IndraLab

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"These patients showed increased levels of pro-inflammatory cytokines, such as TNF, IL-1β and IL-6, and demonstrated clinical improvement after treatment with anti-TNF or anti-IL-1β therapy.In addition, low-penetrance coding and non-coding variants in TNFAIP3 have been suggested to underlie multiple autoimmune diseases, including Crohn’s disease, psoriasis, RA, type 1 diabetes mellitus and susceptibility to allergy and asthma ."

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"In patients with ACPA-negative RA, certain polymorphisms have been identified, including variants in the ankyrin repeat domain 55(ANKRD55)/interleukin 6 signal transduce (IL6ST), B lymphoid tyrosine kinase (BLK), tumor necrosis factor alpha-induced protein 3 (TNFAIP3), GIN1 protein/C5orf30 (GIN1/C5orf30), STAT4, 60S ribosomal protein pseudogene (RPL), and nuclear factor I A (NFIA)genes, suggesting that distinct genetic factors may underlie these two subsets of RA (24, 25)."

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"Finally, the heterogeneity of genetic models in this meta-analysis is high, we should interpret the data with caution.In summary, this meta-analysis provides evidence that TNFAIP3 gene rs2230926 and r[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

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"In this meta-analysis, our data found that TNFAIP3 gene rs6920220, rs2230926, and rs5029937 polymorphisms increased the risk of RA."