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At least 919 records · Page 51Linked to original sources
PubMed1992

The immunogenetic background of scleroderma--an overview.

Currently it may be stated that the MHC associations in scleroderma support the classification of disease subsets, but in no ethnic group is the overall association strong enough for clinical use. In different ethnic groups, the distribution of MHC alleles varies, as does the degree of linkage disequilibrium between alleles of the linked loci. This concept is even relevant to relatively close populations. Thus Whiteside noticed that, if those patients referred from more than 100 miles from the study centre were excluded, then the strength of the DR1 association increased. The environmental contribution to scleroderma is unknown, except in the case of toxin or solvent associated disease. Different causal environmental agents found in different global regions might result in separate MHC associations and hence explain the discrepancies noted above. There are indications that associations between specific subsets of SSc patients and genetic markers will assume greater importance both diagnostically and prognostically. The lung fibrosis group look prime candidates, for example. Genetic markers are also a useful means of relating chemically-induced SSc-like disorders to the classical disease. Vinyl chloride disease provides an example. There is much heterogeneity within the disease, in terms of extent of skin involvement, severity, and of organ involvement. It is clear that the different clinical subsets of scleroderma are characterized by different associated MHC alleles. There are also many cases of clinical overlap with related diseases, and certain of these diseases have a different HLA association, which could detract from the primary HLA type associated with SSc.(ABSTRACT TRUNCATED AT 250 WORDS)

Autoantibodies↗
PubMed1995

Immunogenetics of epitopes of the carboxyl terminus of the human 60-kD Ro autoantigen.

Systemic lupus erythematosus is associated with the presence of autoantibodies which bind several ribonucleoproteins, including Ro (or SS-A). We have explored the relationship of the HLA-DQ and T cell receptor alleles in patients producing autoantibodies binding the 13-kD carboxyl terminus fragment of the 60-kD Ro and with autoantibodies binding a peptide epitope within this fragment (amino acid residues 480-494). Antibodies binding the 13-kD fragment are more likely to be found in the sera of patients with particular DQA1 and DQB1 alleles, while antibodies binding the epitope at 480-494 are found almost exclusively in the sera of patients with a Bg/II 9.8-kb polymorphism of the T cell receptor beta gene. Meanwhile, in these same patient sera the level of autoantibodies binding the complete 60-kD Ro particle is associated with a distinct pattern of alleles at these same immunoregulatory loci. These data demonstrate that component parts of autoantibody responses may be under genetic control which can be distinguished from the HLA associations characteristic of the response to the intact, complete autoantigen.

Amino Acid Sequence↗
PubMedDate not supplied

Immunogenetic studies of multiple sclerosis patients in Caithness County, Scotland.

The present report indicates that there is an increased frequency of HLA-B7 in multiple sclerosis patients compared to unrelated controls and unaffected siblings. HLA-A3 was not significantly increased. The increased frequency of certain HLA antigens was not reflected in increased titres of serum measles antibodies in this group. In contrast to our previous studies, there were only minimal differences in the cellular response to measles antigen in multiple sclerosis patients as compared to siblings and unrelated controls.

Adult↗
PubMed1980

Immunological regulation of experimental cutaneous leishmaniasis. 1. Immunogenetic aspects of susceptibility to Leishmania tropica in mice.

Models of the different disease patterns of cutaneous leishmaniasis can be induced by the same dose of L. tropica promastigotes in various inbred strains of mice. The susceptibility of BALB/c is exceptional, essentially dosage independent (being demonstratable with as few as 20 parasites) and leads to huge progressive lesions with fatal visceral and cutaneous metastasis. Lesions also extend progressively but more slowly in BDA/1 and BDA/2 mice. Strains A C57BL/6 and CBA are relatively resistant to even 2 X 10(7) promastigotes, with arrest of lesion growth within 3 weeks and subsequent gradual healing. Similar resistance of A.SW to 2 X 10(5) is overcome by a larger dose. The major inter-strain differences are H-2 independent, for C57BL/10 congenic mice possessing six different H-2 antigen complexes all show early arrest of lesion growth leading to healing (H-2s, H-2a, H-2k) or mild residual disease (H-2b, H-2d, H-2q). Inter-line differences within the latter group varied between experiments such that no clear rank order emerged. Inexorable disease progression was found in congenic BALB/B, BALB/c, and BALB/K alike, although it was significantly slower in the latter line when infected with smaller doses. Genetic control of BALB/c susceptibility is thus predominantly in the non-H-2 background with only a minor H-2 linked regulatory influence in the later stage. C57BL/6, BALB/c and their F1 hybrid characteristically display "healing", "fatal progressive" and "non-healing" lesions respectively over a wide dose range. "BALB/c-like" susceptibility segregates strictly in the F2 and backcross progeny according to a one predominant gene prediction. A comparison of the present data with those concerning genetic regulation of acute and chronic stages of systemic. L. donovani infection in mice (Bradley, 1977, Blackwell, Freeman & Bradley 1980) reveals differing control for the outcome of cutaneous L. tropica infection, in which other important genetic influences must be involved.

