Molecular analysis of HLA class II genes in primary sjo¨gren's syndrome

Roitberg-Tambur, Anat; Friedmann, Adam; Safirman, C.; Markitziu, A; Ben-Chétrit, Eldad; Rubinow, Alan; Moutsopoulos, Haralampos Μ.; Stavropoulos, Efthymois; Skopouli, Fotini N.; Margalit, Hanah; Brautbar, Chaim

doi:10.1016/0198-8859(93)90130-s

Cited by 44 publications

(18 citation statements)

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“…These associations were further confirmed using meta-analysis. In this case-control study, no association was observed between pSS and the HLA-DBR1*03, *04, *11 or *15 which were associated with pSS in other populations [5,6,14,20]. This result supports that the HLA class II alleles associated with pSS are different among populations.…”

Section: Discussionsupporting

confidence: 61%

“…HLA-DRB1*0803 is the allele shows strongest association with pSS in Chinese population, while it is not associated with the disease in Caucasian and in Jewish [5,6]. This discrepancy might due to the diversity in the frequency of the HLA-DRB1*0803 among populations, where it in south Asia is rather high (approximately 10%) while it is nearly absent in Caucasian and in Jewish [6,26].…”

Section: Discussionmentioning

confidence: 99%

“…The HLA class II alleles associated with pSS are different among populations. For example, HLA-DRB1*15 and HLA-DRB1*03 are associated with pSS in Caucasians [4], the HLA-DRB1*11 is associated with pSS in Jewish [5], while the HLA-DRB1*04 is associated with pSS in Japanese [6]. In addition, a marginal, but not significant association between HLA-DRB1*08 allele and pSS was reported in the Chinese population [6].…”

Section: Introductionmentioning

confidence: 99%

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The amino acid variation within the binding pocket 7 and 9 of HLA-DRB1 molecules are associated with primary Sjögren's syndrome

Huang

Chen

et al. 2015

Journal of Autoimmunity

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Section: Discussionsupporting

confidence: 61%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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The amino acid variation within the binding pocket 7 and 9 of HLA-DRB1 molecules are associated with primary Sjögren's syndrome

Huang

Chen

et al. 2015

Journal of Autoimmunity

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“…The last three AAR are in contact with the T cell receptor (TCR) and therefore, they are important in determining T cell recognition of the peptide -DR complex. The P4 pocket at the reported primary SS-susceptibility alleles across populations: DRB1 * 0301, * 1101, * 1104 and * 0405 (Kang et al 1993;Roitberg-Tambur et al 1993), and DQB1 * 0201 shares a common positively charged amino acid sequence (Gregersen et al 1987;Anaya et al 2005a). Having a positively charged P4 pocket implies that those positive HLA molecules can only present a neutral or negative peptide to T cells (Table I).…”

Section: Major Histocompatibility Complex and Hla Associationsmentioning

confidence: 99%

“…et al (1986),Kang et al (1993),Kerttula et al (1996),Bolstad et al (2001),Anaya et al (2002bAnaya et al ( , 2005a andGottenberg et al (2003); †Kang et al (1993) andMiyagawa et al (1998); ‡Kang et al (1993);{ Papasteriades et al (1988),Roitberg-Tambur et al (1990) andRoitberg-Tambur et al (1993).…”

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confidence: 99%

Genetic Basis of Sjögren′s Syndrome. How Strong is the Evidence?

Anaya

Delgado-Vega

Castiblanco

2006

Journal of Immunology Research

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Sjögren's syndrome (SS) is a late-onset chronic autoimmune disease (AID) affecting the exocrine glands, mainly the salivary and lachrymal. Genetic studies on twins with primary SS have not been performed, and only a few case reports describing twins have been published. The prevalence of primary SS in siblings has been estimated to be 0.09% while the reported general prevalence of the disease is approximately 0.1%. The observed aggregation of AIDs in families of patients with primary SS is nevertheless supportive for a genetic component in its etiology. In the absence of chromosomal regions identified by linkage studies, research has focused on candidate gene approaches (by biological plausibility) rather than on positional approaches. Ancestral haplotype 8.1 as well as TNF, IL10 and SSA1 loci have been consistently associated with the disease although they are not specific for SS. In this review, the genetic component of SS is discussed on the basis of three known observations: (a) age at onset and sex-dependent presentation, (b) familial clustering of the disease, and (c) dissection of the genetic component. Since there is no strong evidence for a specific genetic component in SS, a large international and collaborative study would be suitable to assess the genetics of this disorder.

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Sjögren's syndrome associated with systemic lupus erythematosus: Clinical and laboratory profiles and comparison with primary Sjögren's syndrome

Manoussakis¹,

Georgopoulou²,

Ζιντζαράς³

et al. 2004

Arthritis & Rheumatism

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233

175

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Objective.To address the clinical, serologic, pathologic, and immunogenetic features of sicca syndrome that occurs in systemic lupus erythematosus (SLE), as well as its similarities to, and differences from, sicca syndrome that occurs in primary Sjögren's syndrome (SS).Methods.A cohort of 283 consecutive unselected SLE patients was evaluated for the presence of associated SS using the American–European classification criteria. Clinical and laboratory parameters in SLE patients with SS (SLE–SS) were compared with those in SLE patients without SS (SLE–no SS) and with a group of 86 unselected patients with primary SS.Results.SS was identified in 26 SLE patients (9.2%); the SS preceded the development of lupus in 18 of them (69.2%). Compared with the SLE–no SS group, patients with SLE–SS were significantly older, had a higher frequency of Raynaud's phenomenon, anti‐Ro/SSA, anti‐La/SSB, and rheumatoid factor, but had a significantly lower frequency of renal involvement, lymphadenopathy, and thrombocytopenia. Compared with the primary SS group, SLE–SS patients displayed a clinically similar sicca syndrome, but were significantly younger and had an increased frequency of perivascular infiltrates in the salivary glands associated with anticardiolipin antibodies in the serum. SLE–SS patients had a high frequency of the DRB1*0301 allele. This HLA profile distinguished the SLE–SS group from the SLE–no SS group, who had an increased frequency of DRB1*1501 and DQB1*0602 alleles, but was similar to the HLA profile of the primary SS group, who had an increased frequency of DRB1*0301.Conclusion.SLE–SS appears to constitute a subgroup of patients with distinct clinical, serologic, pathologic, and immunogenetic features, in whom SS is expressed as an overlapping entity and is largely similar to primary SS.

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Molecular analysis of HLA class II genes in primary sjo¨gren's syndrome

Cited by 44 publications

References 22 publications

The amino acid variation within the binding pocket 7 and 9 of HLA-DRB1 molecules are associated with primary Sjögren's syndrome

The amino acid variation within the binding pocket 7 and 9 of HLA-DRB1 molecules are associated with primary Sjögren's syndrome

Genetic Basis of Sjögren′s Syndrome. How Strong is the Evidence?

Sjögren's syndrome associated with systemic lupus erythematosus: Clinical and laboratory profiles and comparison with primary Sjögren's syndrome

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