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Results for “Major Histocompatibility Complex”

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PubMed1983

Identification of the receptor for antigen and major histocompatibility complex on human inducer T lymphocytes.

Human T cell clones and monoclonal antibodies directed at their surface structures were used to define the receptor for the antigen and major histocompatibility complex on inducer T lymphocytes. The results indicated that the receptor is a single complex consisting of the monomorphic T3 molecule with a molecular weight of 20,000 to 25,000 and a clonotypic disulfide linked heterodimer Ti with a molecular weight of 90,000. Sepharose-bound monoclonal antibodies (anti-Ti4 or anti-T3) to the receptor could activate clonal proliferation and inducer function for B cell immunoglobulin secretion and thus substitute for the appropriate combination of major histocompatibility complex gene product and specific antigen.

Antibodies, Monoclonal↗
PubMed1994

Scintigraphic detection of early cardiac rejection by iodine 123-labeled monoclonal antibody directed against monomorphic determinant of major histocompatibility complex class II antigens.

Although it has been shown that early cardiac rejection can be visualized by radioimmunoscintigraphy targeting major histocompatibility complex class II antigen, the use of antibodies that bind to a polymorphic determinant of class II antigen has certain disadvantages for clinical application. This investigation was designed to examine the feasibility of scintigraphic detection of cardiac allograft rejection by using a monoclonal antibody that reacts with a monomorphic determinant of rat IA antigens. Twenty PVG rats (RT1c) and five DA rats (RT1a) underwent heterotopic transplantation with DA hearts. Two of the 20 allografted rats were treated with FK506 (2 mg/kg/day). Seventeen rats were injected intravenously with 80 microCi of iodine 123-labeled monoclonal antibody reactive with a monomorphic determinant of rat major histocompatibility complex class II antigens (Ox6) 16 hours before scintigraphy, and images were compared with those obtained by injection of 123I-labeled monoclonal antibody against a polymorphic determinant of class II antigens (F17-23-6, anti-RT1a) (n = 8). Background activity was higher in rats injected with Ox6 than in rats injected with F17-23-6. Uptake of labeled Ox6 in the grafts reflected the severity of rejection as determined by histopathologic criteria. Rejecting allografts with lymphocyte infiltration but without myocyte necrosis could be identified by the scintigraphy with use of labeled Ox6.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Genetic control of the immune responsiveness to Streptococcus mutans by the major histocompatibility complex of the rat (RT1).

The lymph node cells from 11 strains of rats, differing in the genotype of the major histocompatibility complex of the rat (RT1), were examined on the basis of their proliferative response to the cell wall antigen of Streptococcus mutans. The 11 rat strains fell into three groups: high, intermediate, and low responders. To demonstrate the influence of the major histocompatibility complex on immune responsiveness to S. mutans, further experiments were performed using the RT1-congenic rat strains WKAH.1L(LEW), WKAH. 1AV1(ACI), and WKAH.1J(LEJ), which differ only in the genotype of the RT1 region. Although the background genes of each strain were of WKAH origin, WKAH.1L(LEW) and WKAH.1AV1(ACI) rats showed a low response whereas WKAH.1J(LEJ) rats showed a moderate response to the S. mutans cell wall antigen. The results indicate that the immune response is controlled by the class II gene(s) in RT1. Furthermore, the RT1.D locus products were shown to play an important role in the restriction molecule, since a monoclonal antibody, HOK7, directed to the RT1.Dk locus products reduced the proliferative response of lymph node cells.

Animals↗
PubMed1996

Generation of in vitro natural cytotoxicity of horse lymphocytes against sarcoid-derived tumor cells not expressing major histocompatibility complex antigens.