Animals↗
PubMed1976

Immunogenetic analysis of H-2 mutations. IV. Mapping of and immune reactions to the H-2fa mutation.

H-2fa is a spontaneous mutation that occurred in an (A.CA X A)F1 female mouse and was later transferred on an A-strain background [congenic line A.CA (M506) or M506]. Skin grafts exchanged between M506 and A.CA strains are rejected within 4 weeks after grafting. Significant reaction is observed when these two strains are used as responders and stimulators in mixed lymphocyte culture or in a splenomegaly graft-versus-host assay. The mutant antigen induces strong cell-mediated lymphocytotoxicity. The mutation maps in the K end of the H-2 complex. The capacity of mutant antigens to induce relatively strong lymphocyte proliferation is explained by hypothesizing that the T-cell receptors reacting with K- or D-region products can more easily recognize subtle than drastic alloantigenic differences.

Animals↗
PubMed1985

Immunogenetic studies of respiratory anaphylaxis in selectively bred guinea pigs. Inheritance of atopy, linkage to MHC-complex.

The genetic and immunological basis of respiratory anaphylaxis was studied in two strains of guinea pigs selectively bred for either high or low respiratory anaphylactic response to inhalation of ovalbumin. Individuals of the parental strains, F1-hybrids and backcross offspring were examined for class II MHC type and asthmatic response to ovalbumin. Analysis of the results revealed an association of asthma phenotype and MHC class II type. Apart from the gene(s) in the MHC several other genes seem to be involved in the control of guinea pig asthma.

Anaphylaxis↗
PubMed1983

Frequencies of HLA and Gm immunogenetic markers in Kaposi's sarcoma.

An outbreak of Kaposi's sarcoma in homosexual men has recently been observed in New York and California which differs from the "classic" North American disease with regard to younger age of onset and clinical prognosis. Although the exact mechanism for initiation of either disease is still unknown, a viral mechanism has been suggested in both cases. In order to investigate the possible role of HLA-associated variations in genetic susceptibility, 39 patients with histologically documented Kaposi's sarcoma were typed for HLA-A,B,C antigens. Most of these patients were also typed for HLA-DR antigens and for Gm allotypes. A significant increase in DR5 occurred in both groups. Decreases in B8 and DR3 and an increase in homozygosity for the Gm haplotype 3;5,13 were also noted. These results suggest that HLA and Gm linked immune response factors may play a role in the induction of both these forms of the disease.

HLA Antigens↗
PubMed1986

Immunogenetics of rheumatoid arthritis in Israel.

In an attempt to study the variation of associations between HLA and rheumatoid disease a population of 44 Ashkenazi and 29 non-Ashkenazi patients with Rheumatoid Arthritis were tested for HLA-A, B, C and DR antigens and compared with the relevant control groups. In contrast to the results obtained in Middle European or North American Caucasians, Rheumatoid Arthritis in Israel is not associated with B15 and Cw3, indicating that it is very unlikely that B- and C-locus antigens are involved in coding for disease susceptibility for RA. The allele DR4 which is found associated with RA in almost all populations tested so far was in the total patient group (47.9%) slightly but not significantly more frequent than in the control group (38.3%). This difference was entirely due to a nonsignificant increase in the frequency of DR4 in the Ashkenazi patients (54.5%) compared to controls (40%), while the frequency of DR4 in non-Ashkenazi patients and controls was virtually identical (38.0% vs 36.7%). Another surprising finding was that the frequency of HLA-DR1, which has been reported to be increased in different populations of patients with RA was found to be completely normal in the present study on Israeli patients. The alleles of the Bf and the GLO system did not show any significant difference between patients and controls.(ABSTRACT TRUNCATED AT 250 WORDS)

Antibodies, Antinuclear↗
PubMed1991

Immunogenetic studies of soluble Fc receptor (CD16) antigens in human seminal plasma.

