in a recent study on some sclerosis (MS), we observed the effects of the additive and epistatic interactions between variants of four genes were assembled to induce T-cell hyperactivity with change Asn- (N ) -linked protein glycosylation: namely, Golgi enzymes MGAT1, cytotoxic T-lymphocyte antigen 4 (CTLA-4), interleukin-2 receptor-α (IL2RA) and interleukin-7 receptor-α (IL7RA). As CTLA-4, IL2RA and IL7RA variants associated with type 1 diabetes (T1D), we examined for joint effects on T1D.
Employing logistic regression conditional new family-based data sets, the effects of epistatic and additive were observed using 1423 some x family of Type 1 Diabetes genetically The Consortium collection data. The IL2RA and IL7RA variant has a univariate relationship in MS and T1D, while MGAT1 and CTLA-4 variants are associated with only MS or T1D, respectively. However, similar to MS, MGAT1 haplotype variant interacts with CTLA4 (P = 0.03), and the combination IL2RA and IL7RA (P = 0.01). The combined effect of MGAT1, CTLA4, IL2RA, IL7RA and two interactions using the some Conditional logistic regression was statistically significant (P <5 × 10 (-10)).
The MGAT1-CTLA-4 interaction is repeated (P = 0.01) in 179 families trio of Genetics of Kidneys in Diabetes study. These data are consistent with the N-glycosylation defects of T cells contribute to the pathogenesis of T1D.
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