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PubMed1980

Parasite immunity and the major histocompatibility complex.

Parasite infestations offer fertile ground for investigation of the relationship between immunity, disease and the major histocompatibility complex (MHC). However, due to the complexities of parasite life cycles and the success of parasites in evading the immune response, immune reactions against the parasite often do not parallel protective immunity, and immunity does not imply lack of disease. -- An additional level of complexity is introduced in some forms of parasite immunity by accessory effector cells, e.g., macrophages and eosinophils, that need to be 'activated' for maximal effectiveness, and the 'activated' form of these cells may partly compensate for a deficiency in specific immune responses. -- It is not surprising, therefore, that polygenic effects operate in parasite immunity and reports linking non-MHC genes with parasite immunity far out number those linking MHC genes with it. From the reports that do link MHC genes with parasite immunity, two areas emerge that are interesting. First, the increased incidence of certain HLA genes in people with schistosomiasis who develop hepatosplenic disease may pinpoint individuals at risk of morbidity and direct early treatment to them. Second, mechanisms that intimately involve MHC products but are not linked to a particular MHC haplotype, may indicate newer areas in the investigation of parasite immunity.

Animals↗
PubMed1984

Experimental ultraviolet radiation carcinogenesis: I. Relationship of the major histocompatibility complex to tumor latency and immunogenecity.

The induction of skin tumors by ultraviolet radiation (UV) was compared concurrently in 3 inbred mouse strains (BALB/c, C3H, and C57BL/10) and 7 related H-2 (major histocompatibility complex) congenic strains of mice. The latency period for UV-tumor induction was observed to be shorter in BALB/c mice compared with that in C3H and C57BL/10 animals. Similarly, tumor latency periods in the different H-2 congenic mouse strains tested were comparable to those of their related background strain. The proportion of squamous cell carcinomas to spindle cell fibrosarcomas, as well as the ratio of progressor and regressor tumors, as determined by their ability to grow when transplanted into normal syngenic mice, were comparable for those strains of mice that shared common genetic backgrounds. Interestingly, for all strains of mice analyzed UV-regressor and UV-progressor tumors were found to arise randomly throughout the latency period. These studies suggest that, at least for the three parameters tested, genes or gene products encoded within the major histocompatibility complex do not influence either latency period, histologic type or immunogenicity of UV-induced skin tumors.

Animals↗
PubMed1995

Efficient binding of reduced peptide bond pseudopeptides to major histocompatibility complex class I molecule.

Reduced peptide bond pseudopeptide analogues have been examined for their ability to bind murine class I molecules of the major histocompatibility complex (MHC). Eight pseudopeptide analogues of an antigenic peptide derived from Plasmodium berghei (H-Ser252-Tyr-Ile-Pro-Ser-Ala-Glu-Lys-Ile260-OH) were obtained by systematically replacing one peptide bond at a time by a reduced peptide bond psi (CH2-NH). The resulting analogues were then tested for their binding to a recombinant single chain SC-Kd class I molecule. The comparative results show that five analogues can efficiently mimic the parent peptide while the introduction of the reduced bond between P3-P4, P7-P8, and P8-P9 is deleterious for SC-Kd binding. The fact that more stable pseudopeptides containing reduced peptide bonds can bind major histocompatibility complex molecules is of great interest for the design of peptidomimetics with potential therapeutical properties. Such peptide analogues may prove useful for the development of peptide-based cytotoxic T lymphocyte vaccines.

Amino Acid Sequence↗
PubMed1992

Major histocompatibility complex located complement C4 and steroid 21-hydroxylase gene rearrangements in couples with recurrent spontaneous abortions.

Major Histocompatibility Complex (MHC) class III located complement C4 and steroid 21-hydroxylase (21OH) genes, which form various deletion and duplication units, were studied by TaqI Restriction Fragment Length Polymorphism (RFLP) in 58 Finnish couples who suffered recurrent spontaneous abortions (RSA). The gene rearrangements found in the RSA couples did not differ from those in the controls.

Abortion, Habitual↗
PubMed1991

Chromosomal localization of the major histocompatibility complex (MHC) in the rhesus monkey and chimpanzee by fluorescence in situ hybridization.

Genes for the major histocompatibility complex (MHC) were localized by fluorescence in situ hybridization to the long arm of rhesus monkey chromosome 5. This localization contradicts previous reports, based on genetic investigation of somatic cell hybrids, that placed the MHC on chromosome 2 of this species. In the chimpanzee, the MHC loci were localized to 5p21.3, corresponding precisely to their location on human chromosome 6p21.3.

