Cytokines and the immune-neuroendocrine network: What did we learn from infection and autoimmunity?
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.
Correa
Silvia G
SG
Immunology, Department of Biochemical Chemistry, CIBICI (CONICET), Faculty of Chemical Sciences, National University of Cordoba, Haya de la Torre y Medina Allende, 5000 Cordoba, Argentina. scorrea@bioclin.fcq.unc.edu.ar
Maccioni
Mariana
M
Rivero
Virginia E
VE
Iribarren
Pablo
P
Sotomayor
Claudia E
CE
Riera
Clelia M
CM
D000818:Animals; D001327:Autoimmune Diseases / Q000276:immunology; D015551:Autoimmunity; D005075:Biological Evolution; D016207:Cytokines / Q000276:immunology*; D006801:Humans; D007239:Infections / Q000276:immunology; D018836:Inflammation Mediators / Q000276:immunology; D009490:Neurosecretory Systems / Q000276:immunology*; D051193:Toll-Like Receptors / Q000276:immunology*
D016207:Cytokines; D018836:Inflammation Mediators; D051193:Toll-Like Receptors