OBJECTIVE: To analyze in vitro lymphocyte-mediated immune responses of horses with sarcoids against allogeneic sarcoid cells containing endogenous retrovirus but not expressing major histocompatibility complex antigens. DESIGN: Lymphocyte-mediated immune reactions were assessed by means of proliferative responses in mixed lymphocyte tumor cell culture (MLTC) assay and lymphocyte-mediated cytotoxicity against various equine target cells. ANIMALS: 12 horses with sarcoid tumors and 15 control horses. PROCEDURE: Blood lymphocytes were cocultured in MLTC with allogeneic sarcoid cells (Mc-1, BayMc-1), equine testis cells, or normal equine dermal fibroblasts. Lymphocytes were assayed for proliferative responses by [3H]thymidine uptake and for cytotoxicity against the same targets by 51Cr release assay. The lymphocyte populations were analyzed for some common surface markers. RESULTS: Lymphocytes from horses with sarcoids exerted an anamnestic proliferative response in MLTC against Mc-1 cells, but this procedure never generated cytotoxic lymphocytes. However, lymphocytes from all horses cultured in medium with 10% allogeneic serum only had selective. natural cytotoxicity against Mc-1 that was generated without DNA synthesis. Approximately 80% of the lymphocytes disappeared during culture; however the remaining population of small, viable lymphocytes indicated a decrease of CD4+ T lymphocytes, but numbers of T cells with receptors for Helix pomatia A hemagglutinin were unaffected. Few lymphocytes had Fc-receptors for IgG, were complement-reactive positive cells or were B cells expressing surface immunoglobulin. CONCLUSIONS: Results may indicate a natural defense system, which preferentially recognizes and lyses tumor cells that are deficient in surface expression of major histocompatibility complex antigens, without intervention of conventional T-cell receptors or antibodies.

Animals↗
PubMed1982

The role of the human major histocompatibility complex in cytotoxic T-cell responses to virus-infected cells.

The human major histocompatibility complex (HLA) has been demonstrated to play two roles in the generation and expression of cytotoxic T-lymphocyte responses to virus-infected cells: (1) cytotoxic T cells can only recognize viral antigens in conjunction with antigens encoded by HLA-A and -B genes; and (2) HLA-linked genes may control the capacity to generate T-cell responses to a given virus or to virus in conjunction with particular self HLA-A and -B antigens. Analysis of T-cell responses generated in vivo to Epstein-Barr virus suggests that human T cells may recognize virus in conjunction with antigens other than the class I HLA polymorphic specificities.

Chromosome Mapping↗
PubMed1989

Restriction fragment length polymorphism analysis of major histocompatibility complex genes in the non-obese diabetic mouse strain and its non-diabetic sister strains.

It has been suggested that one of the recessive genes controlling diabetes in non-obese diabetic mice is linked to the major histocompatibility complex. We, therefore, performed restriction fragment length polymorphism studies of major histocompatibility complex genes (class I, II, and III) in non-obese diabetic mice in comparison with those of their non-diabetic sister strains, non-obese non-diabetic, cataract, and ILI mice which were derived from the same Jcl-ICR mice as the non-obese diabetic mouse was. When class II and III probes and a minimum of four restriction enzymes were used, class II and III genes of non-obese diabetic mice were indistinguishable from those of cataract and ILI mice but totally different from those of non-obese non-diabetic mice. The studies also indicated that A beta, E beta, and C4-Slp genes of non-obese diabetic, cataract, and ILI mice, and A alpha, A beta, E beta and C4-Slp genes of non-obese non-diabetic mice are different from those of BALB/c and C57BL/6 mice, respectively. While non-obese non-diabetic mice expressed the E alpha gene, non-obese diabetic, cataract, and ILI mice appeared to carry a deletion in the 5' end of the E alpha gene resulting in failure to transcribe the E alpha gene. When class I probe was used, cataract mice showed very different band patterns from those of the other ICR-derived mice. It is suggested that non-obese diabetic, non-obese non-diabetic, and ILI mice contain only a single class I D region gene.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1978

A safe blood transfusion procedure for immunization against major histocompatibility complex determinants in man.

A standardized procedure is proposed for deliberate immunizations against human major histocompatibility complex determinants. The data presented demonstrate its effectiveness and, by using a number of necessary precautions, this procedure has proven to be very safe. The following points are especially important: (1) exclusive utilization of regular blood donors as immunizers; (3) use of whole blood as an immunizing agent; and (3) use of small immunizing stimuli rather than large transfusions. This procedure can be recommended for the production of monospecific anti-HLA antisera and it may be useful if and when a deliberate transfusion policy for prospective kidney recipients is adopted.

