrated in the apical and basal cytoplasm of all cells covering the villus. Cells at the tip of the villus, in addition, showed staining of the lateral surfaces. Ileal enterocytes demonstrated the most intense immunostaining appearing in the cytoplasm and along baso-lateral surface membranes. Quantitative analyses confirmed that a highly significant (p less than 0.0001) difference in expression of class II antigens occurred in the three regions of the small intestine, which corroborated the qualitative findings. This regional variation of class II molecules by the absorptive epithelium may influence regional differences in antigen presenting functions and immune responsiveness to ingested antigens.

Animals↗
PubMed1993

[Aberrant expression of major histocompatibility complex class II antigen in inflammatory myopathies].

Although major histocompatibility complex (MHC) class I molecules have been consistently demonstrated on muscle fibers of patients with inflammatory myopathies (IM), results concerning the expression of MHC class II molecules have been conflicting and mechanism of the expression remains to be elucidated. Expression of MHC and neural cell adhesion molecules (N-CAM) was analyzed in 38 cases of IM and in 13 cases of normal and disease controls by the immunocytochemical method. The sarcolemmaL HLA-ABC molecules were seen in all IM cases, and were visualized on the every muscle fiber in 68% of the cases. In contrast, the HLA-DR, -DP, or -DQ expression was seen on scattered fibers in 37%, 11%, 5% of IM cases, respectively. The HLA-DR reactivity was often seen on muscle fibers in the vicinity of infiltrating cells or on the perifascicular fibers. The HLA-DR positive fibers did not express N-CAM, suggesting a degenerating/regenerating process of muscle fibers was not contributory to the aberrant expression of MHC class II molecules. The perifascicular HLA-DR expression was related to the perifascicular atrophy and was more frequent in polymyositis complicated with interstitial pneumonitis. Those results suggest that increased expression of MHC class I molecules precede the aberrant expression of MHC class II molecules, and the perifascicular atrophy might reflect immunopathological processes.

Adult↗
PubMed2000

Relationship between gingival hyperplasia and class II histocompatibility antigens in renal transplant recipients.

Gingival hyperplasia, a well-known side effect of ciclosporin A (CS-A), is much more prominent when CS-A is used in combination with calcium channel blockers, especially dihydropyridines. On the other hand, it is interesting to note that this complication is not observed in all patients using this drug combination. This study was conducted in order to investigate the relationship (if any) between major histocompatibility complex antigens and gingival hyperplasia. Seventy-six renal transplantation patients were evaluated by an experienced dentist for gingival hyperplasia. The patients were then divided into two groups according to the presence (group 1, n = 18) or absence (group 2, n = 58) of gingival hyperplasia. There was no significant difference between the two groups regarding age, sex, transplant age, donor type, antihypertensive and immunosuppressive therapy protocols, and CS-A levels. HLA-DR2 antigen was present in 63% of the patients with gingival hyperplasia and in 34% of the patients without gingival hyperplasia. However, the HLA-DR1 antigen frequencies were found to be 11 and 22% in group 1 and group 2, respectively. In patients receiving nifedipine as an antihypertensive therapy, gingival hyperplasia developed more often than in patients receiving verapamil or diltiazem. As a result, in renal allograft recipients with HLA-DR1 antigen, gingival hyperplasia was seen less frequently than in HLA-DR2-positive patients. It is believed that the presence of these antigens regulates the response of the patients to either CS-A and/or calcium channel blockers.

Adult↗
PubMed1993

HMT, encoded by H-2M3, is a neoclassical major histocompatibility class I antigen.

H-2M3 encodes HMT, the major histocompatibility complex (MHC) class I heavy chain of the maternally transmitted antigen (Mta). Like classical MHC class I genes, the expression of M3 can be stimulated by gamma-interferon and its message can be detected from mid-gestational embryos (day 8) through adulthood. HMTb, a nonimmunogenic allelic form of HMT, differs from the common HMTa molecule by four amino acids, of which only two (residues 31 and 95) are located in the alpha 1 and alpha 2 domains that form the peptide-binding groove. Recognition of site-directed mutants by Mta-specific cytotoxic T lymphocytes was hardly affected by the substitution of Met for Val31 but was abolished by the substitution of Gln for Leu95, which is located in the beta-sheet floor of the peptide-binding groove. Thus a single amino acid difference is responsible for the immunological silence of HMTb.