Animals↗
PubMed1978

At least two loci of the major histocompatibility complex can determine mixed lymphocyte stimulation in the rat.

Analysis of a recombinant haplotype of the major histocompatibility complex showed that two genetically separable loci (or groups of loci), LD--1 and LD--2, determine mixed lymphocyte stimulation in the rat. LD--1 maps into the H--1B region which contains the Ir genes and is associated with strong, mixed lymphocyte stimulation. LD--2 maps into the H--1A region and determines weak stimulation. LD--1 and LD--2 determinants can be detected by primed lymphocyte typing.

Animals↗
PubMed1983

Major histocompatibility complex (MHC)-linked genes affecting development.

Genes affecting growth and development which are linked to the major histocompatibility complex have been found in the mouse (t-complex) and in the rat (growth and reproduction complex, grc), and there is some evidence that they also exist in humans. The genes of the t-complex have different effects depending upon the specific combinations involved: skeletal and fertility abnormalities, complete or partial embryonic mortality, high transmission ratios (segregation distortion) in males, high level of linkage disequilibrium with H-2, and suppression of recombination over the adjacent portion of the chromosome. The grc in the homozygous state causes small body size, sterility in the male and reduced fertility in the female, partial embryonic mortality, and a high level of linkage disequilibrium with RT1. It also interacts epistatically with the heterozygous Tal (tail anomaly lethal) gene to cause complete embryonic death. Mice carrying t-haplotypes and rats carrying the grc have an antigen in the male germ cells which cross-reacts very strongly (t-antigen). Suggestive evidence for such genes in humans comes from (1) studies on the relationship between skeletal defects and HLA haplotypes; (2) the association of specific HLA and complement haplotypes with a high transmission ratio in males, linkage disequilibrium among certain HLA and complement specificities and suppression of recombination in some MHC haplotypes; and (3) the lack of homozygotes in an isolated inbreeding population of desert nomads (Kel Kummer Tuaregs). In addition, immunogenetic studies on couples having chronic spontaneous abortions suggest that there is an unusually high incidence of homozygosity for the HLA-D/DR and HLA-A loci in these couples, and this finding is consistent with the presence of linked loci which behave like t or grc.

Animals↗
PubMed1992

The optimal number of major histocompatibility complex molecules in an individual.

A straightforward argument is presented to calculate the number of different major histocompatibility complex (MHC) molecules in an individual that maximizes the probability of mounting immune responses against a large number of foreign peptides. It is assumed that increasing the number of MHC molecules per individual, n, has three different effects: (i) it increases the number of foreign peptides that can be presented; (ii) it increases the number of different T-cell receptors (TCRs) positively selected in the thymus; but (iii) it reduces the number of TCRs by negative selection. The mathematical analysis shows that n = 1/f maximizes the number of different TCRs that pass through positive and negative selection and that n = 2/f maximizes the probability to mount immune responses against a large fraction of foreign peptides. Here f is the fraction of TCRs deleted by one MHC molecule. Both results depend on approximations that are discussed in the paper. The model presented has implications for our understanding of the evolutionary forces acting on the MHC.

Animals↗
PubMed1990

Major histocompatibility complex genes and susceptibility to systemic lupus erythematosus.

Susceptibility to systemic lupus erythematosus is associated with major histocompatibility complex (MHC)--encoded genes. We have used nucleotide sequence analysis to better define the disease-associated MHC alleles. HLA-DR2, DQw1, and especially the rare allele DQ beta 1. AZH confer high relative risk (RR = 14) for lupus nephritis in a Caucasian population of patients. Pilot studies using historical controls suggest that these genes also confer a high risk in non-Caucasian ethnic groups (RR = 24-78). We have found that DR4 is significantly decreased in patients with lupus nephritis. Fifty percent of the patients with lupus nephritis had either the DQ beta 1.1, the DQ beta 1.AZH, or the DQ beta 1.9 alleles. These alleles share amino acid residues that have been predicted to be the contact points for antigen and the T cell receptor. These HLA alleles appear to have a direct role in the predisposition to lupus nephritis, whereas DR4 may have a "protective" effect.

Alleles↗
PubMed2003

Major histocompatibility complex and mate choice in sand lizards.

In mice and man, females prefer males with a major histocompatibility complex (MHC) genotype different to their own. We tested whether this phenomenon also occurs in the Swedish sand lizard (Lacerta agilis). Females in a laboratory experiment preferred to associate with odour samples obtained from more distantly related males at the MHC class 1 loci. Data on free-ranging lizards suggest that associations between males and females are nonrandom with respect to MHC genotype. However, male spatial distribution and mobility during the mating season suggest that the non-random pairing process in the wild may also be driven by corresponding genetic benefits to males pairing with less related females.

