Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024141 (systemic lupus erythematosus)
 44,322 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

HLA-A, -B and -DR gene frequency distributions in populations of Australia, Melanesia, Micronesia and Polynesia are examined in relationship to known HLA and disease associations in other populations. With the exception of a correlation between Reiter's syndrome and B27, other HLA and disease associations are markedly absent. Recombinant DNA and cellular subtyping analyses suggest that the HLA-DR subtypes predominating in susceptibility to several autoimmune disorders in Caucasoids are rare in Oceania. The high frequency of serum complement component C4A deficiency in Australian Aborigines may explain the high prevalence of systemic lupus erythematosus in this group.
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PMID:HLA and disease in Oceania. 269 21

The immune and endocrine systems and HLA genotype were subjected to a comparative study in patients with systemic and discoid lupus erythematosus (SLE, DLE). The patients suffering from these diseases were found to differ in a number of the parameters of the immune status including the content in blood serum and supernatant of the cultivated mononuclear cells of the soluble molecules HLA-A, HLA-B and HLA-DR. The degree of the SLE and DLE association with the genes and haplotypes of class I HLA complex was different as was the character of the association of HLA-A and HLA-B specificities with the activity of the immune system cells and with hydrocortisone content in plasma. The common immunogenetic syndrome characteristic of SLE and DLE patients has been identified.
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PMID:[Immunologic and immunogenetic heterogeneity of systemic and discoid lupus erythematosus]. 278 86

Correlations of anti-single-stranded (ss) DNA, anti-F(ab')2, and anti-idiotypes to HLA types of 16 healthy family members of a lupus patient were studied. High levels of anti-ss DNA (63%) and anti-F(ab')2 (69%) were detected. Of the 12 family members who expressed HLA-DR2 antigen, 8 had anti-ss DNA and anti-F(ab')2 antibodies. One out of 3 family members who shared the same HLA phenotypes, A1B8DR2, of the proband had high levels of anti-idiotype directed against the proband's F(ab')2 anti-DNA. Though a high prevalence of A1B8DR2, of anti-ss DNA, and of anti-F(ab')2 in healthy family members of a lupus patient was found, anti-idiotypes against anti-DNA were not dependent on HLA-A, B, Dr.
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PMID:Lack of correlation between HLA types and anti-idiotypic production in family members of a lupus patient. 278 88

Patients with U1-nRNP antibodies (n = 35, 31 female, four male) were typed for HLA-A, -B, -C, and -DR antigens and IgG heavy chain allotypes G1m(1), -(2), -(3), G3m(5), and -(21). The patient group was clinically heterogeneous. Four met the American Rheumatism Association criteria for systemic lupus erythematosus, six for progressive scleroderma, and 14 for rheumatoid arthritis. Sicca syndrome was present in seven cases. Twenty three had overlapping features compatible with mixed connective tissue disease (MCTD). Healthy blood donors served as controls for HLA typing (n = 64), Gm typing (n = 228), or both (n = 56). Sixty six per cent of the patients with U1-nRNP antibodies were DR4 positive compared with 28% of the controls (relative risk = 4.9, p = 0.00053). The Gm(1,3;5,21) phenotype was found in 46% of the patients and 25% of the controls (relative risk = 2.47, p = 0.0247). Within the patient group Gm(1,3;5,21) was found only in DR4 positive individuals. The coincidence of HLA-DR4 and Gm(1,3;5,21) increases the relative risk values to 8.0 (compared with the group with neither risk factor). DR4 and Gm(1,3;5,21) primarily seem to be related to U1-nRNP antibody formation and not to disease expression. Patients with or without MCTD did not differ with respect to DR4 or Gm(1,3;5,21) frequency. Disease onset was earlier in patients with HLA-DR4/Gm(1,3;5,21) than in patients without both markers (mean 27.9 v 40.1 years; p less than 0.05).
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PMID:HLA-DR4 and Gm(1,3;5,21) are associated with U1-nRNP antibody positive connective tissue disease. 295 14

Two T-lymphocyte subsets develop in the thymus which differ in the expression of glycoproteins on their cell surface. About 60% of the circulating T cells express the glycoprotein T4, while about 30% have the glycoprotein T8. T4 and T8 cells can be determined in the peripheral blood or various organs with monoclonal antibodies. T4 and T8 cells differ in their antigen recognition, have different functions, and can cause various pathohistological changes. T4 cells recognize the antigen in association with the HLA-D/DR/DP determinants. Upon antigenic stimulation they liberate various factors and initiate and amplify an immune response (T4 = helper/inducer T-cells). They can also be cytotoxic and are mediating effector functions via macrophage activation. T8 cells recognize the antigen in association with HLA-A/B/C determinants. They exert their cytotoxic or suppressive effector functions mainly in viral infections. The T4 or T8 cell-mediated pathohistological changes are discussed in the light of the well studied T-cell infiltrations in lepra lepromatosa or lepra tuberculosa. The T4/T8 cell dyscrasia in the peripheral blood, described in a variety of infectious, autoimmune or immunodeficiency diseases, may be due to enhanced proliferation, selective sequestration, reduced production or the elimination of a subset. T-cell subset analysis in joints, bronchial lavages and tissues has clarified the pathomechanism in a variety of autoimmune diseases, although the etiology remains obscure. For example, in rheumatoid arthritis, multiple sclerosis, and sarcoidosis, a T4 cell-mediated reaction with macrophage activation can be found. T4/T8 cell analysis may also be of value in dissecting heterogenous diseases, e.g. systemic lupus erythematosus. Of value is also the additional demonstration of membrane components reflecting T-cell activation (IL-2 receptor or DR-antigen expression) which serves to identify the activated T-cell subset in peripheral blood. Finally, T4/T8 cell analysis can be helpful in deciding treatment, as the T-cell subsets have a different sensitivity to immunosuppressive drugs.
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PMID:[Analysis of T-cell subpopulations. Pathophysiological concept and significance for clinical medicine]. 315 84

