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PubMed2002

Spatial relation between major histocompatibility complex-restricted antigen receptor-bearing thymocytes and subtypes of thymic epithelial cells.

R73, a monoclonal antibody that recognizes a rat T cell surface antigen of TCR(alphabeta), was used to identify thymocytes that express major histocompatibility complex-restricted antigen receptors, and to define the spatial relation between these receptor-bearing thymocytes and individual thymic cortical and medullary epithelial subtypes by ultrastructural immunohistochemistry. We show that in both the cortex and medulla 1) the thymocytes that reacted with R73 antibodies exhibited three staining patterns: cytoplasmic-only staining, simultaneous cytoplasmic and surface membrane staining, and surface membrane-only staining; 2) the subcapsular/perivascular epithelial cells (ECs) were usually associated with thymocytes expressing perinuclear staining only; and 3) the surface membrane areas of thymocytes that expressed antigen receptors made contact with pale and intermediate ECs, but not with dark cells. These results suggest that thymic selection of major histocompatibility complex restriction and/or tolerance may occur by interaction of the receptors on maturing thymocytes with major histocompatibility complex antigens on thymic ECs in general, and on pale and intermediate subtypes in particular.

Animals↗

PubMed2005

Major histocompatibility genes in the Lake Tana African large barb species flock: evidence for complete partitioning of class II B, but not class I, genes among different species.

The 16 African 'large' barb fish species of Lake Tana inhabit different ecological niches, exploit different food webs and have different temporal and spatial spawning patterns within the lake. This unique fish species flock is thought to be the result of adaptive radiation within the past 5 million years. Previous analyses of major histocompatibility class II B exon 2 sequences in four Lake Tana African large barb species revealed that these sequences are indeed under selection. No sharing of class II B alleles was observed among the four Lake Tana African large barb species. In this study we analysed the class II B exon 2 sequences of seven additional Lake Tana African large barb species and African large barbs from the Blue Nile and its tributaries. In addition, the presence and variability of major histocompatibility complex class I UA exon 3 sequences in six Lake Tana and Blue Nile African large barb species was analysed. Phylogenetic lineages are maintained by purifying or neutral selection on non-peptide binding regions. Class II B intron 1 and exon 2 sequences were not shared among the different Lake Tana African large barb species or with the riverine barb species. In contrast, identical class I UA exon 3 sequences were found both in the lacustrine and riverine barb species. Our analyses demonstrate complete partitioning of class II B alleles among Lake Tana African large barb species. In contrast, class I alleles remain for the large part shared among species. These different modes of evolution probably reflect the unlinked nature of major histocompatibility genes in teleost fishes.

Alleles↗

PubMed1992

Interleukin 2 and interferon alpha modulation of the lymphocyte non-major histocompatibility-restricted lytic activity in glioblastoma patients.

We studied the non-major histocompatibility-restricted cytotoxic activity induced by interleukin 2 (IL-2) and interferon alpha (IFN-alpha) in mononuclear cells of peripheral blood (PBMNC) from glioblastoma patients. We observed a depressed cytotoxic activity against natural killer (NK)-sensitive target cells in PBMNC from all the patients studied. Culture of these PBMNC with IFN-alpha for 5 days augmented the cytotoxic activity against NK-sensitive target cells in a small group of patients. Incubation with IL-2 for 5 days normalizes the decreased cytotoxic activity against NK-sensitive target cells of PBMNC from all the glioblastoma patients studied. When PBMNC from these patients were incubated with IL-2 for 5 days and IFN-alpha was added to the culture medium in the last 2 h of culture, an enhancement of non-major histocompatibility-restricted cytotoxic activity was observed compared with that obtained with either IL-2 or IFN-alpha alone. This improvement of the cytotoxic activity was more relevant when it was tested against NK-resistant target cells. The potential utility of the sequential use of the two cytokines in generating non-major histocompatibility cytotoxic activity in glioblastoma patients is discussed.