Animals↗
PubMed1984

Class 1 major histocompatibility complex antigens on human extra-villous trophoblast.

Using immunohistological techniques, class 1 products of the major histocompatibility complex (MHC) have been demonstrated on various forms of human extra-villous trophoblast in placental tissues taken from first, second and third trimester pregnancies. This contrasts with the absence of class 1 MHC antigens on all forms of villous trophoblast. The extra-villous trophoblast which reacted with antibodies to monomorphic class 1 MHC antigens consistently failed to bind HLA-A or HLA-B antibodies specific for the foetal phenotype. This suggests, but does not prove, that the MHC antigen expression of trophoblast may be restricted to HLA-C or some other undefined class 1 antigen.

Antibody Specificity↗
PubMed1985

SB subregion of the human major histocompatibility complex: gene organization, allelic polymorphism and expression in transformed cells.

The SB region of the human major histocompatibility complex (MHC) has been cloned from cosmid and lambda phage libraries made from the human B-lymphoblastoid cell line Priess (DR4/4, DC4/4, SB3/4). Two alpha genes and two beta genes are encoded in the 100 kb long SB region in the order SB alpha-SB beta-SX alpha-SX beta. The SB alpha and SB beta genes encode the alpha and beta subunits of the SB subset of class II MHC molecules. Both the SX alpha and the SX beta genes are pseudogenes in the haplotype examined. From the isolated clones, the two haplotypes of the Priess cell line, SB3 and SB4, are distinguished by nucleotide sequencing and blot hybridization analyses. Restriction site polymorphisms between the SB3 and SB4 clones were observed only in relatively small regions of the SB beta and SX beta genes. A mouse macrophage cell line was transfected with one of the cosmid clones containing both SB alpha and SB beta genes. Expression of the alpha and beta genes was detected by fluorescene-activated cell sorting (FACS) and two-dimensional gel electrophoresis using SB-specific monoclonal antibodies.

Alleles↗
PubMed1992

Single-residue changes in class I major histocompatibility complex molecules stimulate responses to self peptides.

Single-residue changes were introduced into the murine major histocompatibility complex class I molecule H-2Kb at positions 65 and 69, which are predicted to point up from the alpha-helix of the alpha 1 domain and not into the peptide binding groove. Mutated and wild-type genes were transfected into the murine cell line P815 (H-2d). We present evidence that the changes did not affect the binding of three foreign peptides that are recognized by cytotoxic T lymphocytes (CTL) in association with H-2Kb. Additionally, the mutants provoked strong alloreactive responses in T cells from mice expressing unmutated H-2Kb. The alloreactive CTL were specific for self peptides, which could be extracted from wild-type H-2Kb molecules, recognized in the context of the mutant class I.

Animals↗
PubMed1987

Interferon-mediated enhancement of thyroid major histocompatibility complex antigen expression. A flow cytometric analysis.

Epithelial expression of class II antigens encoded by the major histocompatibility complex (MHC) has been proposed as a means by which autoimmune thyroid disease may be initiated and maintained. We studied a rat thyroid epithelial cell line (FRTL-5), which constitutively expresses class I (OX18) but not class II (OX6 or OX17) determinants to quantify in vitro MHC antigen induction using flow cytometry. Recombinant rat gamma interferon (rIFN-gamma) induced dose-dependent expression of OX6 (I-A) antigen at greater than 48 h (maximum 80-90% of cells in culture at 100 U/ml), which was abrogated by DB-1, a monoclonal antibody to rat IFN-gamma. OX17 antigen (I-E) was also induced (86%) and OX18 (class I) markedly increased under these conditions. Other thyroid-active agents including the calcium ionophore A23187, dibutyryl cyclic AMP, thyroid-stimulating autoantibodies from Graves' disease patients (LATS), and TSH, caused no I-A induction. Supernatants from spleen cells stimulated with plant lectins (concanavalin A or phytohaemagglutinin), but not lectin alone, evoked substantial class II induction, which was inhibited by DB-1. These findings suggest that IFN-gamma is the central mediator of thyroid epithelial class II expression. FRTL-5 provides a powerful model for the analysis of thyroid MHC class II dynamics and a potential means of analysing the role of epithelial class II in autoimmune pathogenesis.

Animals↗
PubMed1988

Association of susceptibility to spontaneous diabetes in rat with genes of major histocompatibility complex.