Two forms of CD16 Fc receptors (FcRIII) have been defined on human leukocytes. Type 1, present on polymorphonuclear neutrophils (PMN), expresses the NA alloantigen system and type 2, present on natural-killer (NK) cells and macrophages, has no known polymorphic variations. We have described the presence of soluble FcRIII antigens in human seminal plasma (SP). These SP antigens retain an affinity for IgG-Fc and are biochemically distinct from leukocytic FcRIII. Their origin within the male reproductive tract and how they relate to FcRIII types 1 and 2 were not known. By using monoclonal antibodies CLB/Gran 11 and Leu 11c that differentially react with FcRIII type 1 and type 2 from different individuals, we studied how SP FcRIII antigens relate to leukocytic FcRIII. CLB/Gran 11 and Leu 11c reactivities with PMN and NK cells from a selected panel of male donors were compared with enzyme-linked immunosorbent assay reactivities of CLB/Gran 11 and Leu 11c with SP samples from these donors. The reactivity pattern with SP samples was shown to be different from findings with donors' PMN, but it corresponded with their NK cells. Our results indicate that SP FcRIII antigens do not manifest the polymorphic variations that are detected by CLB/Gran 11 and Leu 11c on PMN. These findings suggest that SP FcRIII antigens do not originate from PMN.

Adult↗
PubMed1997

Immunogenetic study of sympathetic ophthalmia.

Sympathetic ophthalmia (SO) is very rare but it remains one of the most intractable eye diseases. In clinical manifestations and histopathologic features SO is known to resemble closely Vogt-Koyanagi-Harada's disease (VKH disease). We had reported that VKH disease was significantly associated with HLA-DRB1*04 and -DQB1*04 in Japanese patients. In this study, to investigate an HLA association with SO we performed HLA serological and PCR-based DNA typing in 16 patients and 50 healthy controls. Our study revealed that HLA-DRB1*04 (0405; Pc < 5 x 10(-4)), DQA1*03 (Pc < 5 x 10(-3)), and DQB1*04 (0401; Pc < 5 x 10(-4)) were significantly associated with SO as compared to the healthy controls but there was no significant difference in the frequencies of any DPB1 alleles between the patients and healthy controls. It can be postulated that not only the clinical manifestations but also the genetic predisposition of SO are very similar to those of VKH disease.

Female↗
PubMed2004

Immunogenetics of HLA null alleles: implications for blood stem cell transplantation.

The transplantation of haematopoietic stem cells is a potentially curative therapy for a variety of haematological and non-haematological diseases. Matching of donor and recipient for human leucocyte antigens (HLA) is pivotal for the success of blood stem cell transplantation. HLA null alleles are characterized by the lack of a serologically detectable product. Because serological HLA diagnostics are increasingly replaced by DNA-based typing methods considering only small regions of the genes, null alleles may be misdiagnosed as normally expressed variants. The failure to identify an HLA null allele as a non-expressed variant in the stem cell transplantation setting may result in an HLA mismatch that is highly likely to stimulate allogeneic T cells and to trigger graft-vs-host disease. For some HLA null alleles, the translation into a truncated polypeptide chain seems possible, which thus might act as minor histocompatibility antigens. Because the prevalence of HLA null alleles may be around 0.3% or even higher, a screening strategy for HLA null alleles should, therefore, be implemented in the clinical laboratory. It may consist of the combination of serology and standard molecular typing techniques. As the standard molecular techniques are sometimes troublesome especially for characterizing the cytosine island at the 5' end of HLA class I exon 4 and need continuously be updated, an alternative approach may consist of sequencing all samples from genomic DNA for exons 2-3 or 4 (class I) or exon 2 (class II), including the adjacent intron splicing sites. This approach will detect 36/40 so far known non-expressed variants and has the potential to easily uncover novel variants, thus essentially minimizing the risk of overlooking these challenging variants.

DNA↗
PubMed1982

Analysis of the immunogenetic background of Japanese leprosy patients by the HLA system.

295 lepromatous and 74 tuberculoid leprosy patients were typed for HLA-A, -B and -C and compared to 110 healthy controls. It was found that frequency of HLA-B7 was significantly high and that of Bw54 was significantly low in lepromatous leprosy. HLA-DR and MT types were investigated in 84 lepromatous and 28 tuberculoid patients and compared to 55 controls. Both lepromatous and tuberculoid patients showed a marked increase in DR2 frequency. The relative risk is 8.7 and 5.9. Lepromatous leprosy showed an increase in frequency of MT1 and decreases in those of DRw9 and MT3 too.

HLA Antigens↗