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At least 793 records · Page 44Linked to original sources
PubMed1980

HLA antigens as immunogenetic markers of alcoholism and alcoholic liver disease.

HLA antigens were studied among 94 chronic alcoholics. Concerning A and B-loci, there was no significant change of phenotype frequency (PF) in the HLA typing between the patients and controls (80 healthy subjects). However, there was a significant difference in the PF of CW3 between chronic alcoholics and controls (58.5% in alcoholics vs 30.0% in controls). The corrected p value was less than 0.05 with relative risk value being 3.29 HLA-DR loci were also detected in 26 patients, but there was no significant difference between the patients and controls. All alcoholics were subdivided according to the hepatic morphology, and the PF of HLA was examined. A significant high frequency of HLA CW3 was found in patients with hepatitis (64%) compared to controls (30%). There was also an increased PF of CW3 in the liver cirrhosis group (59% in cirrhosis group vs 30% in controls). In conclusion, chronic alcoholics have a significantly higher PF of HLA-CW3 as compared to controls. This characteristic feature becomes even more distinct in alcoholics with severe hepatic lesions.

Adult↗
PubMed1998

Immunogenetic analysis of the heavy chain variable regions of IgE from patients allergic to peanuts.

Peanuts are one of the most allergenic of the foods, and hypersensitivity responses to peanut allergens can be fatal. Although the nature of the antigenic components of peanuts is being defined at the molecular level, there is little information on the induced IgE antibodies, which are central to the allergic reaction. Recognition sites of IgE antibody molecules arise from the variable regions of heavy and light chains (VH and VL). By using nested polymerase chain reactions with specific primers for the available repertoire of VH genes, together with primers in the constant epsilon region, we have amplified VH sequences of IgE from blood lymphocytes of two patients with peanut allergy. After cloning and sequencing the products, we found a predominance of VH1 family use in both patients, which was not found in control IgM-specific primers. The IgE VH sequences were highly somatically mutated, but in only six of 17 cases was there clear evidence for clustering of amino acids indicative of antigen selection. Previous results from patients with allergy to house dust mites have indicated predominance of VH5 use and little evidence for antigen selection. Although results from two patients allergic to peanuts must be regarded as preliminary, they do suggest that the IgE response to peanuts may have a different VH bias, with a similar mutational pattern.

Adolescent↗
PubMed1986

Immunogenetic markers in chlorpromazine-induced tardive dyskinesia.

The presence and severity of tardive dyskinesia were determined in 66 patients with chronic psychiatric disorders treated with chlorpromazine. The patients were classified according to the presence of antinuclear antibodies, the lupus anticoagulant, and the HLA antigen Bw44. The severity of orofacial dyskinesia was estimated using the Rockland Research Institute Scale. Patients with autoantibodies and the Bw44 antigen had higher tardive dyskinesia scores than those with AAB without the Bw44 antigen and also patients without autoantibodies regardless of their HLA phenotype (P less than 0.01). These studies suggest that the presence of autoantibodies in association with the HLA Bw44 antigen is related to, and can be a predictor of, neurological complications of long-term chlorpromazine therapy.

Antibodies, Antinuclear↗
PubMed1998

Immunogenetic analysis of Buerger's disease in India.

In order to understand the role of HLA linked factors in determining susceptibility to Buerger's disease, we have studied 21 unrelated Asian Indian patients belonging to the North Indian states of Punjab, Haryana, Uttar Pradesh and Delhi, representing mainly a lower socioeconomic background. The data was compared with healthy controls belonging to the same ethnic group. The study revealed an over representation of HLA-B40 (60+61) (chi2=6.12; P<0.02) and DR2 (chi2=10.2; P<0.002). Amongst the patients no particular association or linkage disequilibrium with any of the five alleles of the MIC-A gene could be derived in the small sample size studied.

Adult↗
PubMed1996

Low prevalence of immunogenetic markers of IDDM in adult Koreans with diabetes detected on OGTT.