This study was designed to map the diabetes susceptibility gene(s) associated with the rat major histocompatibility complex (MHC) RT1. We have crossed spontaneously diabetic male rats bearing the recombinant RT1r8 haplotype with female rats of the AC1.1r4 congenic strain. Three diabetic rats were determined to be homozygous for the r4 haplotype by serotyping. The absence of recombination within the MHC was confirmed by inspection of restriction-fragment-length patterns of the diabetic animals and the parental strains. In conjunction with previous breeding studies, this study maps the diabetes susceptibility gene to the right of the RT1-A locus and to the left of the RT1-C locus. A low incidence of diabetes in the F2 (4.5%) emphasizes the multifactorial nature of the susceptibility. The presence of depressed responsiveness of peripheral blood lymphocytes to concanavalin A stimulation increases the prevalence of the overt disease. An unusual feature of the diabetic syndrome in this study is the sparse or absent pancreatic lymphocytic inflammatory response, with true insulitis being a rare finding.

Animals↗
PubMed1982

Isolation of cDNA clones for the human complement protein factor B, a class III major histocompatibility complex gene product.

cDNA clones corresponding to a major histocompatibility class III antigen, the complement protein factor B, have been isolated from a human adult liver cDNA library. The clones, ranging in size from 1.0 to 2.3 kilobases, were identified by direct hybridization with two synthetic oligonucleotide mixtures. Two regions of the factor B amino acid sequence, each with minimal ambiguity in codon assignment, were chosen for synthesis of the oligonucleotides. The sequences of two clones have been partially determined. They contain coding information for the amino acid sequence of the Bb fragment of factor B and the entire 3' -untranslated region.

Adult↗
PubMed1983

Possibility of graft-vs-leukemia determinants independent of the major histocompatibility complex in allogeneic marrow transplantation.

The role of major histocompatibility (MHC) versus non-MHC determinants in the antileukemic effect exerted by engrafted normal marrow (graft-vs-leukemia, GvL) was studied in Rauscher leukemic SJL/J mice. The marrow donor strains included normal syngeneic SJL/J (H-2s), allogeneic C57BL/10 and 129/J (H-2b), congenic B10.S (H-2s, but otherwise genetically identical to the C57BL/10), and also F1 hybrid mice of the SJL/J and B10.S or C57BL/10 strains. Prior to transplant the recipients were exposed to a dose of total body irradiation that was large, but lower than that required to eliminate all hematopoietic precursors, such that GvL activity of the donor marrow would be necessary to avoid leukemic relapse. Total relapse within 60 days was observed when the syngeneic SJL/J donors were used. Transplantation either of the H-2b C57BL/10 or the H-2s B10.S marrow resulted in approximately 50% unrelapsed survival at 4 months. In contrast, only 26% unrelapsed survival was obtained with H-2b 129/J marrow. Marrow from (SJL/J X B10.S)F1 hybrids yielded a survival curve that was intermediate between those for the two parental strains; a similar but somewhat improved pattern was seen with (SJL/J X C57BL/10)F1-hybrid donors. The results suggest that although MHC genetic differences between the donor and recipient may produce a GvL effect in marrow transplantation therapy, other non-MHC determinants may also be capable of exerting an independent GvL effect of at least equivalent strength.

Animals↗
PubMed1987

Recombinant gamma interferon induces class II major histocompatibility complex antigens on insulinoma cells.

Aberrant expression of major histocompatibility (MHC) antigens has been implicated as a factor contributing to organ-specific autoimmunity, such as progressive loss of pancreatic beta cells in type 1 diabetes. We investigated the potential of a rat beta cell tumour, RINM5F, to express enhanced levels of MHC antigens in vitro. To this purpose we treated RINM5F cells in vitro with recombinant rat gamma interferon (rIF gamma). We used monoclonal antibodies to RT1.A (class I) and RT1.B (class II) antigens of the rat MHC in conjunction with flowcytometry and immunoperoxidase techniques to analyse the expression of MHC antigens. Untreated RINM5F cells express low levels of RT1.A, whereas they are negative for RT1.B. Treatment with rIF gamma appeared to increase the expression of RT1.A antigens substantially. Most importantly, RT1.B antigens were newly expressed by rat insulinoma cells in vitro after treatment with rIF gamma. To our knowledge this is the first documentation of the potential of beta cells or their derivatives to express class II MHC antigens following IF gamma-treatment. This mechanism may play an important role in the augmentation and perpetuation of insulitis leading to type 1 diabetes mellitus.

Adenoma, Islet Cell↗