TY - JOUR
T1 - Cutting Edge
T2 - Nlrp10 is essential for protective antifungal adaptive immunity against Candida albicans
AU - Joly, Sophie
AU - Eisenbarth, Stephanie C.
AU - Olivier, Alicia K.
AU - Williams, Adam
AU - Kaplan, Daniel H.
AU - Cassel, Suzanne L.
AU - Flavell, Richard A.
AU - Sutterwala, Fayyaz S.
PY - 2012/11/15
Y1 - 2012/11/15
N2 - Nucleotide-binding domain leucine-rich repeat containing receptors (NLRs) are cytosolic receptors that initiate immune responses to sterile and infectious insults to the host. Studies demonstrated that Nlrp3 is critical for the control of Candida albicans infections and in the generation of antifungal Th17 responses. In this article, we show that the NLR family member Nlrp10 also plays a unique role in the control of disseminated C. albicans infection in vivo. Nlrp10-deficient mice had increased susceptibility to disseminated candidiasis, as indicated by decreased survival and increased fungal burdens. In contrast to Nlrp3, Nlrp10 deficiency did not affect innate proinflammatory cytokine production from macrophages and dendritic cells challenged with C. albicans. However, Nlrp10-deficient mice displayed a profound defect in Candida-specific Th1 and Th17 responses. These results demonstrate a novel role for Nlrp10 in the generation of adaptive immune responses to fungal infection.
AB - Nucleotide-binding domain leucine-rich repeat containing receptors (NLRs) are cytosolic receptors that initiate immune responses to sterile and infectious insults to the host. Studies demonstrated that Nlrp3 is critical for the control of Candida albicans infections and in the generation of antifungal Th17 responses. In this article, we show that the NLR family member Nlrp10 also plays a unique role in the control of disseminated C. albicans infection in vivo. Nlrp10-deficient mice had increased susceptibility to disseminated candidiasis, as indicated by decreased survival and increased fungal burdens. In contrast to Nlrp3, Nlrp10 deficiency did not affect innate proinflammatory cytokine production from macrophages and dendritic cells challenged with C. albicans. However, Nlrp10-deficient mice displayed a profound defect in Candida-specific Th1 and Th17 responses. These results demonstrate a novel role for Nlrp10 in the generation of adaptive immune responses to fungal infection.
UR - http://www.scopus.com/inward/record.url?scp=84868554611&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84868554611&partnerID=8YFLogxK
U2 - 10.4049/jimmunol.1201715
DO - 10.4049/jimmunol.1201715
M3 - Article
C2 - 23071280
AN - SCOPUS:84868554611
SN - 0022-1767
VL - 189
SP - 4713
EP - 4717
JO - Journal of Immunology
JF - Journal of Immunology
IS - 10
ER -