Animals↗
PubMed1988

Effects of tumor necrosis factor on the interferon-gamma-induced major histocompatibility complex class II antigen expression by human endothelial cells.

Effects of tumor necrosis factor-alpha (TNF) and interferon-beta (IFN-beta) on the IFN-gamma-induced major histocompatibility complex (MHC) class II expression on human umbilical vein endothelial (HUVE) cells are reported. TNF inhibited the induction of MHC class II expression by IFN-gamma markedly, when added before or simultaneously with IFN-gamma. However, TNF added to the cells 24 h after IFN-gamma enhanced the expression of MHC class II antigens. IFN-beta inhibited the MHC class II expression irrespective of the time at which it was added to the cells. Addition of IFN-beta, TNF, IFN-gamma, and the combination of IFN-beta and IFN-gamma or TNF and IFN-gamma, resulted in all cases in an enhanced MHC class I antigen expression. Antibodies directed against IFN-beta reversed the inhibition of MHC class II expression by both TNF and IFN-beta. The enhancing effect of TNF could not be inhibited by anti-IFN-beta indicating that TNF mediates enhancement of IFN-gamma-induced MHC class II expression via a pathway other than IFN-beta. The role of TNF in the up-regulation as well as in the down-regulation of MHC class II expression in inflammatory processes is discussed.

Antigen-Antibody Reactions↗
PubMedDate not supplied

A gene in the human major histocompatibility complex class II region controlling the class I antigen presentation pathway.

Major histocompatibility complex (MHC) class I molecules export peptides to the cell surface for surveillance by cytotoxic T lymphocytes. Intracellular peptide binding is critical for the proper assembly and transport of class I molecules. This mechanism is impaired as a result of a non-functional peptide supply factor gene (PSF) in several human mutant cell lines with genomic lesions in the MHC. We have now identified PSF in the MHC class II region by deletion mapping in mutants and chromosome-walking. PSF is homologous to mammalian and bacterial ATP-dependent transport proteins, suggesting that it operates in the intracellular transport of peptides.

Amino Acid Sequence↗
PubMed1987

Gamma interferon, but not Mycobacterium leprae, induces major histocompatibility class II antigens on cultured rat Schwann cells.

In order to investigate the possible role of Schwann cells in immune reactions, and in particular their involvement in the response to infection with Mycobacterium leprae, it was determined under what conditions Schwann cells express major histocompatibility complex class II (MHC class II) antigens, since these molecules are thought to have a key role in antigen presentation during cellular immune responses. In situ and in vitro preparations from newborn and adult rat sciatic nerves were used as a model system to examine this question. Schwann cells in dissociated cell cultures did not express immunohistochemically detectable amounts of MHC class II antigens. Teased nerve preparations from the sciatic nerves of healthy adult rats showed no detectable immunolabelling of either myelin-forming or non-myelin-forming Schwann cells. When dissociated Schwann cell cultures derived from the sciatic nerves of either neonatal or adult rats were treated with 10, 50 or 100 units of gamma interferon, MHC class II antigens were detectable on the surface of some Schwann cells 48 h after addition of the interferon. By 72 h, 32.29 +/- 3.9% of Schwann cells in the cultures from neonatal rats and 53.32 +/- 5.4% of Schwann cells in cultures from adult rats, identified by the presence of intracellular S-100, were clearly MHC class II-positive, especially at doses of 50 and 100 units per ml of gamma interferon. Some, but not all, of the fibroblastic cells were very weakly MHC class II-positive. Infection of the cultures with Mycobacterium leprae did not induce MHC class II antigen expression in either Schwann cells or fibroblasts.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗
PubMed1991

Expression of medial class I histocompatibility antigens on RMA-S mutant cells.