Blood Transfusion↗
PubMed2003

Thermodynamic analysis of the increased stability of major histocompatibility complex class II molecule I-Ek complexed with an antigenic peptide at an acidic pH.

The differential scanning calorimetry analysis of the murine major histocompatibility complex class II molecule, I-E(k), in complex with an antigenic peptide derived from mouse hemoglobin, showed that the thermal stability at the mildly acidic pH is higher than that at the neutral pH. Although the thermal unfolding of I-E(k)-hemoglobin was irreversible, we extracted the equilibrium thermodynamic parameters from the kinetically controlled heat capacity curves. Both the denaturation temperatures and the enthalpy changes were almost independent of the heating rate over 1 degrees C per min. The linear relation between the denaturation temperature and the calorimetric enthalpy change provided the heat capacity changes, which are classified into one for the mildly acidic pH region and another for the neutral pH region. The equilibrium thermodynamic parameters showed that the increased stability at the mildly acidic pH is because of the entropic effect. These thermodynamic data provided new insight into the current structural model of a transition to an open conformation at the mildly acidic pH, which is critical for the peptide exchange function of major histocompatibility complex class II in the endosome.

Acids↗
PubMed1980

Evidence of similar organization of the chromosomes carrying the major histocompatibility complex in man and other primates.

The chromosome localization and gene synteny of the major histocompatibility complex (MHC) of the great apes and rhesus monkey were investigated using somatic cell hybrids. The presence of the MHC antigens was determined either with a microadsorption technique employing primate alloantisera, or with a radioimmune assay. The enzymes phosphoglucomutase 3 (PGM3), glyoxalase 1 (GLO1), mitochondrial superoxide dismutase (SOD2), and soluble maleic enzyme (ME1) were assayed in those hybrids where electrophoretic separations could be achieved. A chromosome homologous to the human No. 6 was found in the chimpanzee, gorilla, orangutan and rhesus monkey, and its genomic organization is similar to that of man.

Animals↗
PubMed1985

Trans-acting element(s) operating across species barriers positively regulate expression of major histocompatibility complex class II genes.

Raji, a human B lymphoma line, expresses high levels of major histocompatibility complex (MHC) class II antigens. Conversely, none of the detectable human Ia antigens is present in RJ 2.2.5, an immunoselected Raji variant. Clonal analysis, biochemical characterization, and nucleic acid hybridization studies of hybrids between mouse spleen cells and RJ 2.2.5 show that MHC class II gene expression is regulated in trans by a factor which, as judged by dominance studies, has the characteristics of an activator. Such a positive trans acting factor is expressed in mouse spleen cells, and is able to implement MHC class II gene expression across species boundaries. Expression of this factor in spleen cells strongly suggests that it plays a role in in vivo regulation of Ia expression. Additional data suggest that different subsets of class II genes such as DR and DQ may, in part, be regulated by different mechanisms. It has also been possible to show that the amount of In chain-specific mRNA, present at reduced levels in RJ 2.2.5 cells compared to the parental Raji cells, drastically increased in human X mouse cells hybrids reexpressing human Ia antigens, suggesting that the In chain gene and the class II genes, although located on different chromosomes, are regulated in a concerted fashion, either directly through the same implementing factor, or indirectly through a cascade mechanism.

Animals↗
PubMed2004

Analysis of the major histocompatibility complex in graft rejection revisited by gene expression profiles.

