Association of HLA Class II Alleles and Haplotypes with Type 1 Diabetes in Tunisian Arabs

Hajjej, Abdelhafidh; Almawi, Wassim Y.; Stayoussef, Mouna; Hattab, Lasmar; Hmida, Slama

doi:10.1055/a-0754-5586

Cited by 6 publications

(12 citation statements)

References 36 publications

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“…45 HLA class II allele frequency in the samples from self-identified Tunisian Arab women is consistent with prevalence rates reported earlier. 11,18,46 This study demonstrated a significant association of specific DRB1* or protective aspect to these alleles, respectively. This was in evident disagreement with studies on Brazilian, 47 Danish, 37,48 Japanese, 49 Kazakh, 40 and South Indian 25 women, which demonstrated the association of other DRB1 alleles with an increased risk of RPL, namely, DRB1*03:01:01, and DRB1*07/*07.…”

Section: Discussionmentioning

confidence: 50%

“…12,16 HLA alleles and respective haplotypes were shown previously to be selectively distributed according to ethnic/racial background, 10,11,17 and to (positively or negatively) influence the disease outcome of several immune and inflammatory disorders. 13,18,19 In particular, a remarkable association between specific class II alleles and corresponding haplotypes with disorders of immunity was noted. This was highlighted by the positive association of DRB1*03:01:01 and DQB1*02:01:01, and the negative association of DRB1*11:01:01 and DQB1*03:01:01 with autoimmune type 1 diabetes, 20 and the powerful association of DRB1*04-DQB1*03 haplotype with increased risk to rheumatoid arthritis.…”

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confidence: 99%

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Maternal HLA class II alleles and haplotypes associated with altered risk of recurrent pregnancy loss: A case‐control study

Aimagambetova,

Kapasheva,

Bahia

et al. 2024

American J Rep Immunol

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ProblemThis study analyzed the contribution of DRB1, DQB1, and DPB1 HLA class II alleles and resulting 3‐locus haplotypes to the overall risk of idiopathic recurrent pregnancy loss (RPL).Method of studyThe study participants included 188 Tunisian participants comprising 84 women with established diagnoses of RPL, and 104 matched multiparous females as controls. Genotyping of HLA alleles was done by PCR‐SSP.ResultsThe allelic frequencies of DPB1, DRB1, and DQB1 were consistent with Hardy‐Weinberg equilibrium among control subjects. Among class II alleles, DRB1*04:01:01 (p = .03), DRB1*08:01:01 (p = .04), and DPB1*01:01:01 (p = .04) were positively associated, whereas DPB1*04:01:01 (p = .012) and DPB1*14:01:01 (p = .006) were negatively associated with risk of RPL. The association of DRB1 and DPB1 alleles with RPL was lost after correction for multiple comparisons. The prevalence of the seven determined DQB1 alleles was not significantly different among case and control groups. Higher prevalence of DRB1*07:01:01∼ DQB1*02:01:01∼DPB1*04:01:01 (0.0417 vs. 0.000; p = .049) coupled with lower prevalence of DRB1*13:01:01∼DQB1*06:01:01∼DPB1*02:01:01 (0.0167 vs. 0.1000; p = .014) haplotypes was noted in women with RPL, thus could be considered as an RPL at‐risk and RPL‐protective haplotype, respectively.ConclusionThe study establishes weak/no contribution of class II alleles and corresponding 3‐locus haplotypes to the altered risk of RPL among Tunisian women and does not confirm previous findings on other Arab‐speaking populations of an HLA association with RPL.

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Section: Discussionmentioning

confidence: 50%

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confidence: 99%

Maternal HLA class II alleles and haplotypes associated with altered risk of recurrent pregnancy loss: A case‐control study

Aimagambetova,

Kapasheva,

Bahia

et al. 2024

American J Rep Immunol

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“…The absence of IAA analysis was a limitation in our study because we could not know whether diabetes in this young age group presented this Ab or if it corresponded to monogenic diabetes. For that, HLA-typing should be tested to confirm the autoimmune origin of T1D in these children [ 43 ], and the extended family history of type 1 diabetes must be considered [ 44 ].…”

Section: Discussionmentioning

confidence: 99%

Autoantibodies to Zinc Transporter 8 and SLC30A8 Genotype in Type 1 Diabetes Childhood: A Pioneering Study in North Africa

