Role of SOCS proteins in inflammation and autoimmune diseases
Tomohiro Fukaya, Mayu Suzuki, Ryota Sakaguchi, Hideo Yasukawa, Akihiko Yoshimura
Abstract
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Tomohiro Fukaya, Mayu Suzuki, Ryota Sakaguchi, Hideo Yasukawa, Akihiko Yoshimura
Abstract
Open-access reader
Various cytokines are involved in the regulation of the immune system and inflammation. Dysregulation of cytokine signaling can cause a variety of diseases, including allergies, autoimmune diseases, inflammation, and cancer. Most cytokines utilize the so-called Janus kinase-signal transducers and activators of transcription (JAK-STAT) pathway. This pathway is negatively regulated by suppressors of cytokine signaling (SOCS) proteins. SOCS proteins bind to JAK or certain cytokine receptors, thereby suppressing further signaling events. Studies using conditional knockout mice have shown that SOCS proteins are key physiological pathological regulators of inflammation as well as immune homeostasis. Recent studies have also demonstrated that SOCS1 and SOCS3 are important regulators of adaptive immunity, especially helper T cell differentiation.
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Various cytokines are involved in the regulation of the immune system and inflammation. Dysregulation of cytokine signaling can cause a variety of diseases, including allergies, autoimmune diseases, inflammation, and cancer. Most cytokines utilize the so-called Janus kinase-signal transducers and activators of transcription (JAK-STAT) pathway. This pathway is negatively regulated by suppressors of cytokine signaling (SOCS) proteins. SOCS proteins bind to JAK or certain cytokine receptors, thereby suppressing further signaling events. Studies using conditional knockout mice have shown that SOCS proteins are key physiological pathological regulators of inflammation as well as immune homeostasis. Recent studies have also demonstrated that SOCS1 and SOCS3 are important regulators of adaptive immunity, especially helper T cell differentiation.
Key concepts: SOCS3, Suppressor of cytokine signaling 1, Suppressor of cytokine signalling, Inflammation, Janus kinase, Cytokine, Signal transduction, stat