In the Asian populations, it is not uncommon for adult patients with NIDDM to eventually lose beta-cell function and develop IDDM. Accepting that IDDM is an autoimmune disease, which occurs on a genetic background, it could by hypothesized that by measuring autoantibody prevalence and HLA DQ gene polymorphism, known important prediagnostic markers of IDDM, the prevalence of adult-onset IDDM in patients with previously undiagnosed NIDDM patients could be estimated. To do this, anti-GAD prevalence and HLA DQ A1 and DQ B1 polymorphisms after PCR amplification of genomic DNA were analyzed in 121 newly diagnosed diabetic patients of Yonchon cohort and compared to the results with those of 100 matched health control subjects. We also compared the results with those of other populations to assess the difference of genotype distribution. The overall prevalence of anti-GAD antibodies was 1.7% (2 of 121) in patients with previously undiagnosed NIDDM, whereas 1 of 100 controls had positive antibodies. Among those who were positive, their titer of antibodies to GAD were not high. No statistically significant differences in the distribution of either mean levels of anti-GAD or DQA1 and DQB1 alleles were found comparing NIDDM patients to controls. Interestingly, the frequency of DQB1*non-Asp-57 and DQA1*Arg-52 alleles in the Korean adult control population was similar to that of US Caucasians (DQB1*non-Asp-57: 0.431 vs. 0.475; DQA1*Arg-52: 0.492 vs. 0.463). The low prevalence of anti-GAD antibodies and HLA-DQA1 and DQB1 susceptibility alleles among recent-onset NIDDM patients, not different compared to controls suggests that diabetes in Korean adults is unlikely to have an autoimmune component to its pathogenesis.

Adult↗
PubMed1991

Immunogenetics of systemic lupus erythematosus in Spanish patients: differential HLA markers.

HLA-DR3 antigen included in the compound phenotype B18BfF1 (but not the one linked to the B8BfS compound phenotype) was found to be significantly increased in our SLE patients. It is remarkable that in our Southern-Mediterranean population, B18BfF1DR3 individuals (but not B8BfSDR3) are prone to SLE with renal disease, in contrast with other Northern European and Caucasoid populations. Also, patients with autoantibodies to Ro/La have a significant increase of the B8DR3 compound phenotype. Production of autoantibodies against Ro alone was associated to DR2 and production of anti-Sm/nRNP to DR3 (either B18BfF1 or B8BfS associated) only in the subgroup without renal disease. The distinctive HLA and autoimmune associations to SLE with and without renal disease suggests that both clinical forms may not share a common identical pathogenesis.

Autoantibodies↗
PubMed1982

Immunogenetic studies of the platelet-specific antigen P1A1 (Zw(a)).

The phenotype frequency of the platelet-specific antigens P1A1/A2 ( = Zw(a,b)) in the German population (N = 711) is 97.75% and 2.25% respectively. The corresponding gene frequencies are P1A1 0.85; P1A2 0.15. The P1A1 determinant is codominantly inherited (19 families; 151 family members). There is a strong gene dosage effect between P1A1 homo and heterozygous individuals. No definite linkage of the locus P1A1 versus the loci HLA-ABC, ABO, or Rh was found.

Antilymphocyte Serum↗
PubMed1983

Multiple sclerosis: immunogenetic analyses of sib-pair double case families. II. Studies on the association of multiple sclerosis with C2, C4, BF, C3, C6, and GLO polymorphisms.

The complement component polymorphisms of C2, C4, BF, C3, C6, and the enzyme polymorphism GLO were studied in 13 sib-pair double case families with multiple sclerosis. A significant association was seen between MS patients and the C4 haplotype A4,B2 as compared with their healthy siblings. This finding seems to parallel reports on C2 hypocomplementemia in MS patients since C4 A4,B2 in normal individuals was also seen to be in linkage disequilibrium with the C2 deficiency allele (C2QO) by other investigators.

Complement C2↗
PubMed1988

Hypothesis: immunogenetic analysis of spontaneous autoimmune thyroiditis in obese strain (OS) chickens: a two-gene family model.

Analysis of the number of genes involved in the regulation of the expression of SAT in OS, by means of crosses with the unrelated inbred CB line, gave the following results: 1) The production of Tg-AAb is regulated by one or two genes; 2) the sensitivity of the thyroid to autoimmune attack is under the control of about 3 genes; 3) the expression of SAT, as measured by mononuclear cell infiltration of the thyroid gland, is thus encoded by at least 4-5 genes (approximately 2 of which regulate the immune system hyperreactivity against antigens of the thyroid, and 3 of which regulate the sensitivity of the target organ to an attack by the immune system. It should, however, not be forgotten that this calculation, which results in 5 genes as being crucial for the development of SAT, is only valid for the combination of the OS and the CB inbred line. A different number might have arisen with the use of a different inbred line for crossing experiments. 4) The genes involved in the genetic control of SAT can be divided into two categories, major and minor genes. One family of major genes regulates the hyperreactivity of the immune system and perhaps its specificity for thyroid antigens. A second family of major genes encodes the target organ susceptibility to the attack of the immune system. The minor genes modulate the expression of the major genes and are especially important in animals with an incomplete set of major genes. The influence of sex hormones and the MHC are examples of such genes. MHC genes play an important role in outbred populations, but they are not a prerequisite for the development of the disease. Fully developed, early onset SAT is only seen in an animal where all major genes are present. The existence of two-gene families, each composed of relatively few genes, might guarantee to a species that SAT will not be too frequent in outbred populations.

Animals↗