The non‐inherited maternal HLA haplotype affects the risk for type 1 diabetes

Åkesson, Kristina; Carlsson, Annelie; Ivarsson, Sten-A.; Johansson, Christer; Weidby, B. M.; Ludvigsson, Johnny; Gustavsson, B.; Lernmark, Åke; Kockum, Ingrid

doi:10.1111/j.1744-313x.2008.00802.x

Cited by 6 publications

(8 citation statements)

References 39 publications

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“…These findings are consistent with a dominant protective effect from the noninherited maternal allele DRB1*13 in mothers and increased risk from both inherited and noninherited DRB1*04 alleles in mothers, although this hypothesis was not evaluated directly. Similar parent‐specific effects of DRB1 variants on risk and protection have also been reported for type 1 diabetes (Akesson et al 2009; Feitsma et al 2007).…”

Section: Resultssupporting

confidence: 73%

Comparative immunogenetics of autism and schizophrenia

Crespi

Thiselton

2011

Genes, Brain and Behavior

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Autism and schizophrenia are highly heritable neurodevelopmental disorders, each mediated by a diverse suite of genetic and environmental risk factors. Comorbidity and familial aggregation of such neurodevelopmental disorders with other disease-related conditions can provide important insights into their etiology. Epidemiological studies have documented reduced rates of rheumatoid arthritis, a systemic autoimmune condition, in schizophrenia, and recent work has shown increased rates of rheumatoid arthritis in first-degree relatives of autistic individuals, especially mothers. Advances in understanding the genetic basis of rheumatoid arthritis have shown that much of the genetic liability to this condition is due to risk and protective alleles at the HLA DRB1 locus. These data allow robust testing of the hypotheses that allelic variation at DRB1 pleiotropically modulates risk of rheumatoid arthritis, autism and schizophrenia. Systematic review of the literature indicates that reported associations of DRB1 variants with these three conditions are congruent with a pleiotropic model: DRB1*04 alleles have been associated with increased risk of rheumatoid arthritis and autism but decreased risk of schizophrenia, and DRB1*13 alleles have been associated with protection from rheumatoid arthritis and autism but higher risk of schizophrenia. These convergent findings from genetics and epidemiology imply that a subset of autism and schizophrenia cases may be underlain by genetically based neuroimmune alterations, and that analyses of the causes of risk and protective effects from DRB1 variants may provide new approaches to therapy.

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Section: Resultssupporting

confidence: 73%

Comparative immunogenetics of autism and schizophrenia

Crespi

Thiselton

2011

Genes, Brain and Behavior

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“…In this study, the offspring of mothers positive for these alleles had a lower risk of RA (OR 0.25; p ¼ 0.003) [116]. Akesson et al found a significant association of HLA-DR4 þ and HLA-DR3 þ NIMAs with type 1 diabetes [117]. Guthrie et al found the association between HLA-DRA þ NIMAs to be statistically significant only in females with a younger onset of RA which gives us a possible explanation for conflicting results in studies evaluating NIMAs role in female biased autoimmunity [118].…”

Section: Non-inherited Maternal Antigens (Nimas)mentioning

confidence: 62%

Autoimmune disease and gender: Plausible mechanisms for the female predominance of autoimmunity

Quintero

Amador-Patarroyo

Montoya-Ortiz

et al. 2012

Journal of Autoimmunity

274

205

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A large number of autoimmune diseases (ADs) are more prevalent in women. The more frequent the AD and the later it appears, the more women are affected. Many ideas mainly based on hormonal and genetic factors that influence the autoimmune systems of females and males differently, have been proposed to explain this predominance. These hypotheses have gained credence mostly because many of these diseases appear or fluctuate when there are hormonal changes such as in late adolescence and pregnancy. Differences in X chromosome characteristics between men and women with an AD have led researchers to think that the genetic background of this group of diseases also relates to the genetic determinants of gender. These hormonal changes as well as the genetic factors that could explain why women are more prone to develop ADs are herein reviewed.

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“…Both risk and protective NIMA effects have been reported for RA (8, 14). NIMA effects do not appear to play a strong role in type 1 diabetes mellitus, although some evidence for an association has been reported (12, 15). We tested the hypothesis that maternal histocompatibility antigens, specifically those for HLA–DRB1, may contribute to the risk of SLE.…”

Section: Discussionmentioning

confidence: 99%

Analysis of maternal–offspring HLA compatibility, parent‐of‐origin effects, and noninherited maternal antigen effects for HLA–DRB1 in systemic lupus erythematosus

Bronson¹,

Komorowski²,

Ramsay³

et al. 2010

Arthritis & Rheumatism

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Objective. Genetic susceptibility to systemic lupus erythematosus (SLE) is well established, with the HLA class II DRB1 and DQB1 loci demonstrating the strongest association. However, HLA may also influence SLE through novel biologic mechanisms in addition to genetic transmission of risk alleles. Evidence for increased maternal-offspring HLA class II compatibility in SLE and differences in maternal versus paternal transmission rates (parent-of-origin effects) and nontransmission rates (noninherited maternal antigen [NIMA] effects) in other autoimmune diseases have been reported. Thus, we investigated maternal-offspring HLA compatibility, parent-of-origin effects, and NIMA effects at DRB1 in SLE.Methods. The cohort comprised 707 SLE families and 188 independent healthy maternal-offspring pairs (total of 2,497 individuals). Family-based association tests were conducted to compare transmitted versus nontransmitted alleles (transmission disequilibrium test) and both maternally versus paternally transmitted (parent-of-origin) and nontransmitted alleles (using the chi-square test of heterogeneity). Analyses were stratified according to the sex of the offspring. Maternally affected offspring DRB1 compatibility in SLE families was compared with paternally affected offspring compatibility and with independent control maternaloffspring pairs (using Fisher's test) and was restricted to male and nulligravid female offspring with SLE.Results. As expected, DRB1 was associated with SLE (P < 1 ؋ 10 ؊4 ). However, mothers of children with SLE had similar transmission and nontransmission frequencies for DRB1 alleles when compared with fathers, including those for the known SLE risk alleles HLA-DRB1*0301, *1501, and *0801. No association between maternal-offspring compatibility and SLE was observed.Conclusion. Maternal-offspring HLA compatibility, parent-of-origin effects, and NIMA effects at DRB1 are unlikely to play a role in SLE.

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The non‐inherited maternal HLA haplotype affects the risk for type 1 diabetes

Cited by 6 publications

References 39 publications

Comparative immunogenetics of autism and schizophrenia

Comparative immunogenetics of autism and schizophrenia

Autoimmune disease and gender: Plausible mechanisms for the female predominance of autoimmunity

Analysis of maternal–offspring HLA compatibility, parent‐of‐origin effects, and noninherited maternal antigen effects for HLA–DRB1 in systemic lupus erythematosus

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