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РЖ ВИНИТИ 34 (BI39) 97.01-04К1.163

IFN-'альфа''бета' reconstitutes the deficiency in lipid A-activated AKR macrophages for nitric oxide synthase [Text] / Hong Jiang [et al.] // J. Immunol. - 1996. - Vol. 157, N 1. - P305-312 . - ISSN 0022-1767
Перевод заглавия: Интерферон (IFN) 'альфа''бета' ликвидирует дефицит в активированных липидом A макрофагах мышей AKR в отношении синтазы оксида азота
Аннотация: AKR mouse peritoneal macrophages (PM) have a defect in their response to lipid A for nitric oxide (NO)-mediated tumor cytotoxicity, which was related to a lower level of C1q synthesis and reconstituted by exogenous IFN-'гамма' or C1q. Were used AKR-PM as a model to further define the role of IFN-'альфа''бета' in modulation of induction of macrophage nitric oxide synthase (NOS) in response to lipid A. The AKR-PM produced a significantly lower level of IFN-'альфа''бета' than responsive C3H-PM in response to lipid A. AKR-PM failed to increase NOS mRNA synthesis and NO generation when exposed to lipid A. This partial deficiency of AKR-PM to lipid A stimulation was reconstituted completely by exogenous IFN-'альфа''бета' for both synthesis of NOS mRNA and release of NO. The failure of AKR-PM to produce NOS to lipid A stimulation appears to be related to reduced secretion of IFN-'альфа''бета' and the resultant failure to express TNF-A type II receptor (TNF-RII) mRNA, which in turn decreases TNF-'альфа' binding to its receptor for autocrine induction of NOS. Insufficient synthesis and secretion of endogenous IFN-'альфа''бета' may be the primary reason for AKR-PM refractoriness to induction of NOS in response to lipid A. Furthermore, the close correlation between lack of IFN-'альфа''бета' secretion and decreased TNF-RII mRNA synthesis may implicate a critical role for IFN-'альфа''бета' in the upregulation of macrophage TNF-RII receptor expression for autocrine induction of NOS during lipid A stimulation. США, Noble Ctr. Biomed. Res., Oklahoma Citi, OK 73104-5046. Библ. 32

ГРНТИ	34.43.29

ВИНИТИ 341.43.29.29.11
Рубрики: МАКРОФАГИ
ДЕФИЦИТ СИНТАЗЫ АЗОТА
ВОССТАНОВЛЕНИЕ
ИНТЕРФЕРОН АЛЬФА/БЕТА
МЫШИ AKR

Доп.точки доступа:
Jiang, Hong; Rummage, John A.; Zhou, Anqiang; Chen, Zhenfang; Herriott, Mary J.; Stewart, Charles A.; Kolosov, Mikhail; Leu, Richard W.

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