Interleukins cellular role

Specific cellular immunity is a type of (more specialized) acquired immunity which is based primarily on T lymphocytes. Several subpopulations of T lymphocytes are differentiated in the thymus, where one subset has identical structures on the cell surface to recognize a specific set of antigen. Each subpopulation performs different effector functions. The dominant T-cell type involved is the so-called cytotoxic T lymphocyte. In addition, T-helper cells are important for enhancing the immune response. By synthesizing and secreting various cytokines such as interferon y (INF-y or interleukin 2 (IL-2), T-lymphocytes also have an important role in controlling other major parts of the immune system. 

Interleukin-6 (IL-6) is a principal cellular regulatory factor, and also plays a role in bone remodeling. IL-6 exercises its effect by binding to a receptor (IL-6R), which leads to signal transduction and activation of intracellular cascades. Information from studies performed both in vitro and in vivo show IL-6 as an autocrine/paracrine factor of the osteoclasts. Recent studies describe especially increased expression of IL-6R mRNA in the osteoclasts engaged in increased bone resorption. It can be judged that IL-6 itself is in a sophisticated way involved in bone resorption, and that especially the expression of its receptor (IL-6R) correlates with resorption activity of the osteoclasts (LI). 

Ellman, C., Corbett, J.A., Misko, T.P., McDaniel, M., and Beckerman, K.P. (1993). Nitric oxide mediates interleukin-Ip-induced cellular cytotoxicity. A potential role for nitric oxide in the ovulatory process. J. Clin. Invest. 92 3053-3056. 

The dream of Stewart Adams, to find not only a palliative treatment but also a cure for rheumatoid diseases, did unfortunately not come true. [180] Pro-inflammatory cytokines like interleukin-1 and -6, or the tumour-necrosis factor-a (TNF-a) play key roles in diseases of the rheumatoid spectrum, and impact a multitude of signalling cascades within the immune system. Accumulating insight into the pathophysiology, biochemistry, cellular and molecular biology of these illnesses has clearly improved the opportunities for their treatment at the... 

Inflammation plays a key role in the etiology of aAerosclerosis /139). A plethora of interleukins, cytokines, intercellular matrix modifying enzymes, and cell types interact to promote foam cell, fatty streak, and atheromatous plaque formation (140). PPAR-a has emerged as an important mediator of vascular inflammation and cellular redox status (141). The nuclear factor kB (NF-kB) pathway regulates the expression adhession molecules, interleukin-6, cyclooxygenase-2, and endotheUn- (141). CRP is an important modulator of and marker for atherosclerotic disease (142,143). PPAR-a agonism with fibrate therapy decreases serum CRP levels (94,144). 

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