Commentary: IL-17 in Chronic Inflammation: From Discovery to Targeting

A recent article titled “IL-17 in chronic inflammation: From discovery to targeting,” by Beringer et al. (2016), greatly reviewed the biology of interleukin-17 (IL-17) family members highlighting the contributions of IL-17 cytokines toward diseases and IL-17-based treatment options. Authors attractively reported how preclinical and clinical studies have provided a solid scientific justification for targeting IL-17 and/or IL-17 receptor (IL-17RA) in human diseases such as inflammatory and autoimmune disorders. Here, I wish to implement the description of the biological properties of IL-17A on the cardiovascular system, the novel underlying mechanisms on platelets aggregation, and thrombus formation, and to report the contribution of IL-17A/IL-17RA axis in the association of autoimmune diseases with cardiovascular risk.

[1]  A. Yoshimura,et al.  Critical Link Between Epigenetics and Transcription Factors in the Induction of Autoimmunity: a Comprehensive Review , 2016, Clinical Reviews in Allergy & Immunology.

[2]  P. Miossec,et al.  IL-17 in Chronic Inflammation: From Discovery to Targeting. , 2016, Trends in molecular medicine.

[3]  P. Cutler,et al.  Biomarkers for cardiovascular risk assessment in autoimmune diseases , 2015, Proteomics. Clinical applications.

[4]  F. D’Acquisto,et al.  Interleukin-17A Exacerbates Ferric Chloride-Induced Arterial Thrombosis in Rat Carotid Artery , 2014, International journal of inflammation.

[5]  R. D. de Winter,et al.  Neutrophils, neutrophil extracellular traps and interleukin-17 associate with the organisation of thrombi in acute myocardial infarction , 2012, Thrombosis and Haemostasis.

[6]  P. Miossec,et al.  Simvastatin inhibits the pro-inflammatory and pro-thrombotic effects of IL-17 and TNF-α on endothelial cells , 2012, Annals of the rheumatic diseases.

[7]  Jing Yuan,et al.  IL-17A Facilitates Platelet Function through the ERK2 Signaling Pathway in Patients with Acute Coronary Syndrome , 2012, PloS one.

[8]  P. Miossec,et al.  Combination of IL-17 and TNFα induces a pro-inflammatory, pro-coagulant and pro-thrombotic phenotype in human endothelial cells , 2012, Annals of the rheumatic diseases.

[9]  A. Mammen.  Autoimmune myopathies: autoantibodies, phenotypes and pathogenesis , 2011, Nature Reviews Neurology.

[10]  F. D’Acquisto,et al.  IL-17A increases ADP-induced platelet aggregation. , 2011, Biochemical and biophysical research communications.

[11]  F. D’Acquisto,et al.  From IL-15 to IL-33: the never-ending list of new players in inflammation. Is it time to forget the humble aspirin and move ahead? , 2010, Biochemical pharmacology.

[12]  F. D’Acquisto,et al.  Interleukin 17 sustains rather than induces inflammation. , 2009, Biochemical pharmacology.

[13]  M. Lotze,et al.  Interleukin-17 promotes angiogenesis and tumor growth. , 2003, Blood.

[14]  T. Pullar,et al.  Rheumatoid arthritis and macrovascular disease. , 2003, Rheumatology.

[15]  M. Seldin,et al.  Herpesvirus saimiri encodes a new cytokine, IL-17, which binds to a novel cytokine receptor. , 1995, Journal of immunology.

[16]  M. Seldin,et al.  Herpesvirus Saimiri encodes a new cytokine, IL-17, which binds to a novel cytokine receptor. , 1995, Immunity.