Immunity to fungal infections
Key Points Fungi can interact with humans in multiple ways, establishing symbiotic, commensal, latent or pathogenic relationships. Although the burdens of fungal diseases may rival those of many of the best-known bacterial diseases, humans have evolved with ubiquitous or commensal fungi in host–fung...
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description | Key Points
Fungi can interact with humans in multiple ways, establishing symbiotic, commensal, latent or pathogenic relationships. Although the burdens of fungal diseases may rival those of many of the best-known bacterial diseases, humans have evolved with ubiquitous or commensal fungi in host–fungus relationships that for the most part are positive or neutral.
The co-evolution of humans and fungi suggests that complex mechanisms exist to allow the host immune system to respond to fungi and, likewise, that fungi have developed sophisticated mechanisms to antagonize immune responses. Indeed, fungal diseases represent an important paradigm in immunology, as they can result either from lack of recognition or from overactivation of the inflammatory response.
We are entering an exciting period of transition from studying the molecular and cellular bases of the virulence of fungal pathogens to determining the mechanisms of immune adaptations that maintain homeostasis with fungi.
As the immune system cannot ignore fungi, a fine balance between pro- and anti-inflammatory signals is required for a stable host–fungus relationship, the disruption of which leads to pathological consequences. Thus, the challenge for future studies is to gain a better understanding of the control of inflammation, the molecular bases of regulation and rupture, and the way in which innocuous but opportunistic fungal pathogens maintain 'friendly' relationships, or evade or subvert host inflammation.
The use of multidisciplinary approaches, including functional genomics, proteomics and bioinformatics, will have important biomedical implications. These may include the identification of new susceptibility genes, the identification of more accurate biomarkers that predict inflammatory fungal disorders, and the development of multi-pronged therapeutic approaches that target specific inflammatory or metabolic end points in fungal infections and diseases.
In this article, Luigina Romani describes the immune mechanisms that have evolved to recognize and respond to fungi. She explains how the failure of either pro-inflammatory or tolerogenic immune responses can lead to the development of fungal diseases.
Fungal diseases represent an important paradigm in immunology, as they can result from either a lack of recognition by the immune system or overactivation of the inflammatory response. Research in this field is entering an exciting period of transition from studying the molecular and cellular bas |
doi_str_mv | 10.1038/nri2939 |
format | Article |
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Fungi can interact with humans in multiple ways, establishing symbiotic, commensal, latent or pathogenic relationships. Although the burdens of fungal diseases may rival those of many of the best-known bacterial diseases, humans have evolved with ubiquitous or commensal fungi in host–fungus relationships that for the most part are positive or neutral.
The co-evolution of humans and fungi suggests that complex mechanisms exist to allow the host immune system to respond to fungi and, likewise, that fungi have developed sophisticated mechanisms to antagonize immune responses. Indeed, fungal diseases represent an important paradigm in immunology, as they can result either from lack of recognition or from overactivation of the inflammatory response.
We are entering an exciting period of transition from studying the molecular and cellular bases of the virulence of fungal pathogens to determining the mechanisms of immune adaptations that maintain homeostasis with fungi.
As the immune system cannot ignore fungi, a fine balance between pro- and anti-inflammatory signals is required for a stable host–fungus relationship, the disruption of which leads to pathological consequences. Thus, the challenge for future studies is to gain a better understanding of the control of inflammation, the molecular bases of regulation and rupture, and the way in which innocuous but opportunistic fungal pathogens maintain 'friendly' relationships, or evade or subvert host inflammation.
The use of multidisciplinary approaches, including functional genomics, proteomics and bioinformatics, will have important biomedical implications. These may include the identification of new susceptibility genes, the identification of more accurate biomarkers that predict inflammatory fungal disorders, and the development of multi-pronged therapeutic approaches that target specific inflammatory or metabolic end points in fungal infections and diseases.
In this article, Luigina Romani describes the immune mechanisms that have evolved to recognize and respond to fungi. She explains how the failure of either pro-inflammatory or tolerogenic immune responses can lead to the development of fungal diseases.