Aged↗

PubMed1990

Induction of major histocompatibility complex antigens within the myocardium of patients with active myocarditis: a nonhistologic marker of myocarditis.

The histologic diagnosis of active myocarditis is frequently difficult to establish. A nonhistologic marker of immune activation would be clinically useful in identifying cases of immune-mediated myocarditis. A viral etiology with subsequent autoimmunity to cardiac antigens has been implicated in human myocarditis. Because autoimmunity and viral disease are commonly associated with increased expression of major histocompatibility complex (MHC) antigens on targeted tissue, we examined endomyocardial biopsy samples from patients with active myocarditis for abnormal levels of MHC antigen expression. Thirteen patients with active myocarditis and eight control patients with other well-defined cardiac diagnoses (coronary disease, amyloidosis or neoplasm) were studied. A sensitive radioimmunoassay was developed that utilized monoclonal antibodies to human MHC class I and class II antigens in order to quantitate the expression of both of these antigens within each biopsy. Abnormal MHC class I and class II antigen expression was present in 11 of 13 myocarditis specimens and 1 of 8 control samples (specificity 88%, sensitivity 84.6%). Active myocarditis samples had approximately a 10-fold increase in MHC class I and class II expression. Immunoperoxidase staining localized abnormal MHC expression primarily within microvascular endothelium and along myocyte surfaces (11 of 13). This study is the first to demonstrate a marked increase in major histocompatibility complex antigen expression within the myocardium of patients with active myocarditis. The identification of abnormal histocompatibility antigen expression within an endomyocardial biopsy may prove a useful adjunct to the histologic diagnosis of myocarditis.

Adult↗

PubMed1995

Fresh venous allografts in peripheral arterial reconstruction in dogs. Effects of histocompatibility and of short-term immunosuppression with cyclosporine A and mycophenolate mofetil.

To date, no arterial substitute has been shown to be as effective as the autologous saphenous vein in peripheral revascularization procedures. In the present study, the venous allograft was evaluated as a vascular substitute in terms of patency and induction of host immune reactivity, whether used in major histocompatibility complex-incompatible, major histocompatibility complex-incompatible dogs. The immunosuppressive drug therapies were given for a period of 31 days, beginning 1 day before transplantation, and consisted of the use of cyclosporine A, mycophenolate mofetil, or a combination of both. All histoincompatible allografts were thrombosed at 4 or 8 weeks after transplantation with antibody development and cell-mediated cytotoxicity in the graft, whereas histocompatible allografts showed late stenosis without immunologic reactions directed toward donor cells. Given alone, neither cyclosporine A nor mycophenolate mofetil improved the overall patency of venous allografts; thrombosis occurred shortly after cessation of immunosuppression. Still, the cyclosporine A-mycophenolate mofetil combination therapy led to a 100% patency rate at 20 weeks after implantation and immune reactions were markedly reduced. This study shows that the fresh vein allograft is still an attractive and functional alternative to the autologous saphenous vein if the host immunologic reactions are controlled by cyclosporine A-mycophenolate mofetil immunosuppression.

Animals↗

PubMed1991

Histocompatibility antigen subtypes in black women with class A1 or class GB diabetes mellitus.

Insulin-dependent diabetes mellitus is associated with an increased frequency of certain histocompatibility antigens located on chromosome six, the most common types being B-8, B-15, DR-3, DR-4, and DR-7. We therefore theorized that screening for these subtypes may allow the identification of those women with gestational diabetes who will remain euglycemic on dietary modification (class A1) compared with those who will require insulin to achieve euglycemia (class GB). From 1982 to 1987, 228 black women with gestational diabetes were screened for the above histocompatibility antigens. As theorized, certain histocompatibility antigen subtypes were more common in women with class GB gestational diabetes mellitus; DR-2 (41.8% versus 23.7% p = 0.015), B-15 (p = 0.07), and DR-3 (p = 0.08). However, because of the low sensitivity (42%), specificity (75%), and positive predictive value (36%), this test is impractical in the clinical management of women with gestational diabetes mellitus.

