Neutralization or Absence of the Interleukin-23 Pathway Does Not Compromise Immunity to Mycobacterial Infection.
From: Discovery Research and Experimental Pathology and Pharmacology, Schering-Plough Biopharma, 901 California Ave., Palo Alto, CA 94304-1104, USA.
Infection and immunity
- Publish Date: Nov 2006
- ISSN: 0019-9567
- Volume: 74
- Issue: 11
- Pages: 6092-9
- Medium: Print
- Language: English
- Citation (JAMA): Chackerian Alissa A, Chen Shi-Juan, Brodie Scott J, et al. Neutralization or Absence of the Interleukin-23 Pathway Does Not Compromise Immunity to Mycobacterial Infection.. Infect. Immun. Nov 2006;74:6092-9
Abstract
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.
Mesh Headings (Keywords): Animals, Female, Granuloma, Interleukin-12, Interleukin-23, Interleukin-23 Subunit p19, Mice, Mice, Inbred C57BL, Mice, Knockout, Mycobacterium bovis, Receptors, Interleukin, Signal Transduction, Tuberculosis
Check for Full Text / PubMed Unique Identifier (PMID): 16923792
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