Cutting edge: Nlrp10 is essential for protective antifungal adaptive immunity against Candida albicans
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 antifung...
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Veröffentlicht in: | The Journal of immunology (1950) 2012-11, Vol.189 (10), p.4713-4717 |
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container_title | The Journal of immunology (1950) |
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creator | Joly, Sophie Eisenbarth, Stephanie C Olivier, Alicia K Williams, Adam Kaplan, Daniel H Cassel, Suzanne L Flavell, Richard A Sutterwala, Fayyaz S |
description | 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. |
doi_str_mv | 10.4049/jimmunol.1201715 |
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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. 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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.</description><subject>Animals</subject><subject>Apoptosis Regulatory Proteins - genetics</subject><subject>Apoptosis Regulatory Proteins - immunology</subject><subject>Candida albicans</subject><subject>Candida albicans - immunology</subject><subject>Candidiasis - genetics</subject><subject>Candidiasis - immunology</subject><subject>Candidiasis - pathology</subject><subject>Carrier Proteins - genetics</subject><subject>Carrier Proteins - immunology</subject><subject>Cytokines - genetics</subject><subject>Cytokines - immunology</subject><subject>Dendritic Cells - immunology</subject><subject>Dendritic Cells - pathology</subject><subject>Immunity, Cellular</subject><subject>Immunity, Innate - genetics</subject><subject>Macrophages - immunology</subject><subject>Macrophages - pathology</subject><subject>Mice</subject><subject>Mice, Knockout</subject><subject>NLR Family, Pyrin Domain-Containing 3 Protein</subject><subject>Th1 Cells - immunology</subject><subject>Th1 Cells - pathology</subject><subject>Th17 Cells - immunology</subject><subject>Th17 Cells - pathology</subject><issn>0022-1767</issn><issn>1550-6606</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFUctOwzAQtBCIlsKdE_KRS8qu7SQNNxTxkiq4wDnaxHblKo8SO0j9e0IfXDmtNDuzO5ph7BphrkBld2vXNEPb1XMUgCnGJ2yKcQxRkkByyqYAQkSYJumEXXi_BoAEhDpnEyEhRbGAKbP5EIJrV9zolbnnb3W_QeDOc-O9aYOjmtuu55u-C6YK7ttwGlE7tKtxQ5o2O2xnw4UtpxW51geeU6udJk516Spq_SU7s1R7c3WYM_b59PiRv0TL9-fX_GEZVUpBiKzStACZKZPJ2MQgVQqoS5AEZLVIq1IKnZUas7RUYDJUqSJLEs2iRCsyOWO3-7uj4a_B-FA0zlemrqk13eCLMR1MBEoR_09FmSXjIyVHKuypVd953xtbbHrXUL8tEIrfIopjEcWhiFFyc7g-lI3Rf4Jj8vIH9hmGTQ</recordid><startdate>20121115</startdate><enddate>20121115</enddate><creator>Joly, Sophie</creator><creator>Eisenbarth, Stephanie C</creator><creator>Olivier, Alicia K</creator><creator>Williams, Adam</creator><creator>Kaplan, Daniel H</creator><creator>Cassel, Suzanne L</creator><creator>Flavell, Richard A</creator><creator>Sutterwala, Fayyaz S</creator><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>7T5</scope><scope>7T7</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>M7N</scope><scope>P64</scope></search><sort><creationdate>20121115</creationdate><title>Cutting edge: Nlrp10 is essential for protective antifungal adaptive immunity against Candida albicans</title><author>Joly, Sophie ; Eisenbarth, Stephanie C ; Olivier, Alicia K ; Williams, Adam ; Kaplan, Daniel H ; Cassel, Suzanne L ; Flavell, Richard A ; Sutterwala, Fayyaz S</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c440t-f4da80394e935e5034701db03a0afd27cb32d9bd197b40e91474afa31e8b1f293</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Animals</topic><topic>Apoptosis Regulatory Proteins - genetics</topic><topic>Apoptosis Regulatory Proteins - immunology</topic><topic>Candida albicans</topic><topic>Candida albicans - immunology</topic><topic>Candidiasis - genetics</topic><topic>Candidiasis - immunology</topic><topic>Candidiasis - pathology</topic><topic>Carrier Proteins - genetics</topic><topic>Carrier Proteins - immunology</topic><topic>Cytokines - genetics</topic><topic>Cytokines - immunology</topic><topic>Dendritic Cells - immunology</topic><topic>Dendritic Cells - pathology</topic><topic>Immunity, Cellular</topic><topic>Immunity, Innate - genetics</topic><topic>Macrophages - immunology</topic><topic>Macrophages - pathology</topic><topic>Mice</topic><topic>Mice, Knockout</topic><topic>NLR Family, Pyrin Domain-Containing 3 Protein</topic><topic>Th1 Cells - immunology</topic><topic>Th1 Cells - pathology</topic><topic>Th17 Cells - immunology</topic><topic>Th17 Cells - pathology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Joly, Sophie</creatorcontrib><creatorcontrib>Eisenbarth, Stephanie C</creatorcontrib><creatorcontrib>Olivier, Alicia K</creatorcontrib><creatorcontrib>Williams, Adam</creatorcontrib><creatorcontrib>Kaplan, Daniel H</creatorcontrib><creatorcontrib>Cassel, Suzanne L</creatorcontrib><creatorcontrib>Flavell, Richard A</creatorcontrib><creatorcontrib>Sutterwala, Fayyaz S</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>Immunology Abstracts</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><jtitle>The Journal of immunology (1950)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Joly, Sophie</au><au>Eisenbarth, Stephanie C</au><au>Olivier, Alicia K</au><au>Williams, Adam</au><au>Kaplan, Daniel H</au><au>Cassel, Suzanne L</au><au>Flavell, Richard A</au><au>Sutterwala, Fayyaz S</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Cutting edge: Nlrp10 is essential for protective antifungal adaptive immunity against Candida albicans</atitle><jtitle>The Journal of immunology (1950)</jtitle><addtitle>J Immunol</addtitle><date>2012-11-15</date><risdate>2012</risdate><volume>189</volume><issue>10</issue><spage>4713</spage><epage>4717</epage><pages>4713-4717</pages><issn>0022-1767</issn><eissn>1550-6606</eissn><abstract>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.</abstract><cop>United States</cop><pmid>23071280</pmid><doi>10.4049/jimmunol.1201715</doi><tpages>5</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Animals Apoptosis Regulatory Proteins - genetics Apoptosis Regulatory Proteins - immunology Candida albicans Candida albicans - immunology Candidiasis - genetics Candidiasis - immunology Candidiasis - pathology Carrier Proteins - genetics Carrier Proteins - immunology Cytokines - genetics Cytokines - immunology Dendritic Cells - immunology Dendritic Cells - pathology Immunity, Cellular Immunity, Innate - genetics Macrophages - immunology Macrophages - pathology Mice Mice, Knockout NLR Family, Pyrin Domain-Containing 3 Protein Th1 Cells - immunology Th1 Cells - pathology Th17 Cells - immunology Th17 Cells - pathology |
title | Cutting edge: Nlrp10 is essential for protective antifungal adaptive immunity against Candida albicans |
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