BACKGROUND: The precise role of major histocompatibility complex (MHC) molecules in graft rejection remains incompletely understood. The important role of foreign peptides in the alloimmune response was recently recognized. METHODS: We performed a comparative study of the functions of minor antigens Class I, Class II, and CD1 in murine cardiac allograft rejection by investigating the expression of a large panel of immune and inflammatory genes. To investigate the role of MHC Class II and I, our protocol analyzed allograft recipients deficient in MHC Class II and b2 microglobulin (b2-M), a critical component of the Class I heterodimer. We also included CD1 deficient recipients to differentiate effects in the beta2-M deficient strain due to CD1 deficiency versus the combined inactivation of CD1 and Class I. The serum cytokines tumor necrosis factor (TNF)-alpha interleukin (IL)-6, interferon (IFN)-gamma and IL-1beta were evaluated posttransplant by ELISA. The intragraft expression of 55 chemokines, chemokine receptors, and CD markers were measured by ribonuclease protection assay. The data were analyzed through hierarchical clustering dendrograms and self-organizing maps. RESULTS: The analysis indicates that each gene deficiency induces both the upregulation and the downregulation of distinct subsets of genes and that similar kinetics of rejection can be attributed to different molecular mechanisms. CONCLUSIONS: The study provides novel insights into the role of classical and non-classical MHC molecules in graft rejection.

Animals↗
PubMed1994

Recombination in the class III region of the mouse major histocompatibility complex.

The sites of meiotic recombination in the class II region of the mouse major histocompatibility complex (MHC) are clustered at hotspots. To search for hotspots in the class III region, we mapped recombinational breakpoints of 79 Ab:H2-D recombinants with 11 DNA markers; these included Tnx, the gene for an extracellular matrix protein, tenascin X, the Notch-related Int3 gene, and a microsatellite marker, D17Mit13, none of which had previously been mapped precisely. The results gave the gene order of Eb-61.1-Int3-Tnx-Cyp21/C4-Bf-Hsp68c-D17Mit13+ ++-Tnfa/Tnfb-D. The crossover sites in 40 of the 79 recombinants were confined within the Eb/Int3:Tnx/Cyp21 interval. The result demonstrated that an unequal distribution of recombination is a general feature of the mouse MHC, suggesting the presence of a recombinational hotspot within the Int3:Tnx interval.

Animals↗
PubMed2000

Genes of the class II and class III major histocompatibility complex are associated with typhoid fever in Vietnam.

The influence of genes of the major histocompatibility complex (MHC) class II and class III loci on typhoid fever susceptibility was investigated. Individuals with blood culture-confirmed typhoid fever and control subjects from 2 distinct geographic locations in southern Vietnam were genotyped for HLA-DRB1 and HLA-DQB1 alleles, the gene that encodes tumor necrosis factor (TNF)-alpha (TNFA [-238] and TNFA [-308]), the gene that encodes lymphotoxin-alpha, and alleles of the TNF-alpha microsatellite. HLA-DRB1*0301/6/8, HLA-DQB1*0201-3, and TNFA*2 (-308) were associated with susceptibility to typhoid fever, whereas HLA-DRB1*04, HLA-DQB1*0401/2, and TNFA*1 (-308) were associated with disease resistance. The frequency of all possible haplotypes of the 3 individually associated loci were estimated and were found to be significantly different in typhoid case patients and control subjects (chi2=55.56, 32 df; P=.006). Haplotypes that were either protective (TNFA*1 [-308].DRB1*04) or predisposed individuals to typhoid fever (TNFA*2 [-308].DRB1*0301) were determined. This report identifies a genetic association in humans between typhoid fever and MHC class II and III genes.

Alleles↗
PubMed1983

Toxicity but not arthritogenicity of Mycoplasma arthritidis for mice associates with the haplotype expressed at the major histocompatibility complex.

The use of inbred and congenic mouse strains established that toxicity and death induced by Mycoplasma arthritidis associates with the haplotype expressed at the murine major histocompatibility complex. Mice bearing H-2k and H-2d are susceptible, whereas those bearing H-2b are much more resistant. Mice susceptible to toxicity exhibited massive peritoneal adhesions and a decreased ability to clear organisms from the peripheral circulation. However, the severity of acute arthritis developing over a 3-month period was not statistically related to the haplotype expressed at the major histocompatibility complex. Lymphocyte activation in vitro by a soluble T-cell mitogen is also dependent on a similar haplotype expression.

Animals↗
PubMed1989

Influence of non-major histocompatibility complex differences on the severity of lymphocytic choriomeningitis.