Fakhfakh

Kmiha

Tahri

et al. 2022

Journal of Diabetes Research

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Background. Type 1 diabetes (T1D) occurs as a result of insulin deficiency due to destructive lesions of pancreatic β cells. In addition to classical autoantibodies (Abs) to islet cell antigens, antizinc transporter 8 Abs (ZnT8-Ab) have been recently described in T1D. Objective. As no data on ZnT8-Ab in Tunisian patients has been reported, we aim to evaluate the relationships between ZnT8-Ab, ZnT8 coding gene (SLC30A8) promoter polymorphism, and T1D risk in newly diagnosed children. Methods. ZnT8-Ab were measured in the serum of T1D newly affected children ( n = 156 ) who were admitted to the pediatric department of the Hedi Chaker University Hospital of Sfax. Rs13266634 was genotyped in T1D children and 79 of their first-degree parents. The SPSS software was used to analyze the serological data. Allelic association analysis was conducted with family-based association tests implemented in the FBAT program v1.5.1. Results. ZnT8-Ab was detected in 66/156 (42.3%) of T1D newly diagnosed children. Among them, 6 (9%) presented ZnT8-Ab as the only humoral marker. The inclusion of ZnT8-Ab increased the number of Ab-positive patients to 90% and reduced the negative ones by 27%. There was no evidence of any overtransmission of any allele of the rs13266634 C/T polymorphism from parents to affected T1D children, nor of any correlation with any clinical or serological parameter. After the T1D disease onset age adjustment, a significant association was observed with the C allele suggesting that it could have a susceptibility role. Conclusion. ZnT8-Ab appears as a relevant diagnostic marker for T1D in Tunisian children, especially at the onset of the disease as teenagers.

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“…More or less long extended HLA haplotypes have been studied with some success in certain diseases; Berger's Disease in 1984 [163], type I diabetes in 1992 [164], and some extended HLA haplotypes were also defined in 1991 [165]. However, relatively few studies have been done up until now; some of them were in microscopic polyangiitis [166], celiac disease [167], kidney disease [168,169], diabetes [170], and psoriatic arthritis [171]. Technical difficulties of this type of study may be in part overcome by nowadays more advanced technologies.…”

Section: Hla Haplotypes and Disease Associationmentioning

confidence: 99%

Evolution and molecular interactions of major histocompatibility complex (MHC)-G, -E and -F genes

Arnaiz‐Villena

Suárez-Trujillo

Juárez

et al. 2022

Cell. Mol. Life Sci.

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Classical HLA (Human Leukocyte Antigen) is the Major Histocompatibility Complex (MHC) in man. HLA genes and disease association has been studied at least since 1967 and no firm pathogenic mechanisms have been established yet. HLA-G immune modulation gene (and also -E and -F) are starting the same arduous way: statistics and allele association are the trending subjects with the same few results obtained by HLA classical genes, i.e., no pathogenesis may be discovered after many years of a great amount of researchers’ effort. Thus, we believe that it is necessary to follow different research methodologies: (1) to approach this problem, based on how evolution has worked maintaining together a cluster of immune-related genes (the MHC) in a relatively short chromosome area since amniotes to human at least, i.e., immune regulatory genes (MHC-G, -E and -F), adaptive immune classical class I and II genes, non-adaptive immune genes like (C2, C4 and Bf) (2); in addition to using new in vitro models which explain pathogenetics of HLA and disease associations. In fact, this evolution may be quite reliably studied during about 40 million years by analyzing the evolution of MHC-G, -E, -F, and their receptors (KIR—killer-cell immunoglobulin-like receptor, NKG2—natural killer group 2-, or TCR-T-cell receptor—among others) in the primate evolutionary lineage, where orthology of these molecules is apparently established, although cladistic studies show that MHC-G and MHC-B genes are the ancestral class I genes, and that New World apes MHC-G is paralogous and not orthologous to all other apes and man MHC-G genes. In the present review, we outline past and possible future research topics: co-evolution of adaptive MHC classical (class I and II), non-adaptive (i.e., complement) and modulation (i.e., non-classical class I) immune genes may imply that the study of full or part of MHC haplotypes involving several loci/alleles instead of single alleles is important for uncovering HLA and disease pathogenesis. It would mainly apply to starting research on HLA-G extended haplotypes and disease association and not only using single HLA-G genetic markers.

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Association of HLA Class II Alleles and Haplotypes with Type 1 Diabetes in Tunisian Arabs

Cited by 6 publications

References 36 publications

Maternal HLA class II alleles and haplotypes associated with altered risk of recurrent pregnancy loss: A case‐control study

Maternal HLA class II alleles and haplotypes associated with altered risk of recurrent pregnancy loss: A case‐control study

Autoantibodies to Zinc Transporter 8 and SLC30A8 Genotype in Type 1 Diabetes Childhood: A Pioneering Study in North Africa

Evolution and molecular interactions of major histocompatibility complex (MHC)-G, -E and -F genes

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