Soluble XXXX @entity5003 receptor type I induces release of constitutive @entity5003 alpha.

@entity558 @entity137 @entity634 @entity635 @entity19 @entity5003 @entity5132 @entity637
@entity634 and @entity635 are proinflammatory cytokines involved in the pathogenesis of many infectious and noninfectious inflammatory diseases. To reduce @entity5003 @entity137 , extracellular domains of the soluble (s) IL-1R are shed from cell membranes and prevent triggering of cell-bound receptors. We investigated to what extent @entity19 sIL-1RI can neutralize the @entity5003 produced by @entity558 -stimulated macrophages. When @entity19 peritoneal macrophages were incubated with @entity558 , addition of sIL-1RI significantly inhibited the bioactivity of @entity5003 . Stimulation of cells with sIL-1RI alone induced no bioactive @entity5003 . When immunoreactive cytokine concentrations were measured with specific radioimmunoassays, sIL-1RI alone appeared to induce a significant release of @entity634 in a concentration-dependent manner. This effect was independent of new protein synthesis. The production of @entity635 or @entity637 was not influenced by sIL-1RI. There was no interference of sIL-1RI with the @entity634 radioimmunoassay. In @entity19 , an i.v. injection of sIL-RI alone induced a rapid release of @entity634 , but not of @entity637 or @entity635 . Treatment of @entity19 with sIL-1RI improved the survival during a lethal infection with @entity5132 . In conclusion, sIL-1RI induces a rapid release of @entity634 from cells, as well as into the systemic circulation. Although this @entity634 may be inactivated in circulation by the same sIL-1RI, this phenomenon probably has immunostimulatory effects at local levels where the sIL-1RI-induced @entity634 acts in a paracrine or autocrine manner.