Black People↗

PubMed1986

Class I histocompatibility antigens and insulin receptors: evidence for interactions.

We provide evidence for an interaction between mouse class I major histocompatibility complex antigens and insulin receptors. Antibodies against class I but not class II major histocompatibility complex antigens immunoprecipitate photoaffinity-labeled hepatic insulin receptors. Haplotype specificity is demonstrated by reciprocal precipitation using anti-class I antibodies and three strains of mice. Antibodies against the 45-kDa products of either the H-2K or H-2D locus and rabbit anti-mouse beta 2-microglobulin antibodies were shown to precipitate insulin receptors. We also demonstrate the specific binding of 125I-labeled insulin and 125I-labeled epidermal growth factor, but not 125I-labeled glucagon or 125I-labeled atrial natriuretic factor, to solubilized plasma membranes immunoprecipitated with anti-H-2K antibody. These observations suggest a specific interaction between class I major histocompatibility complex antigens and certain hormone receptors.

Animals↗

PubMed1988

Evidence for a trans-acting factor that regulates the transcription of class II major histocompatibility complex genes: genetic and functional analysis.

The study of specific trans-acting transcription factors in prokaryotes and lower eukaryotes has been greatly facilitated by genetic analysis of mutant strains deficient in such factors. We have developed such a system to study mammalian trans-acting factors that regulate the transcription of class II major histocompatibility complex genes, using the mutant cell lines RM2 and RM3. These cells, derived from the human B-cell line Raji, specifically fail to transcribe their class II major histocompatibility complex genes. Here we show that a transfected HLA-DR alpha class II major histocompatibility complex gene, like the endogenous HLA-DR alpha genes, is efficiently transcribed in Raji cells but not in RM2 or RM3 cells, demonstrating that the mutant cells are deficient in a specific trans-acting factor required for transcription of these genes. HLA-DR expression in RM2 and RM3 cells is rescued by fusion to another B-cell line but not by fusion to each other. Thus, the defects in the two cell lines are recessive and noncomplementing and define a locus whose wild-type product we designate TF-X1. We show that TF-X1 influences the activity of a 24-base-pair B-cell-specific cis-acting transcription element in the HLA-DR alpha promoter. However, in three different biochemical assays, we detect no difference between wild-type and mutant cells in the DNA-binding proteins that interact with these DNA sequences. Thus, the defective version of TF-X1 may be a DNA-binding protein that binds to the HLA-DR alpha promoter but fails to activate transcription. Alternatively, TF-X1 may not be a DNA-binding protein at all.

Base Sequence↗

PubMed1988

Complete amino acid sequence of human plasma Zn-alpha 2-glycoprotein and its homology to histocompatibility antigens.

In the present study the complete amino acid sequence of human plasma Zn-alpha 2-glycoprotein was determined. This protein whose biological function is unknown consists of a single polypeptide chain of 276 amino acid residues including 8 tryptophan residues and has a pyroglutamyl residue at the amino terminus. The location of the two disulfide bonds in the polypeptide chain was also established. The three glycans, whose structure was elucidated with the aid of 500 MHz 1H NMR spectroscopy, were sialylated N-biantennas. The molecular weight calculated from the polypeptide and carbohydrate structure is 38,478, which is close to the reported value of approximately equal to 41,000 based on physicochemical measurements. The predicted secondary structure appeared to be comprised of 23% alpha-helix, 27% beta-sheet, and 22% beta-turns. The three N-glycans were found to be located in beta-turn regions. An unexpected finding was made by computer analysis of the sequence data; this revealed that Zn-alpha 2-glycoprotein is closely related to antigens of the major histocompatibility complex in amino acid sequence and in domain structure. There was an unusually high degree of sequence homology with the alpha chains of class I histocompatibility antigens. Moreover, this plasma protein was shown to be a member of the immunoglobulin gene superfamily. Zn-alpha 2-glycoprotein appears to be a truncated secretory major histocompatibility complex-related molecule, and it may have a role in the expression of the immune response.