The RMA-S mutant T cell line is defective in H-2b restricted antigen presentation and has markedly reduced surface expression of Kb and Db. We examined RMA-S for the expression of the medial class I histocompatibility antigens Qa1b and Mta. While RMA-S targets varied in their susceptibility to lysis by cytotoxic T lymphocytes (CTL) specific for Qa1b, Mta levels were detectable but consistently low compared to the parent RMA cell line. Addition of synthetic ND1 alpha 1-26 or ND1 alpha 1-17 peptides that mimic MTF alpha (the ligand of Mta) increased killing of RMA-S by anti-Mta alpha CTL to levels comparable to or better than RMA, with 300 nM peptide being fully effective. None of the MTF peptides increased the killing of RMA-S by anti-H-2b or anti-Qa1b CTL, even at the highest (1 microM) peptide concentrations. RMA-S cells treated with 100 microM of either the ND1 alpha 4-26 or ND1 alpha 1-26 peptides showed a small increase in the fluorescent staining for beta 2-microglobulin but not for H-2Kb or H-2Db. These results show that Mta and Qa1b, although affected, are not obliterated by the defect in RMA-S cells; that the association of MTF peptides with HMT is exclusive; and that MTF enters the endoplasmic reticulum in the same fashion as other endogenous peptides.

Animals↗
PubMed1986

Shared T cell recognition sites on human histocompatibility leukocyte antigen class II molecules of patients with seropositive rheumatoid arthritis.

Seropositive rheumatoid arthritis (RA) in adult and juvenile patients is associated with the serologic marker HLA-DR4. This association is incomplete; about one-third of the patients lack the disease-associated HLA-DR4 haplotype. The main biological function of class II molecules is to restrict the recognition of antigen by T lymphocytes. We therefore tested the hypothesis that patients with seropositive RA share T cell recognition sites for an unknown antigen and that such T cell "epitopes" are not identified by conventional serologic typing. We generated alloreactive human T cell clones by stimulating peripheral blood lymphocytes of normal donors against a lymphoblastoid cell line from a juvenile patient with seropositive RA. A panel of clones that recognized only HLA-Dw14 cells on a panel of homozygous typing cells was used to analyze class II molecules of adult patients with seropositive RA. By inhibition studies using monoclonal antibodies, the epitopes recognized by the different clones could be further characterized and assigned either to DR- or to DQ-encoded cell surface products. By using four different clones, it was possible to identify Dw14-associated T cell epitopes on all seropositive rheumatoid patients tested who typed HLA-DR4-positive and also on all eight DR4-negative patients tested. Approximately one-half of nonrheumatoid DR4-positive donors carried one or more determinants recognized by these clones; the expression of these allodeterminants in DR4-negative nonrheumatoid patients was rare (less than 10%). Thus, alloreactive human T cell clones are powerful tools to define T cell recognition sites on class II molecules that are not identified by conventional typing. Using T cell clones with specificities for determinants expressed on Dw14 homozygous typing lines, we were able to demonstrate shared epitopes on cells of all patients tested with seropositive RA irrespective of their HLA-D or HLA-DR type. These data suggest that major histocompatibility complex class II antigens of RA patients might be much more homogeneous than demonstrated by the incomplete HLA-DR4 association.

Arthritis, Rheumatoid↗
PubMed1992

Cell subsets responding to purified hepatocytes and evidence of indirect recognition of hepatocyte major histocompatibility complex class I antigen. II. In vitro-generated "memory" cells to class I+ class II- hepatocytes.

Purified hepatocytes stimulate the development of L3T4-, Ly2+ allospecific cytolytic T cells from naive splenocytes after 5 days in primary mixed lymphocyte-hepatocyte culture (MLHC). Previous studies indicate that the immunogenicity of purified hepatocytes relates to the expression of MHC class I antigen. The purpose of the following experiments was to identify the cell subsets that specifically recognize hepatocyte MHC class I antigen. We employed primed lymphocyte testing (PLT) in order to test for a "second set" response. Cells from primary MLHC reverted to a functionally quiescent state when they were grown in culture for an additional 7-9 days. The cells were then tested for cytotoxicity or rechallenged with allogeneic, syngeneic, or "third party" hepatocytes and tested for proliferation. Allocytotoxicity was low on day 12 in MLHC, but the sensitized cell population demonstrated peak proliferation in response to allogeneic hepatocytes 48 hr after restimulation. When bulk PLT cells were immunodepleted, both L3T4+, Ly2- and L3T4-, Ly2+ T cell subsets demonstrated a "second set" response to allogeneic hepatocytes consistent with specific recognition of and retention of "memory" for hepatocyte MHC class I alloantigen.

Animals↗