Engineering cell and tissue surfaces with SA-FasL protein provides a practical, efficient, and safe means of localized immunomodulation with important implications for autoimmunity and transplantation.
The gut bacteria compositional changes observed in VIP<sup>-/-</sup> mice was consistent with gut microbial structure changes reported for certain inflammatory and autoimmune disorders.
The T cell-instructed IL-1β resulted in systemic inflammation, whereas absence of TNFR or Fas signaling protected mice from CD4<sup>+</sup> T cell-driven autoimmunity.
IL-17-producing CD8<sup>+</sup> (Tc17) cells are enriched in active lesions of patients with multiple sclerosis (MS), suggesting a role in the pathogenesis of autoimmunity.
A reversible S-adenosyl-l-homocysteine hydrolase (SAHH) inhibitor, DZ2002, modulates the pathologic processes of various inflammatory diseases and autoimmune diseases.
Our meta-analysis showed that the FAS -670 A/G polymorphism was associated with the risk of autoimmune diseases (GG vs. GA: OR=1.079, 95% CI=1.004-1.160, P=0.038), especially in Caucasians (GG vs. GA: OR=1.12, 95% CI=1.03-1.23, P=0.012), Asians (G vs. A: OR=0.89, 95% CI=0.83-0.96, P=0.002), systemic lupus erythematosus (SLE) (G vs. A: OR=0.85, 95% CI=0.77-0.94, P=0.001), multiple sclerosis (MS) (GG+GA vs. AA: OR=0.83, 95% CI=0.70-0.99, P=0.043), systemic sclerosis (SSc) (GG vs. GA: OR=1.20, 95% CI=1.07-1.36, P=0.003) and Hashimoto's thyroiditis (HT) (G vs. A: OR=1.45, 95% CI=1.10-1.90, P=0.008); the FAS -1377 G/A polymorphism was associated with the risk of autoimmune diseases (A vs. G: OR=1.11, 95% CI=1.03-1.20, P=0.008), especially in Asians (A vs. G: OR=1.15, 95% CI=1.05-1.25, P=0.002) and high quality studies (A vs. G: OR=1.14, 95% CI=1.05-1.24, P=0.002).
Activation of the Absent in Melanoma 2 (AIM2) inflammasome is crucial for immune defense, but it can also cause inflammatory and autoimmune diseases, including psoriasis.
These findings offer a mechanistic model where during islet autoimmunitymiR142-3p/Tet2-mediated Treg instability contributes to autoimmune activation and progression.
CD200/CD200R1 signalling is associated with the prevention of autoimmune diseases; however, the role of CD200/CD200R1 signalling in the pathogenesis of psoriasis remains unknown.
IL-1 system is involved in the induction and maintenance of chronic inflammation associated with several autoimmune diseases and cancer, mainly due to its capacity to promote the secretion of inflammatory mediators.
IL-1 system is involved in the induction and maintenance of chronic inflammation associated with several autoimmune diseases and cancer, mainly due to its capacity to promote the secretion of inflammatory mediators.
Cumulative evidence suggests that MASP-2, and even other components of the LP, are largely redundant in human defenses and that individuals with MASP-2 deficiency do not seem to be particularly prone to infectious or autoimmune diseases.
Here, we show that mice lacking immune inhibitory receptor VISTA or programmed death-1 homolog (PD-1H KO) on a BALB/c background spontaneously develop cutaneous and systemic autoimmune diseases resembling human lupus.
Moreover, the mapped network in B lymphocytes comprised two additional hub proteins involved in both inflammation and autoimmunity: HSPA8 (Heat Shock Protein Family A Member 8 also known as HSC70) and HSP90AA1 (Heat Shock Protein 90 Alpha Family Class A Member 1).
Moreover, the mapped network in B lymphocytes comprised two additional hub proteins involved in both inflammation and autoimmunity: HSPA8 (Heat Shock Protein Family A Member 8 also known as HSC70) and HSP90AA1 (Heat Shock Protein 90 Alpha Family Class A Member 1).
Moreover, the mapped network in B lymphocytes comprised two additional hub proteins involved in both inflammation and autoimmunity: HSPA8 (Heat Shock Protein Family A Member 8 also known as HSC70) and HSP90AA1 (Heat Shock Protein 90 Alpha Family Class A Member 1).
Abnormalities in leptin-adiponectin (adipocyte biology), oxidative stress and autoimmunity are among the mechanisms studied regarding pathogenesis of PCOS.