The role of the non-major histocompatibility complex (MHC) genetic background in the development of lymphocytic choriomeningitis (LCM) was examined for a range of mouse strains of the H-2k haplotype. The onset of meningitis relative to the time of injection of LCM virus was delayed and the maximal level of cellular extravasation into cerebrospinal fluid was lower in C3H/HeJ and CBA/H compared with AKR/J, B10.Br and BALB/c.H-2k mice. Adoptive transfer experiments indicated that the C3H mice are genuine low responders, but immune spleen cells from the CBA/H were as potent on a cell-for-cell basis as those from the AKR/J. Further analysis with CBA/H, AKR/J and (CBA/H x AKR/J)F1 mice showed that the pattern of high response for the AKR/J was dominant, with the differential kinetics of the development of meningitis correlating with the cellularity of the cervical lymph nodes. Thus, the generation of the LCM inflammatory process is not dictated solely by the MHC phenotype.

Animals↗
PubMed1985

Mapping of steroid 21-hydroxylase genes adjacent to complement component C4 genes in HLA, the major histocompatibility complex in man.

The genes for four components (C) of complement in the human major histocompatibility complex (HLA) have been aligned previously in a series of overlapping cosmid cloned inserts. Those inserts, which contained the two C4 genes C4A and C4B, hybridized with human adrenal mRNA, indicating that they contain a gene expressed in the adrenal. The mRNA fraction of 2.4 kilobases (kb) hybridizes with genomic DNA of 4.5 kb, which is duplicated and lies about 1.5 kb 3' of both the C4A and the C4B complement genes. Sequencing of a 430-base section and comparison with the published cDNA sequence of bovine cytochrome P-450 21-hydroxylase, peptide sequences of porcine 21-hydroxylase, and a cDNA sequence of a rat liver cytochrome P-450 identified the gene as coding for human steroid 21-hydroxylase [steroid,hydrogen-donor:oxygen oxidoreductase (21-hydroxylating), EC 1.14.99.10]. Mapping of the gene was helped by use of a synthetic oligonucleotide based on the bovine cDNA sequence.

Adrenal Glands↗
PubMed1993

Human natural killer (NK) alloreactivity and its association with the major histocompatibility complex: ancestral haplotypes encode particular NK-defined haplotypes.

As ancestral haplotypes of the major histocompatibility complex (MHC) appear to define identical MHC haplotypes in unrelated individuals, unrelated individuals sharing the same ancestral haplotype should also share the same NK-defined allospecificities that have recently been shown to map to the human MHC. To test this prediction, multiple cell lines from unrelated individuals sharing the same ancestral haplotypes were tested for the NK-defined allospecificities. It was found that cells sharing the same ancestral haplotypes do have the same NK-defined specificities. Furthermore, the NK-defined phenotype of cells that possess two different ancestral haplotypes can be predicted from the NK-defined phenotypes of unrelated cells that are homozygous for the ancestral haplotypes concerned. Although the group 1 and 2 NK-defined allospecificities can be explained to some extent by HLA-C alleles, evidence is presented that additional genes may modify the phenotype conferred by HLA-C.

Alleles↗
PubMedDate not supplied

Mapping of the class II region of the human major histocompatibility complex by pulsed-field gel electrophoresis.

The class II region of the human major histocompatibility complex (MHC) encodes a polymorphic set of cell surface glycoproteins involved in the regulation of the immune response. Each glycoprotein is a heterodimer composed of a alpha-chain of relative molecular mass (Mr) 34,000 (34 K) and a beta-chain of Mr = 28K. The products of the class II region have been characterized by the mixed lymphocyte reaction, serology, primed lymphocyte typing and DNA cloning. DR, DQ and DP, three subregions containing both alpha- and beta-chains, and two additional loci, DZ alpha and DO beta, locate this gene cluster on the short arm of chromosome 6. The precise genomic organization of these loci have been difficult to determine. Here we describe the use of pulsed-field gel electrophoresis together with restriction endonucleases having few genomic restriction sites and Southern blotting, to determine the order of the subregions and to derive a map for the human class II region. The order of these loci is similar to that of the homologous loci in the murine class II region. Our study establishes the use of pulsed-field gel electrophoresis in mapping large regions of the genome in higher eukaryotes.

Cell Line↗