RGD Reference Report - Neutralization or absence of the interleukin-23 pathway does not compromise immunity to mycobacterial infection. - Rat Genome Database

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Neutralization or absence of the interleukin-23 pathway does not compromise immunity to mycobacterial infection.

Authors: Chackerian, Alissa A  Chen, Shi-Juan  Brodie, Scott J  Mattson, Jeanine D  McClanahan, Terrill K  Kastelein, Robert A  Bowman, Edward P 
Citation: Chackerian AA, etal., Infect Immun. 2006 Nov;74(11):6092-9. doi: 10.1128/IAI.00621-06. Epub 2006 Aug 21.
RGD ID: 39457937
Pubmed: PMID:16923792   (View Abstract at PubMed)
PMCID: PMC1695481   (View Article at PubMed Central)
DOI: DOI:10.1128/IAI.00621-06   (Journal Full-text)

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.



RGD Manual Disease Annotations    Click to see Annotation Detail View

  
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
IL23AHumanBovine Tuberculosis  ISOIl23a (Mus musculus) RGD 
Il23aRatBovine Tuberculosis  ISOIl23a (Mus musculus) RGD 
Il23aMouseBovine Tuberculosis  IMP  RGD 

Objects Annotated

Genes (Rattus norvegicus)
Il23a  (interleukin 23 subunit alpha)

Genes (Mus musculus)
Il23a  (interleukin 23, alpha subunit p19)

Genes (Homo sapiens)
IL23A  (interleukin 23 subunit alpha)


Additional Information