β Scribed by Joost J. Oppenheim; Igal Gery
No coin nor oath required. For personal study only.
facliir { LAI'i in V.)72, as an (w/irily firdiliiccil h]' cidturcd litinuin pcnphcrdl li/mii/ (idliercnt leukmyti's which wax directly tniliigcnic Jor murine Ihyiniicylcs but not fur iittmuncicijni//ctciit /icn/ihcriil lynifihocytcs. Unman LAF aim \yncrgistically augmented the mitnuenic efjccts iij the !eetin.\ (JinA and I'lIA on mnrine t/iymoeytes and s/ilcnic T tym/i/iocyti's'. Since then I.AF has been shown to prinnote lymphocyte differentiation and pinclions and even to affect a variety of nmdymphocytic target cells. In neiv (d the many biological activities attributed to tins macrophage-denvcd factor, LAF wa.s renamed 'interleukin I' ( IL I) at the Seeont/ International Fymphokuie M'orkshofi at Frmatingcn. Switzerland, in 1979-. Partly as a conseiiuence of the resultant controversy, this term has become widely known and will be used in this revieic. even though, as J. J. Oppenheim and Igal (iery show. IL I is more than a sii^nal between leukocytes.
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## Abstract Interleukinβ1 (ILβ1) is considered to be involved in the pathogenesis of Graves' disease. The aim of this study was to test whether the ILβ1βΞ² gene promoter region and exon 5 and ILβ1 receptor antagonist (ILβ1Ra) gene intron 2 polymorphisms could be useful genetic markers for susceptibi
The present study was carried out to compare the threshold doses of interleukin-1 beta (IL-1 beta) necessary to elicit febrile and adrenocorticotrophic hormone (ACTH) responses. The results show that intravenous injection of a small dose of IL-1 beta (0.2 micrograms/kg) did not stimulate ACTH secret