HLA-A,B,C and DR antigens were tested in 75 Cape Coloured systemic lupus erythematosus (SLE) patients, and the GLO I and Bf markers in 51. The patients with HLA-DR2 had a relative risk significantly greater than one (p=0.0005). Twenty-two (29%) patients had only one detectable DR antigen. Of these, 11 (50%) were found to have DR2 only. The HLA-DR7 antigen was associated with severe disease (p less than 0.02). Bf and GLO I markers were not associated with SLE.
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PMID:HLA-A,B,C, and DR antigens, GLO I and Bf marker profiles in 75 Cape coloured patients with systemic lupus erythematosus (SLE). 318 91

Strong expression of MHC Class I determinants had been observed on the erythrocytes of three genetically C4 deficient patients who all had SLE. In a study of 35 other SLE patients who were not C4 deficient, 30 showed a marked increase in the expression of MHC Class I on their erythrocytes. There was a correlation between the expression of erythrocyte Class I and disease activity. The polymorphic HLA determinants were detected by haemagglutination with human cytotoxic antisera from untransfused pregnant women. A shared monomorphic epitope of HLA-A, -B and -C, and beta 2-microglobulin were detected by haemagglutination with monoclonal antibodies. A monoclonal antibody for a monomorphic epitope on MHC Class II alpha and beta chains did not react. Erythrocytes from a group of RA patients and a group of normal controls had moderate and low expression respectively. We suggest that MHC Class I may be induced on erythrocytes maturing in a milieu containing mediators derived from activated cells of the immune system. Aberrant tissue expression of MHC antigens may be more widespread than has been previously recognized in diseases mediated by immune mechanisms.
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PMID:Expression of MHC class I determinants on erythrocytes of SLE patients. 330 28

The distribution of HLA-A, B, and DR alleles has been studied in 100 Chinese patients with systemic lupus erythematosus and in 100 healthy Chinese controls. Complement components factor B, C4A and C4B were studied in 72 patients and 61 controls. There was no significant difference between patients and controls in the distribution of HLA-A, HLA-B, factor B and C4B alleles, but there was a significant excess of HLA-DR2 and C4A null in the patients. An unusual variant of C4B was found in 6 patients and 1 control. The possible role of haplotypes is considered in interpreting these results and relating them to previous findings in Chinese.
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PMID:Strong association between the major histocompatibility complex and systemic lupus erythematosus in southern Chinese. 343 19

The complement components C4A, C4B, and factor B, and the HLA-A, B, C, DR, DQ, and DRw antigens were analyzed in 103 patients (66 Caucasian, 37 black) with systemic lupus erythematosus (SLE) and 98 control subjects (63 Caucasian, 35 black). Only the C4A null (silent) allele was significantly increased in SLE (0.254 versus 0.095 in Caucasians, p = 0.033; 0.200 versus 0.071 in blacks, p = 0.046). The absence of any detectable C4A gene products (homozygous C4A null or C4A*Q0,Q0) was found in 11.1 percent of Caucasian patients but in no control subjects (p = 0.006 with relative risk of 16.86). HLA-DR2 was significantly associated with Caucasian SLE (R2 = 0.63, p less than 0.0012). Multivariate analysis demonstrated that the HLA-DR2 antigen and C4A null allele contributed independently to the risk of SLE (relative risk 3.0 and 3.2, respectively); when HLA-DR2 and the homozygous C4A null phenotype were present together, the relative risk of SLE was 24.9. Both HLA-B8 and HLA-DR3 were increased in SLE, but these antigens are in linkage disequilibrium with the C4A null allele; the presence of HLA-B8 or DR3 did not contribute further to the risk of SLE. It is concluded that the HLA-DR2 antigen and the C4A null allele are independent and additive risk factors for development of SLE.
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PMID:Relationship between C4 null genes, HLA-D region antigens, and genetic susceptibility to systemic lupus erythematosus in Caucasian and black Americans. 346 13

For 75 patients with systemic lupus erythematosus (SLE), 39 laboratory and clinical characteristics, including HLA-A, B, C and DR typing, were analysed using a cluster analysis technique. Three groups were identified. Group I (46 patients) was characterized by infrequently severe disease, good response to therapy and infrequent multisystem involvement. Group II (24 patients) was characterized by a severe course of disease (although the tendency to remit after therapy was not unusual), and frequently, renal involvement and pericarditis. Group III (5 patients) was characterized by more severe renal disease. Of the 75 patients studied, 38.7% possessed HLA-DR3, compared to 17.4% of controls. Group I patients did not differ from controls but 80% of Group II patients and 4/5 Group III patients had DR3. Cluster analysis identifies subsets of SLE patients who show marked differences in disease course and severity, correlated with possession of the HLA B8, DR3 phenotype.
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PMID:Heterogeneity of systemic lupus erythematosus elucidated by cluster analysis. The influence of HLA. 347 Mar 92


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