Cytokines and autoimmunity

Abstract

SUMMARYAlthough the immunopathology of most autoimmune diseases has been well defined, responsible for the breakdown of self-tolerance and which lead to the development of syste organ-specific autoaggression are still unclear. Evidence has accumulated which supports a role for a disregulated production of cytokines by leucocytes and possibly other cells in the pathogenesis of some autoimmune diseases. However, due to the complexity and heterogeneity of cytokine effects in the regulation of the immune response, it is difficult to determine whether abnormalities in the patterns of eytokine production are primary or secondary to the pathological process. Confusion is also caused by the fact that the biological activities of cytokines are multiple and often overlapping, and consequently it is difficult to focus on a unique effect of any one cytokine. Characterization of the potential and actual involvement of cytokines is important not only for a better understanding of the pathogenesis of autoimmune conditions, but particularly because of the implications for the development of immunotherapeutic strategies for the prevention and treatment of the diseases.

Activin-A: a novel dendritic cell–derived cytokine that potently attenuates CD40 ligand–specific cytokine and chemokine production

“…However, uncontrolled cytokine/chemokine release within this microenvironment can also result in inappropriate T-and B-cell responses and subsequent immunopathology. [21][22][23] In this regard, the immune system has evolved to coordinately express mediators that attenuate exaggerated or inappropriate responses so as to minimize tissue damage and immunopathology (eg, prostaglandin E 2 (PGE 2 ), adenosine triphosphate (ATP), transforming growth factor-␤ [TGF-␤]). 24 Activin-A is a homodimer of activin-␤A subunits and was first described as a reproductive factor that accentuates the release of follicle-stimulating hormone.…”

A possible inhibitory action of diaminodiphenyl sulfone on tumour necrosis factor-α production from activated mononuclear cells on cutaneous lupus erythematosus

“…TNF‐α is not a disease‐specific cytokine, but is rather a pivotal proinflammatory cytokine produced by various cell types such as macrophages, neutrophils, fibroblasts, lymphocytes, mast cells and epithelial cells. TNF‐α has been reported to have a central role in both the modulation of immune functions such as neutrophil and lymphocyte trafficking and the expression of cellular adhesion molecules, 18 and also in inducing class II major histocompatibility complex 19 and T‐cell‐mediated cytotoxicity 20,21 . Furthermore, direct tissue damage generated by TNF‐α has been described in autoimmune pulmonary inflammation in lupus‐prone mice 22 .…”

“…TNF-a has been reported to have a central role in both the modulation of immune functions such as neutrophil and lymphocyte trafficking and the expression of cellular adhesion molecules, 18 and also in inducing class II major histocompatibility complex 19 and T-cellmediated cytotoxicity. 20,21 Furthermore, direct tissue damage generated by TNF-a has been described in autoimmune pulmonary inflammation in lupus-prone mice. 22 We had previously reported the infiltration of CD68+ and CD3+ lymphocytes in DLE lesions.…”

Tacrine Derivatives in Neurological Disorders: Focus on Molecular Mechanisms and Neurotherapeutic Potential

“…Glial cells activated during brain inflammation may produce proinflammatory mediators, which have been linked to the neuropathology that produces cognitive impairments in neurological diseases [ 43 , 44 ]. In neurodegenerative illnesses, the balance between proinflammatory and anti-inflammatory cytokines also has an impact on the course of the disease [ 15 , 45 ]. According to Zhang et al, hippocampal injection of a tacrine analogue known as 4-(bis(pyridin-2-ylmethyl)amino)-N-(3- ((1,2,3,4-tetrahydroacridin-9-yl) amino)propyl)butanamide could effectively attenuate A β 1-42 oligomers-induced cognitive dysfunction by activating the CREB/BDNF signaling pathway, decreasing tau phosphorylation [ 46 ].…”