Amino Acid Sequence↗

PubMed1990

Concerted evolution of class I genes in the major histocompatibility complex of murine rodents.

Full-length cDNA sequences of two class I major histocompatibility complex molecules from the DA strain of Rattus norvegicus are reported. One codes for the classical class I restriction element RT1.Aa, which maps to the locus in the rat major histocompatibility complex homologous to H-2K in the mouse. The other probably codes for a soluble nonclassical class I molecule present in DA rat serum; a short deletion in the fifth exon implies that the translated product will terminate in the membrane-spanning region. These sequences have been compared with mouse classical class I sequences as well as with three published rat class I cDNA partial sequences. The results show, first, that "locus-specific" substitutions from the H-2K, H-2D, and H-2L data set are scrambled in the RT1.Aa molecule; a majority of these substitutions have H-2D/L-specific features. Second, the data show that the four rat sequences are strikingly similar to one another regardless of locus or haplotype of origin; they share a number of apparently species-specific features that distinguish them all from mouse classical class I sequences, which likewise share distinctive features of their own. The results suggest that segmental sequence exchange plays a major role in determining the evolution of sequence in class I major histocompatibility complex molecules.

Amino Acid Sequence↗

PubMed1983

In vitro generation of cytotoxic cells specific for human minor histocompatibility antigens by lymphocytes from a normal donor potentially primed during pregnancy.

A normal female donor (H9) is described, whose cells generate strong cytotoxicity against a human minor histocompatibility antigen in vitro. These cytotoxic T lymphocytes are generated after secondary restimulation with cells from an HLA-A, -B, -C, and -DR-matched donor and are HLA restricted (HLA-B7). No other donor could be identified whose cells responded to this antigen. The two children of donor H9 are virtually HLA identical to her and one of the children expresses the relevant minor histocompatibility antigen. These data suggest that priming in vivo during pregnancy has facilitated cytotoxic T cell response to human minor histocompatibility antigens in vitro.

Cytotoxicity, Immunologic↗

PubMed1989

No increased histocompatibility antigen-sharing in couples with idiopathic habitual abortions.

Sharing of major histocompatibility antigens between spouses has been claimed to play an aetiological role in couples with unexplained, habitual spontaneous abortions. On the other hand there is evidence that a subset of habitually aborting women exists, in whom autoimmune aberrations seem to be of importance. In the present study, 56 couples with unexplained habitual abortions were histocompatibility typed for HLA-A, -B and -DR specificities, as were a group of 33 fertile control couples with two or more children and no spontaneous abortions. The DR-typing was done partly by use of the restriction fragment length polymorphism (RFLP). There was no significant difference in the distribution of histocompatibility antigens between the habitually aborting women and the control women. No increased HLA-antigen sharing could be demonstrated between spouses in aborting couples compared with controls, neither in each single locus nor in the combination of all loci (all P-values greater than 0.2). Neither could any increased HLA-antigen sharing in sub-groups of aborting couples with and without autoimmunity be demonstrated. It can be concluded from these data that compatibility between spouses for HLA-A, -B and DR-antigens per se only plays a minor role in the aetiology of habitual abortion.

Abortion, Habitual↗

PubMed1995

Regulation of transgenic class II major histocompatibility genes in murine Langerhans cells.

