The immune system responds to the microorganisms through the release of pro-inflammatory cytokines with expansion of T cells followed by deletion or anergy. Naïve T cells can develop into effector T helper cells (Th), actually distinguished in Th1, Th2 and Th17, and T regulatory cells (T regs) depending on the stimulus and on the local cytokine milieu. Early response to the bacterial infection requires Th1 and, often, Th17 cytokine production to limit bacterial growth. In a second time, the early pro-inflammatory response may switch to an anti-inflammatory response driven by Tregs cells. A dysregulation of the timing of cytokine response with low levels of regulatory cytokines in the late phase of infection may induce a chronic inflammatory state (with a persistent Th1/Th17 cytokine profile) and develop many autoimmune and inflammatory diseases such as Rheumatoid Arthritis, Diabetes, Atherosclerosis, Autoimmune Myocardititis, Crohn’disease, Multiple Sclerosis.

Il network citochinico, dalla risposta alle infezioni all’induzione di autoimmunità

IMBESI, SELENE CARMELA;MINCIULLO, PAOLA LUCIA;GANGEMI, Sebastiano
2011

Abstract

The immune system responds to the microorganisms through the release of pro-inflammatory cytokines with expansion of T cells followed by deletion or anergy. Naïve T cells can develop into effector T helper cells (Th), actually distinguished in Th1, Th2 and Th17, and T regulatory cells (T regs) depending on the stimulus and on the local cytokine milieu. Early response to the bacterial infection requires Th1 and, often, Th17 cytokine production to limit bacterial growth. In a second time, the early pro-inflammatory response may switch to an anti-inflammatory response driven by Tregs cells. A dysregulation of the timing of cytokine response with low levels of regulatory cytokines in the late phase of infection may induce a chronic inflammatory state (with a persistent Th1/Th17 cytokine profile) and develop many autoimmune and inflammatory diseases such as Rheumatoid Arthritis, Diabetes, Atherosclerosis, Autoimmune Myocardititis, Crohn’disease, Multiple Sclerosis.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11570/1912068
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