IL-12 and IL-23 share the p40 subunit, which heterodimerizes respectively with IL-12 p35 or IL-23 p19 subunits to form IL-12 or IL-23. IL-12 p40 exists as a monomer and as a homodimer (IL-12 p80). IL-12 induction is relevant in asthmatic airway inflammation. IL-12 expression can be induced by mouse parainfluenza type I (Sendai) virus and its source is airway epithelial cells. In that experimental model, IL-12 induction is followed by excessive expression of IL-12 p40 that could be further enhanced in IL-12 p35-deficient mice. Overexpression of IL-12 p80 causes macrophage accumulation and contributes to airway inflammation and consequent morbidity during viral bronchitis. Amplified epithelial IL-12 p40 expression and augmented concentrations of BAL fluid IL-12 p40 (but not IL-12 p70) has been detected in asthmatic subjects. It has been demonstrated that p80, but not IL-12 or p40, induces macrophage chemotaxis that is independent of IL-12 and mediated through the cytoplasmic tail of IL-12b1. Additional studies with transgenic mice suggest that overexpression of IL-12 p80 prior to a viral infection increases the number of resident airway macrophages, and this primes the host for a protective response against a lethal respiratory viral infection. In addition, it has been suggested that p80 functions as a competitive antagonist of IL-12 p70. Mouse Con A-activated splenocytes display identical binding affinities for p80 and IL-12, and in these cells p80 competitively inhibited IL-12 binding and IL-12-dependent proliferation. Furthermore, p80 is able to inhibit IL-12-dependent IFNg production in freshly isolated splenocytes.
原厂资料：
Description:
IL-12 and IL-23 share the p40 subunit, which heterodimerizes respectively with IL-12 p35 or IL-23 p19 subunits to form IL-12 or IL-23. IL-12 p40 exists as a monomer and as a homodimer (IL-12 p80). IL-12 induction is relevant in asthmatic airway inflammation. IL-12 expression can be induced by mouse parainfluenza type I (Sendai) virus and its source is airway epithelial cells. In that experimental model, IL-12 induction is followed by excessive expression of IL-12 p40 that could be further enhanced in IL-12 p35-deficient mice. Overexpression of IL-12 p80 causes macrophage accumulation and contributes to airway inflammation and consequent morbidity during viral bronchitis. Amplified epithelial IL-12 p40 expression and augmented concentrations of BAL fluid IL-12 p40 (but not IL-12 p70) has been detected in asthmatic subjects. It has been demonstrated that p80, but not IL-12 or p40, induces macrophage chemotaxis that is independent of IL-12 and mediated through the cytoplasmic tail of IL-12b1. Additional studies with transgenic mice suggest that overexpression of IL-12 p80 prior to a viral infection increases the number of resident airway macrophages, and this primes the host for a protective response against a lethal respiratory viral infection. In addition, it has been suggested that p80 functions as a competitive antagonist of IL-12 p70. Mouse Con A-activated splenocytes display identical binding affinities for p80 and IL-12, and in these cells p80 competitively inhibited IL-12 binding and IL-12-dependent proliferation. Furthermore, p80 is able to inhibit IL-12-dependent IFNg production in freshly isolated splenocytes.
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