I-E is a class II major histocompatibility complex molecule normally expressed by Langerhans cells. A series of transgenic mice were developed previously that carry E alpha d gene constructs with promoter-region deletions that cause expression of I-E by different cell types when maintained on a B6 (I-E[-]) genetic background. To study cis-acting gene sequences that regulate expression of class II proteins by Langerhans cells, we identified transgenic I-E expression by tissue immunoperoxidase staining and by epidermal cell suspension immunofluorescence cytometry. Mice with a transgene containing 1.4 kilobase pairs (kb) of flanking sequence 5' to the E alpha initiation site expressed barely detectable levels of I-E on a tiny percentage of Langerhans cells, indicating that sequences promoting Langerhans cell expression of E alpha exist between 2.0 and 1.4 kb 5' of the E alpha initiation site. Removal of an additional 170 bp of 5' flanking sequence caused near-normal levels of expression by approximately one third of epidermal Langerhans cells, which contrasts with studies that showed minimal transgene expression by splenic dendritic cells in these animals. Thus, sequences between 1.4 and 1.23 kb 5' of the E alpha initiation site decrease expression of I-E by epidermal Langerhans cells, but enable I-E expression by splenic dendritic cells. These studies identify Langerhans cell-specific regulatory sequences and genetic regions controlling major histocompatibility complex class II gene expression in Langerhans cells and splenic dendritic cells. The genetic regions identified may be particularly important because differential regulation of class II major histocompatibility complex protein synthesis by Langerhans cells and dendritic cells may be crucial to immune functions of intact animals.

Animals↗

PubMed1983

Histocompatibility antigens in coal miners with pneumoconiosis.

Twenty-five histocompatibility antigens have been measured in 100 coal miners with pneumoconiosis attending a pneumoconiosis medical panel and the results compared with a panel of 200 normal volunteers not exposed to dust. Chest radiographs were read independently by three readers according to the ILO U/C classification. On a combined score, 40 men were thought to have simple pneumoconiosis and 60 men complicated pneumoconiosis. The number of antigens tested and associations between antigens caused difficulties in assessing the statistical significance of differences in prevalence of antigens between groups of men. Using stringent criteria for statistical significance, no significant differences were found in antigen prevalences between miners and controls, or miners with simple or complicated pneumoconiosis. When a less stringent statistical approach was applied, three antigens appeared to have abnormal prevalences in these 100 miners by comparison with the normal volunteers. More detailed examination of these antigen prevalences in relation to radiographic category of pneumoconiosis did not provide any supportive evidence that these slight associations were of statistical or clinical significance. Reports on histocompatibility antigens in miners with pneumoconiosis are reviewed briefly and the results compared. There is no good evidence that any of the histocompatibility antigens so far tested are associated with a clinically important altered risk of simple or complicated pneumoconiosis when dust is inhaled.

Aged↗

PubMed2005

Influence of maternal-fetal histocompatibility and MHC zygosity on maternal microchimerism.

To investigate the relationship between maternal-fetal histocompatibility and maternal microchimerism, we developed a sensitive quantitative PCR assay for the neomycin resistance gene (neoR), and, in a mouse model system, used neoR as a noninherited maternal allele marker of maternal cells to detect and quantitate maternal microchimerism in tissues of neoR(-/-) N2 backcross progeny of (neoR(+/-))F(1) females mated with neoR(-/-) males. Using this approach, we obtained evidence for the presence of chimeric maternal cells in the brain, spleen, and thymus of all weanling and adult mice so tested. The numbers of chimeric maternal cells present in the spleen did not differ significantly from those in the thymus regardless of age or maternal-fetal histocompatibility. At all ages, brain tissue had higher level of maternal microchimerism than lymphoid tissue in mice MHC identical with their mothers, but the levels were similar in mice MHC disparate with their mothers. The levels of chimeric maternal cells in both brain and lymphoid tissue of mice with homozygous syngenicity and maternal allogenicity were similar, and tended to be higher than tissue-specific levels in mice with either combined maternal-fetal allogenicity or heterozygous syngenicity. Thus, MHC homozygous progeny had higher levels of maternal microchimerism than MHC heterozygous progeny. We conclude that normal mice possess small numbers of maternal cells in spleen, thymus, brain, and probably most other tissues, and that maternal-fetal histocompatibility influences the levels of these cells by mechanisms related to MHC zygosity of the progeny.

Alleles↗

PubMed1974

Localization of histocompatibility and organ specific antigens on mouse spermatozoa.

