Cytokines pathophysiology

B cells also have impact on T-cell differentiation. B-cell antigen presentation plays an important role at promoting Th2 responses and pathophysiology during allergic disorders. It has been shown that B-cell -/- mice and in mice selectively deficient in MHCII on B cells had decreased Th2 cytokines IL-4 and IL-5 [152]. Also in another study it has been reported that B-cell-derived exosomes can present allergen peptides and activate allergen-specific T cells to proliferate and produce Th2 cytokines IL-5 and IL-13 [42]. 

Inflammatory cytokines have been implicated in the pathophysiology of HF.9 Several proinflammatory (e.g., tumor necrosis factor-a [TNF-a], interleukin-1, interleukin-6, and interferon-y) and anti-inflammatory cytokines (e.g., interleukin-10) are overexpressed in the failing heart. The most is known about TNF-a, a pleiotrophic cytokine that acts as a negative inotrope, stimulates cardiac cell apoptosis, uncouples 3-adrenergic receptors from adenylyl cyclase, and is related to cardiac cachexia. The exact role of cytokines and inflammation in HF pathophysiology continues to be studied. 

Although it appears that severe IL-4-regulated enteropathy is not required for immune expulsion of T. spiralis, it is still possible that Th2 cytokines can act in a direct fashion to create an environment unfavourable for intestinal parasites. It remains to be shown directly whether these effects are sufficient to expel parasites. Indeed, there is considerable evidence to support a variety of pathophysiological effects of IL-4 and/or TNF on the gut. These effects may be mediated by factors including cytokines and mast-cell products (e.g. leukotrienes and 5-hydroxytryptamine). 7. spiralis infections result in increased fluid and mucus secretion into the lumen as well as increased intestinal propulsive activity and more rapid intestinal transit (Castro et al, 1979 Russell, 1986 Vermillion and Collins, 1988 Vermillion et al., 1991 Weisbrodt et al, 1994 Barbara et al, 1997). The increased contractility of radial and longitudinal muscle is greater in high-... 

Inhibition of cytokine activity in vivo by administration of monoclonal antibodies (and, more recently, by gene knockout studies) continues to elucidate the physiological and pathophysiological effect of various cytokines. 

Kwan TS, Padrines M, Theoleyre S, Heymann D, Fortun Y (2004) IL-6, RANKL, TNF-alpha/IL-1 interrelations in bone resorption pathophysiology. Cytokine Growth Factor Rev 15 49-60... 

Ischaemic stroke is the third leading cause of death in industrialized countries. The debilitating or lethal consequences of transient or temporary reductions in cerebral blood flow are not only caused by necrosis in the infarct zone itself, but also by pathophysiological events in the peri-infarct zone [14]. Apparently, the release of inflammatory mediators such as cytokines and NO contributes to tissue inflammatory injury. There is also evidence for apoptosis in the peri-infarct zone. These processes offer novel targets for therapeutic strategies. In this respect, the potential of neurotrophic factor treatment is described in Section 2.4.2.6. 

Pace TW, Hu F, Miller AH Cytokine-effects on glucocorticoid receptor function Relevance to glucocorticoid resistance and the pathophysiology and treatment of major depression. Brain Behav Immun 2007 21(1) 9. [PMID 17070667]... 

Nearly all cells express kinin receptors that mediate the activities of both bradykinin and kallidin. The activation of these G-protein coupled receptors causes relaxation of venular smooth muscle and hypotension, increased vascular permeability, contraction of smooth muscle of the gut and airway leading to increased airway resistance, stimulation of sensory neurons, alteration of ion secretion of epithelial cells, production of nitric oxide, release of cytokines from leukocytes, and the production of eicosanoids from various cell types [11,12]. Because of this broad spectrum of activity, kinins have been implicated as an important mediator in many pathophysiologies including pain, sepsis, asthma, rheumatoid arthritis, pancreatitis, and a wide variety of other inflammatory diseases. Moreover, a recent report demonstrated that bradykinin B2 receptors on the surface of human fibroblasts were upregulated three-fold beyond normal in patients with Alzheimer s disease, implicating bradykinin as a participant in the peripheral inflammatory processes associated with that disease [13]. 

Several pathophysiological mechanisms have been proposed, including adverse effects of protease inhibitors on hepatocyte and fat cell function (143), mitochondrial toxicity from nucleoside analogues (144), excess of reactive oxygen species (145), and cytokine-mediated events... 

Furthermore, the immunologic pathway involved in the pathophysiology of AD is complex (table 2). It presents a degree of complexity which has not been appreciated with allergic rhinitis and asthma. In AD both Thl and Th2 T cell products play a role in chronic inflammation, which is maintained by both IL-5 (Th2) and IFN-y (Thl) [51]. In addition recent studies have demonstrated different cytokine expressions in acute (predominantly IL-16) and in chronic (mainly IL-12 and GM-CSF) lesions [52, 53]. 

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