<?xml version="1.0" encoding="UTF-8"?><xml><records><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Freches, Danielle</style></author><author><style face="normal" font="default" size="100%">Korf, Hannelie</style></author><author><style face="normal" font="default" size="100%">Olivier J Denis</style></author><author><style face="normal" font="default" size="100%">Havaux, Xavier</style></author><author><style face="normal" font="default" size="100%">Huygen, Kris</style></author><author><style face="normal" font="default" size="100%">Marta Romano</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Mice genetically inactivated in interleukin-17A receptor are defective in long-term control of Mycobacterium tuberculosis infection.</style></title><secondary-title><style face="normal" font="default" size="100%">Immunology</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Immunology</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Animals</style></keyword><keyword><style  face="normal" font="default" size="100%">Cytokines</style></keyword><keyword><style  face="normal" font="default" size="100%">Enzyme-Linked Immunosorbent Assay</style></keyword><keyword><style  face="normal" font="default" size="100%">Flow Cytometry</style></keyword><keyword><style  face="normal" font="default" size="100%">mice</style></keyword><keyword><style  face="normal" font="default" size="100%">Mice, Inbred C57BL</style></keyword><keyword><style  face="normal" font="default" size="100%">Mice, Knockout</style></keyword><keyword><style  face="normal" font="default" size="100%">Mycobacterium tuberculosis</style></keyword><keyword><style  face="normal" font="default" size="100%">Receptors, Interleukin-17</style></keyword><keyword><style  face="normal" font="default" size="100%">Tuberculosis</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2013</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2013 Oct</style></date></pub-dates></dates><number><style face="normal" font="default" size="100%">231</style></number><volume><style face="normal" font="default" size="100%">140</style></volume><pages><style face="normal" font="default" size="100%">220-31</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Interleukin-17A (IL-17A), a pro-inflammatory cytokine acting on neutrophil recruitment, is known to play an important role during Mycobacterium tuberculosis infection, but the role of IL-17A receptor signalling in immune defence against this intracellular pathogen remains poorly documented. Here we have analysed this signalling using C57BL/6 mice genetically inactivated in the IL-17 receptor A subunit (IL-17RA(-/-) ). Although early after infection bacterial growth was controlled to the same extent as in wild-type mice, IL-17RA(-/-) mice were defective in exerting long-term control of M.&amp;nbsp;tuberculosis infection, as demonstrated by a progressively increasing pulmonary bacterial burden and shortened survival time. Compared with infected wild-type mice, IL-17RA(-/-) mice showed impaired recruitment of neutrophils to the lungs at the early but not the late stage of infection. Pulmonary tumour necrosis factor-&amp;alpha;, IL-6 and particularly IL-10 levels were decreased in the absence of IL-17RA signalling, whereas IL-1&amp;beta; was increased. CD4(+) -mediated and &amp;gamma;&amp;delta;-mediated IL-17A production was dramatically increased in IL-17RA(-/-) mice (confirming part of their phenotype), whereas production of interferon-&amp;gamma; and expression of the bactericidal enzyme inducible nitric oxide synthase were not affected. Collectively, our data suggest that early but not late neutrophil recruitment is essential for IL-17A-mediated long-term control of M.&amp;nbsp;tuberculosis infection and that a functional interferon-&amp;gamma; response is not sufficient to control M.&amp;nbsp;tuberculosis growth when the IL-17RA pathway is deficient. As treatment of auto-immune diseases with anti-IL-17A antibodies is actually being tested in clinical studies, our data suggest that caution should be taken with respect to possible reactivation of tuberculosis.&lt;/p&gt;
</style></abstract><issue><style face="normal" font="default" size="100%">2</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/23721367?dopt=Abstract</style></custom1><section><style face="normal" font="default" size="100%">220</style></section></record></records></xml>