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Review
. 2007 Dec;19(6):377-82.
doi: 10.1016/j.smim.2007.10.009. Epub 2007 Nov 28.

Th17 cells and mucosal host defense

Shean J Aujla  1 , Patricia J Dubin, Jay K Kolls
Affiliations
Review

Th17 cells and mucosal host defense

Shean J Aujla et al. Semin Immunol. 2007 Dec.

Abstract

Th17 cells are a new lineage of T-cells that are controlled by the transcription factor RORgammat and develop independent of GATA-3, T-bet, Stat 4 and Stat 6. Novel effector molecules produced by these cells include IL-17A, IL-17F, IL-22, and IL-26. IL-17RA binds IL-17A and IL-17F and is critical for host defense against extracellular planktonic bacteria by regulating chemokine gradients for neutrophil emigration into infected tissue sites as well as host granulopoiesis. Moreover, IL-17 and IL-22 regulate the production of antimicrobial proteins in mucosal epithelium. Although TGF-beta1 and IL-6 have been shown to be critical for development of Th17 cells from naive precursors, IL-23 is also important in regulating IL-17 release in mucosal tissues in response to infectious stimuli. Compared to Th1 cells, IL-23 and IL-17 show limited roles in controlling host defense against primary infections with intracellular bacteria such as Mycobacterium tuberculosis suggesting a predominate role of the Th17 lineage in host defense against extracellular pathogens. However, in the setting of chronic biofilm infections, as that occurs with cystic fibrosis or bronchiectasis, Th17 cells may be key contributors of tissue injury.

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Figures

Figure 1
Figure 1
Changes in splenic neutrophil progenitors eighteen hours after pulmonary challenge with K. pneumoniae. WT or IL-17RA KO mice were challenged with 104 CFU of K. pneumoniae and spleens were harvested at 18 hours and CFU-GM and high proliferative potential (HPP) colonies were measured using colony formation in methylcellulose (n=6−7 mice per group, * denotes p <0.05 compared to WT control by Mann-Whitney non parametric testing).
Figure 2
Figure 2
Lack of susceptibility of IL-17RA deficient mice to primary Mycobacterium tuberculosis infection. WT or IL-17RA were challenged with 100 CFU of H37Rv M. tuberculosis and sacrificed at serial time points to determine lung CFU. As a positive control, TNFR p55 KO mice were infected as well. As opposed to mice deficient in TNFR p55 signaling, IL-17RA showed control of M tb growth similar to WT mice (n=6−7 mice per group, * denotes p <0.05 compared to WT control by Mann-Whitney non parametric testing).
Figure 3
Figure 3
Proposed model of IL-17 signaling in human airway epithelium. IL-17RA and IL-17RC can associate to potentially form a heterodimeric receptor. Antibodies against IL-17RA depicted in light blue can effectively block IL-17A and IL-17F. However due to the relatively lower affinity of soluble IL-17RA:Fc depicted in dark blue, can bind can neutralize IL-17A but is ineffective blocking IL-17F resulting in only partial abrogation of IL-17 induced CXC chemokines.
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