Cytokines and the immune-neuroendocrine network: What did we learn from infection and autoimmunity?

被引：39

作者：

Correa, Silvia G. ^{[1
]}

Maccioni, Mariana ^{[1
]}

Rivero, Virginia E. ^{[1
]}

Iribarren, Pablo ^{[1
]}

Sotomayor, Claudia E. ^{[1
]}

Riera, Clelia M. ^{[1
]}

机构：

[1] Univ Nacl Cordoba, Fac Chem Sci, CONICET, CIBICET,Dept Biochem Chem, RA-5000 Cordoba, Argentina

来源：

CYTOKINE & GROWTH FACTOR REVIEWS | 2007年 / 18卷 / 1-2期

关键词：

inflammation; Toll-like receptors; stress; hypothalamic-pituitary-adrenal axis; sympathetic nervous system;

D O I：

10.1016/j.cytogfr.2007.01.011

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 [生物化学与分子生物学]; 081704 [应用化学];

摘要：

The initial view of the neuroendocrine-immune communication as the brake of immune activation is changing. Recent evidence suggests that the optimization of the body's overall response to infection could be actually the role of the immune-endocrine network. In gradually more complex organisms, the multiplicity of host-pathogen interfaces forced the development of efficient and protective responses. Molecules such as cytokines and Toll-like receptors (TLRs) are distributed both in the periphery and in the brain to participate in a coordinated adaptive function. When sustained release of inflammatory mediators occurs, as in autoimmune diseases, undesirable pathological consequences become evident with different manifestations and outcomes. Clearly, organisms are not well adapted to that disregulated condition yet, suggesting that additional partners within neuroendocrine-immune interactions might emerge from the evolutionary road. (c) 2007 Elsevier Ltd. All rights reserved.

引用

页码：125 / 134

页数：10

共 82 条

[1]

Up-regulation of the inflammatory cytokines IFN-γ and IL-12 and down-regulation of IL-4 in cerebral cortex regions of APPSWE transgenic mice [J].