Regular ArticleThe Role of IL-4 in Regulation of Murine Collagen-Induced Arthritis
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Regulatory effect of nicotine on the differentiation of Th1, Th2 and Th17 lymphocyte subsets in patients with rheumatoid arthritis
2018, European Journal of PharmacologyCitation Excerpt :Low numbers of Th2 cells are present in RA and it may have a protective role in RA (Guggino et al., 2014). Th2 cells and its cytokine interleukin (IL)−4 is thought to exert a protective function in RA and collagen-induced arthitis (CIA)(Schulze-Koops and Kalden, 2001; Myers et al., 2002). The Th1/Th2 ratio in RA patients is increased and is positively correlated with disease activity.
Group 2 Innate Lymphoid Cells Attenuate Inflammatory Arthritis and Protect from Bone Destruction in Mice
2018, Cell ReportsCitation Excerpt :Beside the prominent downregulation of IL-1β by IL-4/13+ ILC2s, which is a key effector cytokine in arthritis (Ji et al., 2002; Lamacchia et al., 2012), IL-4 itself acts as a regulatory cytokine in arthritis, as it fosters Th2 cell commitment, induces Ig class switching to the Th2-associated isotypes IgG1 and IgE (Nelms et al., 1999), and has the ability to suppress synoviocyte proliferation (Dechanet et al., 1993). In accordance, most (Horsfall et al., 1997; Joosten et al., 1997; Myers et al., 2002) but not all (Ohmura et al., 2005) studies showed that IL-4 has attenuating effects on arthritis. Studies of IL-13 and arthritis are limited, and although IL-13 is found in RA (Liu et al., 2016; Siloşi et al., 2016; Tokayer et al., 2002), only one study addressed its functional role by showing that IL-25/IL-13 has an attenuating effect on arthritis (Liu et al., 2016; Siloşi et al., 2016; Tokayer et al., 2002).
Antiinflammatory properties of a peptide derived from interleukin-4
2013, CytokineCitation Excerpt :Deficits in IL-4 aggravate severe inflammation in collagen-induced arthritis (CIA), a widely used animal model of rheumatoid arthritis. Overexpression of IL-4 or exogenous administration of IL-4 significantly delayed the onset and reduced the severity of experimental autoimmune encephalomyelitis (EAE) and CIA and attenuated the pathogenesis of Alzheimer’s disease in transgenic mice [1–6]. IL-4 knockout mice have been found to be more sensitive in models of transient focal cerebral ischemia [7].
Effector T cells in rheumatoid arthritis: Lessons from animal models
2011, FEBS LettersCitation Excerpt :IL-4 seems to play a role in the maintenance of tolerance. Tolerance to CII can be induced by the oral administration of CII or the injection of CII-treated splenocytes; and blockade of IL-4 using mAbs or IL-4−/− mice reverses tolerance to CIA [154,155]. Similar to the effect of IL-4 blockade in the CIA model, IL-4 mAbs also diminish tolerance induced after intranasal injection of mBSA in the AIA model [156].
T cell receptor signaling induced by an analog peptide of type II collagen requires activation of Syk
2009, Clinical ImmunologyCitation Excerpt :IL-10 is effective in down-regulating arthritis when administered to mice [36], yet it does not duplicate the effects of IL-4. Our previous data is consistent with the concept that IL-4 has a unique role in the suppression of arthritis that is only partially duplicated by other Th2 cytokines in the absence of IL-4 [37]. Such observations support out hypothesis that antigen interaction with the TCR in the context of the MHC can influence the cytokine profiles which are eventually produced by T cells.
Polymorphisms in the interleukin-4 and IL-4 receptor genes modify risk for chronic inflammatory arthropathies in women
2006, Experimental and Molecular Pathology