Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
11
pubmed:dateCreated
2006-10-23
pubmed:abstractText
Interleukin-23 (IL-23), a member of the IL-12 family, is a heterodimeric cytokine that is composed of the p40 subunit of IL-12 plus a unique p19 subunit. IL-23 is critical for autoimmune inflammation, in part due to its stimulation of the proinflammatory cytokine IL-17A. It is less clear, however, if IL-23 is required during the immune response to pathogens. We examined the role of IL-23 during Mycobacterium bovis BCG infection. We found that IL-23 reduces the bacterial burden and promotes granuloma formation when IL-12 is absent. However, IL-23 does not contribute substantially to host resistance when IL-12 is present, as the ability to control bacterial growth and form granulomata is not affected in IL-23p19-deficient mice and mice treated with a specific anti-IL-23p19 antibody. IL-23p19-deficient mice are also able to mount an effective memory response to secondary infection with BCG. While IL-23p19-deficient mice do not produce IL-17A, this cytokine is not necessary for effective control of infection, and antibody blocking of IL-17A in both wild-type and IL-12-deficient mice also has little effect on the bacterial burden. These data suggest that IL-23 by itself does not play an essential role in the protective immune response to BCG infection; however, the presence of IL-23 can partially compensate for the absence of IL-12. Furthermore, neutralization of IL-23 or IL-17A does not increase susceptibility to mycobacterial BCG infection.
pubmed:commentsCorrections
http://linkedlifedata.com/resource/pubmed/commentcorrection/16923792-11114383, http://linkedlifedata.com/resource/pubmed/commentcorrection/16923792-11390512, http://linkedlifedata.com/resource/pubmed/commentcorrection/16923792-11673546, http://linkedlifedata.com/resource/pubmed/commentcorrection/16923792-11739515, http://linkedlifedata.com/resource/pubmed/commentcorrection/16923792-11801672, http://linkedlifedata.com/resource/pubmed/commentcorrection/16923792-11895957, http://linkedlifedata.com/resource/pubmed/commentcorrection/16923792-12417590, http://linkedlifedata.com/resource/pubmed/commentcorrection/16923792-12610626, http://linkedlifedata.com/resource/pubmed/commentcorrection/16923792-12778462, http://linkedlifedata.com/resource/pubmed/commentcorrection/16923792-14662908, http://linkedlifedata.com/resource/pubmed/commentcorrection/16923792-15127338, http://linkedlifedata.com/resource/pubmed/commentcorrection/16923792-15265921, http://linkedlifedata.com/resource/pubmed/commentcorrection/16923792-15657292, http://linkedlifedata.com/resource/pubmed/commentcorrection/16923792-16002675, http://linkedlifedata.com/resource/pubmed/commentcorrection/16923792-16113296, http://linkedlifedata.com/resource/pubmed/commentcorrection/16923792-16148138, http://linkedlifedata.com/resource/pubmed/commentcorrection/16923792-16157683, http://linkedlifedata.com/resource/pubmed/commentcorrection/16923792-16164029, http://linkedlifedata.com/resource/pubmed/commentcorrection/16923792-16393998, http://linkedlifedata.com/resource/pubmed/commentcorrection/16923792-16670770, http://linkedlifedata.com/resource/pubmed/commentcorrection/16923792-16670771, http://linkedlifedata.com/resource/pubmed/commentcorrection/16923792-16849446, http://linkedlifedata.com/resource/pubmed/commentcorrection/16923792-2647299, http://linkedlifedata.com/resource/pubmed/commentcorrection/16923792-8630732, http://linkedlifedata.com/resource/pubmed/commentcorrection/16923792-9597139, http://linkedlifedata.com/resource/pubmed/commentcorrection/16923792-9746609, http://linkedlifedata.com/resource/pubmed/commentcorrection/16923792-9784532
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0019-9567
pubmed:author
pubmed:issnType
Print
pubmed:volume
74
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
6092-9
pubmed:dateRevised
2009-11-18
pubmed:meshHeading
pubmed:year
2006
pubmed:articleTitle
Neutralization or absence of the interleukin-23 pathway does not compromise immunity to mycobacterial infection.
pubmed:affiliation
Discovery Research and Experimental Pathology and Pharmacology, Schering-Plough Biopharma, 901 California Ave., Palo Alto, CA 94304-1104, USA.
pubmed:publicationType
Journal Article