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This is followed by recruitment of the\n                    <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\n                    \u201018R\u03b2 chain.\n                    <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\n                    \u201018 then uses the same signaling pathway as\n                    <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\n                    \u20101 to activate\n                    <jats:styled-content style=\"fixed-case\">NF<\/jats:styled-content>\n                    \u2010\n                    <jats:styled-content style=\"fixed-case\">kB<\/jats:styled-content>\n                    and induce inflammatory mediators such as adhesion molecules, chemokines and Fas ligand.\n                    <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\n                    \u201018 also binds to the circulating high affinity\n                    <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\n                    \u201018 binding protein (\n                    <jats:styled-content style=\"fixed-case\">BP<\/jats:styled-content>\n                    ), such as only unbound free\n                    <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\n                    \u201018 is active.\n                    <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\n                    \u201018R\u03b1 may also bind\n                    <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\n                    \u201037, another member of the\n                    <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\n                    \u20101 family, but in association with the negative signaling chain termed\n                    <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\n                    \u20101R8, which transduces an anti\u2010inflammatory signal.\n                    <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\n                    \u201018\n                    <jats:styled-content style=\"fixed-case\">BP<\/jats:styled-content>\n                    also binds\n                    <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\n                    \u201037 and this acts as a sink for the anti\u2010inflammatory properties of\n                    <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\n                    \u201037. There is now ample evidence for a role of\n                    <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\n                    \u201018 in various infectious, metabolic or inflammatory diseases such as influenza virus infection, atheroma, myocardial infarction, chronic obstructive pulmonary disease, or Crohn's disease. However,\n                    <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\n                    \u201018 plays a very specific role in the pathogenesis of hemophagocytic syndromes (\n                    <jats:styled-content style=\"fixed-case\">HS<\/jats:styled-content>\n                    ) also termed Macrophage Activation Syndrome. In children affected by\n                    <jats:styled-content style=\"fixed-case\">NLRC<\/jats:styled-content>\n                    4 gain\u2010of\u2010function mutations,\n                    <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\n                    \u201018 circulates in the range of tens of nanograms\/mL.\n                    <jats:styled-content style=\"fixed-case\">HS<\/jats:styled-content>\n                    is treated with the\n                    <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\n                    \u20101 Receptor antagonist (anakinra) but also specifically with\n                    <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\n                    \u201018\n                    <jats:styled-content style=\"fixed-case\">BP<\/jats:styled-content>\n                    . Systemic juvenile idiopathic arthritis or adult\u2010onset Still's disease are also characterized by high serum\n                    <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\n                    \u201018 concentrations and are treated by\n                    <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\n                    \u201018BP.\n                  <\/jats:p>","DOI":"10.1111\/imr.12616","type":"journal-article","created":{"date-parts":[[2017,12,18]],"date-time":"2017-12-18T03:53:15Z","timestamp":1513569195000},"page":"138-153","source":"Crossref","is-referenced-by-count":572,"title":["Interleukin\u201018: Biological properties and role in disease pathogenesis"],"prefix":"10.1111","volume":"281","author":[{"given":"Gilles","family":"Kaplanski","sequence":"first","affiliation":[{"name":"Assistance Publique\u2010H\u00f4pitaux de Marseille Centre Hospitalier Universitaire Conception Service de M\u00e9decine Interne et Immunologie 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