Further studies on the topographic localization of histocompatibility and organ-specific antigens on mouse spermatozoa have been reported. Specific antisera to a histocompatibility antigen (H-2a) and a serum prepared by injecting male mice with syngeneic testicular homogenate were labeled with peroxidase and the antigens were located by immunoelectron microscopy. The organ-specific antigen was located on the sperm head and occasionally on the midpiece, whereas the H-2 antigen was confined to the sperm head. The observations were not quantitative, because of the obvious limitations in the examination of thin sections. The distribution of the 2 antigens may be related to the functions of the various parts of the spermatozoa, although no clear correlation could be suggested. The authors indicate several points of discussion arising from their observations. There is no general agreement at present about the presence or absence of histocompatability antigens on spermatozoa. The reported location of these antigens on spermatozoa conflicts with some earlier results. The present observations must also be considered in relation to the fluid mosaic model of cell membranes, for the localization of antigens to particular sites imples that restrictions are placed on the movement of some membrane constituents.

Biology↗

PubMed1999

Major Histocompatibility Complex in Human - HLA System: Biological Role and Impact for Practical Medicine.

Interactions of HLA constitute the key basis for development of the whole number of pathologies, starting from oncological and infectious diseases, and ending with autoimmune disorders and allergies. The most demonstrable example is oncopathology. The fact is that HLA class I (namely, its non-polymorphic determinants) have recently been shown to be the main target for so called natural (or non-specific) killer cells (NK). Naturally, the profound decrease of class I histocompatibility antigens on the surface of pathologically changed cells, impairing cellular interaction between NK and target cells, "takes them out" from the control of NK. As a result, the body looses one of the most important protective functions. Quite another type of impairment of HLA role in cellular interaction may be the basis of autoimmune diseases. The most successful results were obtained in studies of insulin dependent diabetes. One of the main pathogenic factors was shown to be marked elevation (aberrant expression) of HLA on islet cells (insulin producers). This, in its turn, is the consequence of dysfunction and activation of genes, responsible for "assembly and transport" of HLA class II. The problem about role of HLA in cell interactions in allergy is rather novel, but poor studied trend, however some obtained results are encouraging. The point is that the unique feature in expression of class II histocompatibility antigens, specific for allergy, was revealed for recent years. Expression of class II histocompatibility antigens is appeared to be sharply increased on B lymphocytes of allergic patients.

Journal Article↗

PubMed2005

[Primary study on histocompatibility of three kinds of collagen-chitosan porous scaffolds].

OBJECTIVE: To construct three kinds of collagen-chitosan porous scaffolds with enhanced bio-stability and to investigate the histocompatibility of the scaffolds in vivo. METHODS: Collagen-chitosan porous scaffolds were fabricated by freeze-drying method, cross-linked using dehydrothermal treatment and glutaraldehyde, respectively. The morphology of the uncross-linked scaffold (scaffold 1), dehydrothermal cross-linked scaffold (scaffold 2) and glutaraldehyde cross-linked scaffold (scaffold 3) was studied by scanning electron microscopy. Three kinds of scaffolds were embedded subcutaneously on dorsal surface of 12 rabbit ears. The general and local responses were recorded daily. The bio-stability and histocompatibility of the scaffolds were observed by using HE staining after 3, 7, 14 and 28 days of operation. RESULTS: The scaffolds had three-dimensional porous structures with a porosity of more than 90%, and possessed pore sizes of 120 +/- 10 microm, 80 +/- 15 microm and 170 +/- 20 microm, respectively. All experimental rabbits survived with good general condition during the study. All skin incisions healed well without obvious reactive red or swelling. Histological study showed that scaffold 1 was degraded rapidly with obvious inflammation. The degradation of scaffold 2 was slower than that of scaffold 1 and the inflammation of scaffold 2 was also milder than that of scaffold 1. Scaffold 3 possessed slow degradation property with slight inflammatory reaction, and rapid tissue regeneration. CONCLUSION: The collagen-chitosan porous scaffolds have three-dimensional porous structures that are suitable for tissue regeneration. The bio-stability and histocompatibility of the scaffolds are enhanced after cross-linked. Glutaraldehyde cross-linked is better than dehydrothermal cross-linked, which can facilitate dermal tissue reconstruction.

Animals↗