Regulation of autoimmunity by proinflammatory cytokines
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Quantitative alterations in bovine milk proteome from healthy, subclinical and clinical mastitis during S. aureus infection
2020, Journal of ProteomicsCitation Excerpt :During the early stage of mastitis, oxidative stress begins to develop by ROS production [82] to eliminate invading bacteria which in turn damages the body's cells. Hence, overexpression of angiogenin that boosts cell survival and saves anabolic energy [81] and cofilin-1 that induces T cell hyposensitivity [83] could be an essential adaptive coping mechanism against the onset of the oxidative stress. To understand the interplay among differentially expressed proteins between CM/SCM; STRING analysis was performed to uncover potential interactions to regulate downstream functions in promoting the progression of the disease.
TNF activity and T cells
2018, CytokineCell-Targeted Biologics and Emerging Targets
2016, Kelley and Firestein's Textbook of Rheumatology: Volumes 1-2, Tenth EditionThe role of Th17-associated cytokines in the pathogenesis of experimental autoimmune uveitis (EAU)
2015, CytokineCitation Excerpt :That a specific cytokine possesses both pro- and anti-inflammatory activities is not a surprising observation. For example, an anti-inflammatory effect of the classic proinflammatory cytokine TNF-α has been reported [52,53]. A dual role of TNF-α in type 1 diabetes has also been observed [54].
Low C-peptide levels and decreased expression of TNF and CD45 in children with high risk of type 1 diabetes
2013, Clinical ImmunologyCitation Excerpt :The importance of TNF in the development of T1D has been demonstrated in mice [28], but it's role seems quite double-edged since studies have shown harmful or protective effects depending on timing [29]. Indeed, although TNF is well known as a pro-inflammatory cytokine, there is evidence suggesting anti-inflammatory and immune-suppressive effects as well [30]. Results from a recent study in mice revealed that activated effector T cells boost both suppressive function and expansion of regulatory T cells (Treg) in vivo by a TNF-dependent mechanism, and that sustained Treg-mediated protection from diabetes was dependent on this boost [31].