Enhanced protection to Mycobacterium tuberculosis infection in IL-10-deficient mice is accompanied by early and enhanced Th1 responses in the lung
✍ Scribed by Paul S. Redford; Andre Boonstra; Simon Read; Jonathan Pitt; Christine Graham; Evangelos Stavropoulos; Gregory J. Bancroft; Anne O'Garra
- Publisher
- John Wiley and Sons
- Year
- 2010
- Tongue
- English
- Weight
- 507 KB
- Volume
- 40
- Category
- Article
- ISSN
- 0014-2980
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✦ Synopsis
IL-10 regulates the balance of an immune response between pathogen clearance and immunopathology. We show here that Mycobacterium tuberculosis (Mtb) infection in the absence of IL-10 (IL-10^−/−^ mice) results in reduced bacterial loads in the lung. This reduction was preceded by an accelerated and enhanced IFN-γ response in the lung, an increased influx of CD4^+^ T cells into the lung, and enhanced production of chemokines and cytokines, including CXCL10 and IL-17, in both the lung and the serum. Neutralization of IL-17 affected neither the enhanced production of CXCL10 nor the accumulation of IFN-γ-producing T cells in the lungs, but led to reduced numbers of granulocytes in the lung and reduced bacterial loads in the spleens of Mtb-infected mice. This suggests that IL-17 may contribute to dissemination of Mtb.