HLA class I and II antigens in South African Blacks with Graves' disease

Omar, M. A. K.; Hammond, M. G.; Desai, Rajesh K.; Motala, Ayesha A.; Aboo, Nazimuddin; Seedat, M. A.

doi:10.1016/0090-1229(90)90009-f

Cited by 28 publications

(15 citation statements)

References 11 publications

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“…We previously reported that no significant HLA-DR association was detected in the total group of AfricanAmerican patients with GD (7) in contrast to the well-recognized HLA-DR3 (DR17) associations in Caucasians (1,3). Except for our study, there is only one report on the HLA class I and -DR distributions in patients with GD of African descent (8). The authors found a significant increase of HLA-DR3 and -DR1 in South African patients.…”

Section: Frequencies Of Dr Antigenscontrasting

confidence: 83%

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HLA Class II Associations in African-American Female Patients with Graves' Disease

Yanagawa¹,

DeGroot²

1996

Thyroid

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Graves' disease (GD) is an autoimmune thyroid disease. Development of the disease phenotype is believed to be dependent on environmental factors and the action of several genes either in concert or in independent groups. Genes of, or closely associated to, the human leukocyte antigen (HLA) complex are important in determining genetic predisposition to GD in various ethnic groups. We previously reported that no significant HLA class I or -DR associations were detected in the total group of African-American patients with GD. To further investigate the associations of GD with HLA class II alleles, 52 unrelated African-American female patients with GD and 55 controls were typed for HLA-DRB1, -DQA1, and -DQB1, using sequence-specific oligonucleotide probes to analyze polymerase chain reaction amplified DNA. There were no significant differences in HLA distribution between patients and controls. These findings indicate that the contribution of HLA-DR and DQ regions to susceptibility to GD is small in African-American women.

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Section: Frequencies Of Dr Antigenscontrasting

confidence: 83%

“…Only two studies have analyzed HLA-DR distributions of patients with GD in Africans or African-Americans by serological methods (7,8).…”

Section: Introductionmentioning

confidence: 99%

HLA Class II Associations in African-American Female Patients with Graves' Disease

Yanagawa¹,

DeGroot²

1996

Thyroid

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“…Whereas all these studies were based on limited numbers of patients (n~50) it is noteworthy that only one reported an association with the DRB1 *03 variant [38]. Notably, none of the studies analyzed the DPB1 locus.…”

Section: Genes Predisposing To Gdmentioning

confidence: 99%

The Genetic Basis of Graves Disease

Płoski

Szymański²,

Bednarczuk

2011

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The presented comprehensive review of current knowledge about genetic factors predisposing to Graves’ disease (GD) put emphasis on functional significance of observed associations. In particular, we discuss recent efforts aimed at refining diseases associations found within the HLA complex and implicating HLA class I as well as HLA-DPB1 loci. We summarize data regarding non-HLA genes such as PTPN22, CTLA4, CD40, TSHR and TG which have been extensively studied in respect to their role in GD. We review recent findings implicating variants of FCRL3 (gene for FC receptor-like-3 protein), SCGB3A2 (gene for secretory uteroglobin-related protein 1- UGRP1) as well as other unverified possible candidate genes for GD selected through their documented association with type 1 diabetes mellitus: Tenr–IL2–IL21, CAPSL (encoding calcyphosine-like protein), IFIH1(gene for interferon-induced helicase C domain 1), AFF3, CD226 and PTPN2. We also review reports on association of skewed X chromosome inactivation and fetal microchimerism with GD. Finally we discuss issues of genotype-phenotype correlations in GD.

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“…The association between GD and HLA specificities has also been reported in other ethnic groups: HLA-A2 and HLA-DPBU0501 in Japanese (52); HLA-B46, HLA-DR9, and HLA-DQB1*303 in male Hong Kong Chinese (53); HLA-A10, HLA-B8, and HLA-DQ2 in Asian Indians (54); and HLA-DR3 and HLA-DR1 in native South Africans (55). Whether there are associations between GD and the HLA complex among African-Americans is questioned.…”

Section: Hla Markers and Gdmentioning

confidence: 62%

What is the Evidence of Genetic Factors in the Etiology of Graves' Disease? A Brief Review

Brix¹,

Kyvik²,

Hegedűs³

1998

Thyroid

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Graves' disease (GD) is generally thought of as a multifactorial disorder in which genetic susceptibility interacts with environmental and endogenous factors to cause disease. The importance of genetic factors is suggested by the clustering of GD within families and by a higher concordance rate for disease in monozygotic than in dizygotic twins. This has, however, recently been shown to be less pronounced than previously thought. During the last decade much effort has been put into characterization of the genetic background of GD. Until recently, most studies have examined associations between GD and the human leukocyte antigen (HLA) region, but recent advances in molecular techniques have opened the way for whole genome screening. A number of HLA and non-HLA candidate genes have been proposed, but despite several large investigations within multiplex families no major susceptibility genes have been identified. This brief review discusses relevant articles published from 1940 through 1997 regarding the influence of genetic factors in the etiology of GD. Ongoing studies focus on whole genome screening in multiplex families as well as population-based twin studies. However, the possibility of GD being a heterogeneous disease without a single well-defined genotype and phenotype should be left open.

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HLA class I and II antigens in South African Blacks with Graves' disease

Cited by 28 publications

References 11 publications

HLA Class II Associations in African-American Female Patients with Graves' Disease

HLA Class II Associations in African-American Female Patients with Graves' Disease

The Genetic Basis of Graves Disease

What is the Evidence of Genetic Factors in the Etiology of Graves' Disease? A Brief Review

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