NDLI: Mifepristone (RU486) restores humoral and T cell-mediated immune response in endotoxin immunosuppressed mice.

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Mifepristone (RU486) restores humoral and T cell-mediated immune response in endotoxin immunosuppressed mice.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Rearte, B. Maglioco, A. Balboa, L. Bruzzo, J. Landoni, V. I. Laborde, E. A. Chiarella, P. Ruggiero, R. A. Fernández, G. C. Isturiz, M. A.
Description	Country affiliation: Argentina Author Affiliation: Rearte B ( Instituto de Leucemia Experimental (ILEX)-CONICET, Academia Nacional de Medicina, Buenos Aires, Argentina. barbararearte@yahoo.com.ar)
Abstract	Sepsis and septic shock can be caused by Gram-positive and -negative bacteria and other microorganisms. In the case of Gram-negative bacteria, endotoxin, a normal constituent of the bacterial wall, also known as lipopolysaccharide (LPS), has been considered as one of the principal agents causing the undesirable effects in this critical illness. The response to LPS involves a rapid secretion of proinflammatory cytokines such as tumour necrosis factor (TNF)- , interleukin (IL)-1, IL-6, interferon (IFN)-Î³ and the concomitant induction of anti-inflammatory mediators such as IL-10, transforming growth factor (TGF)-ß or glucocorticoids, which render the host temporarily refractory to subsequent lethal doses of LPS challenge in a process known as LPS or endotoxin tolerance. Although protective from the development of sepsis or systemic inflammation, endotoxin tolerance has also been pointed out as the main cause of the non-specific humoral and cellular immunosuppression described in these patients. In this report we demonstrate, using a mouse model, that mifepristone (RU486), a known glucocorticoid receptor antagonist, could play an important role in the restoration of both adaptive humoral and cellular immune response in LPS immunosuppressed mice, suggesting the involvement of endogenous glucocorticoids in this phenomenon. On the other hand, using cyclophosphamide and gemcitabine, we demonstrated that regulatory/suppressor CD4(+) CD25(+) forkhead boxP3(+) and GR-1(+) CD11b(+) cells do not play a major role in the establishment or the maintenance of endotoxin tolerance, a central mechanism for inducing an immunosuppression state.
File Format	HTM / HTML
ISSN	00099104
e-ISSN	13652249
DOI	10.1111/j.1365-2249.2010.04262.x
Journal	Clinical & Experimental Immunology
Issue Number	3
Volume Number	162
Language	English
Publisher	Wiley-Blackwell
Publisher Date	2010-12-01
Publisher Place	Great Britain (UK)
Access Restriction	Open
Subject Keyword	Discipline Immunology Mifepristone Administration & Dosage T-lymphocytes, Regulatory Drug Effects T-lymphocytes Animals Antigens, Cd Biosynthesis Cyclophosphamide Deoxycytidine Analogs & Derivatives Forkhead Transcription Factors Immunity, Cellular Immunity, Humoral Immunosuppression Immunosuppressive Agents Lipopolysaccharides Mice Mice, Inbred Balb C Pharmacology Receptors, Glucocorticoid Antagonists & Inhibitors Immunology Metabolism Pathology Research Support, Non-u.s. Gov't
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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Mifepristone (RU486) restores humoral and T cell-mediated immune response in endotoxin immunosuppressed mice

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Mifepristone (RU486) restores humoral and T cell-mediated immune response in endotoxin immunosuppressed mice.

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Mifepristone (RU486) restores humoral and T cell-mediated immune response in endotoxin immunosuppressed mice.