IFNy interferon

If the ATP depletion is too great, then apoptosis cannot proceed. Kupffer cell activation involving IFNy (interferon) and TNF-a is part of an inflammatory response in which nitric oxide and various cytokines are produced. 

Fig. 9.2. Simplified schema of the development of T helper type 1 (Th1) and 2 (Th2) cells under the influence of interleukin (IL)-12 and IL-4, respectively, and how these two polarized T cell phenotypes produce cross-inhibitory cytokine profiles and promote different aspects of the host immune response (IFNy, interferon-gamma TNFa, tumour necrosis factor alpha Thr, T helper regulatory cell Th3, T helper type 3 cell).

Abbreviations-. CD, cluster designation (surface markers) ConA, concanavalin A (aT cell mitogen) IFNy, interferon-gamma IL, interleukin PBMC, peripheral blood mononuclear cells TNFa, tumour necrosis factor-alpha. 

ACDy allergic contact dermatitis /CD, irritant contact dermatitis JL, interleukin HLA, human leukocyte antigen ICAMy intercellular adhesion molecule TNF, tumour-necrosis factor IFNy interferon GM-CSFy granulocyte-macrophage-colony-stimulating factor /P, IFN-induced protein M/P, macrophage inflammatory protein... 

Interferon production of PBMCs cultured in the presence of selected DIMS determined by ELISA for IFNa, IFNp (mean data from six healthy individuals) and by Cytometric Bead Array (Becton Dickinson) for IFNy (mean data from four healthy individuals)... 

Inhibitory Smads Smad 6 and Smad 7 function as inhibitors of TGPp signaling. They bind to type I receptors and interfere with phosphorylation of the pathway-restricted Smads. These Smad proteins may be used to modulate and weaken the TGPp receptor. Such transmodulation has been described for the interferon y pathway. Activation of the IFNy pathway leads to increased transcription of Smad 7, which diminishes signal conduction in the TGPp pathway (Ulloa et al., 1999). 

Types I and type II Interferon Signaling IFNa/p IFNy... 

The molecular mechanism of the NO pro-inflammatory activity is also multifaceted NO regulates the inflammatory responses by cell-specific inhibition of the transcription factor NF-kB, IL-ip, interferon-y (IFNy). At sites of inflammation, increased free radical activity is associated with the activation of the neutrophil NADPH-oxidase and/or the uncoupling of a variety of redox systems, leading to a substantial increase in ROS. Free radicals thus produced, have the capacity to mediate tissue destruction, either alone or in concert with proteases [53]. 

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