Fungal diseases represent an important paradigm in immunology, as they can result from either a lack of recognition by the immune system or overactivation of the inflammatory response. Research in this field is entering an exciting period of transition from studying the molecular and cellular bases of fungal virulence to determining the cellular and molecular mechanisms that maintain immune homeostasis with fungi. The fine line between these two research areas is central to our understanding of tissue homeostasis and its possible breakdown in fungal infections and diseases. Recent insights into immune responses to fungi suggest that functionally distinct mechanisms have evolved to achieve optimal host−fungus interactions in mammals.</description><identifier>ISSN: 1474-1733</identifier><identifier>EISSN: 1474-1741</identifier><identifier>DOI: 10.1038/nri2939</identifier><identifier>PMID: 21394104</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>631/250/255/1672 ; 631/250/516 ; 631/326/193/2544 ; 692/700/565 ; Animals ; Antifungal Agents - immunology ; Asthma ; Asthma - immunology ; Asthma - microbiology ; Biomedical and Life Sciences ; Biomedicine ; Dermatitis ; Development and progression ; Disease ; Drug resistance ; Fungal infections ; Fungi ; Fungi - immunology ; Fungi - pathogenicity ; Health aspects ; Homeostasis ; Homeostasis - immunology ; Hormone replacement therapy ; Humans ; Immune response ; Immune system ; Immunity ; Immunity, Innate ; Immunology ; Inflammatory bowel disease ; Mammals ; Mice ; Mycoses ; Mycoses - immunology ; Mycoses - microbiology ; Pathogens ; Physiological aspects ; review-article ; Skin ; Skin Diseases - immunology ; Skin Diseases - microbiology ; T-Lymphocytes - immunology ; T-Lymphocytes - microbiology ; Virulence ; Yeast</subject><ispartof>Nature reviews. Immunology, 2011-04, Vol.11 (4), p.275-288</ispartof><rights>Springer Nature Limited 2011</rights><rights>COPYRIGHT 2011 Nature Publishing Group</rights><rights>Copyright Nature Publishing Group Apr 2011</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c504t-acc84dfa9de5b145c6051a10ab2a2399cbc703807fdcecc151cf8b3ef16f8aa23</citedby><cites>FETCH-LOGICAL-c504t-acc84dfa9de5b145c6051a10ab2a2399cbc703807fdcecc151cf8b3ef16f8aa23</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1038/nri2939$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1038/nri2939$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27903,27904,41467,42536,51297</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21394104$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Romani, Luigina</creatorcontrib><title>Immunity to fungal infections</title><title>Nature reviews. Immunology</title><addtitle>Nat Rev Immunol</addtitle><addtitle>Nat Rev Immunol</addtitle><description>Key Points
Fungi can interact with humans in multiple ways, establishing symbiotic, commensal, latent or pathogenic relationships. Although the burdens of fungal diseases may rival those of many of the best-known bacterial diseases, humans have evolved with ubiquitous or commensal fungi in host–fungus relationships that for the most part are positive or neutral.
The co-evolution of humans and fungi suggests that complex mechanisms exist to allow the host immune system to respond to fungi and, likewise, that fungi have developed sophisticated mechanisms to antagonize immune responses. Indeed, fungal diseases represent an important paradigm in immunology, as they can result either from lack of recognition or from overactivation of the inflammatory response.
We are entering an exciting period of transition from studying the molecular and cellular bases of the virulence of fungal pathogens to determining the mechanisms of immune adaptations that maintain homeostasis with fungi.
As the immune system cannot ignore fungi, a fine balance between pro- and anti-inflammatory signals is required for a stable host–fungus relationship, the disruption of which leads to pathological consequences. Thus, the challenge for future studies is to gain a better understanding of the control of inflammation, the molecular bases of regulation and rupture, and the way in which innocuous but opportunistic fungal pathogens maintain 'friendly' relationships, or evade or subvert host inflammation.
The use of multidisciplinary approaches, including functional genomics, proteomics and bioinformatics, will have important biomedical implications. These may include the identification of new susceptibility genes, the identification of more accurate biomarkers that predict inflammatory fungal disorders, and the development of multi-pronged therapeutic approaches that target specific inflammatory or metabolic end points in fungal infections and diseases.
In this article, Luigina Romani describes the immune mechanisms that have evolved to recognize and respond to fungi. She explains how the failure of either pro-inflammatory or tolerogenic immune responses can lead to the development of fungal diseases.
Fungal diseases represent an important paradigm in immunology, as they can result from either a lack of recognition by the immune system or overactivation of the inflammatory response. Research in this field is entering an exciting period of transition from studying the molecular and cellular bases of fungal virulence to determining the cellular and molecular mechanisms that maintain immune homeostasis with fungi. The fine line between these two research areas is central to our understanding of tissue homeostasis and its possible breakdown in fungal infections and diseases. Recent insights into immune responses to fungi suggest that functionally distinct mechanisms have evolved to achieve optimal host−fungus interactions in mammals.</description><subject>631/250/255/1672</subject><subject>631/250/516</subject><subject>631/326/193/2544</subject><subject>692/700/565</subject><subject>Animals</subject><subject>Antifungal Agents - immunology</subject><subject>Asthma</subject><subject>Asthma - immunology</subject><subject>Asthma - microbiology</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Dermatitis</subject><subject>Development and progression</subject><subject>Disease</subject><subject>Drug resistance</subject><subject>Fungal infections</subject><subject>Fungi</subject><subject>Fungi - immunology</subject><subject>Fungi - pathogenicity</subject><subject>Health aspects</subject><subject>Homeostasis</subject><subject>Homeostasis - immunology</subject><subject>Hormone replacement therapy</subject><subject>Humans</subject><subject>Immune response</subject><subject>Immune system</subject><subject>Immunity</subject><subject>Immunity, Innate</subject><subject>Immunology</subject><subject>Inflammatory bowel disease</subject><subject>Mammals</subject><subject>Mice</subject><subject>Mycoses</subject><subject>Mycoses - immunology</subject><subject>Mycoses - microbiology</subject><subject>Pathogens</subject><subject>Physiological aspects</subject><subject>review-article</subject><subject>Skin</subject><subject>Skin Diseases - immunology</subject><subject>Skin Diseases - microbiology</subject><subject>T-Lymphocytes - immunology</subject><subject>T-Lymphocytes - microbiology</subject><subject>Virulence</subject><subject>Yeast</subject><issn>1474-1733</issn><issn>1474-1741</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNqN0klLxDAUB_AgiuOGn0AZFFwO1bwm3Y6DuAwIgss5pGkyU2kTTVJwvr0ZZ1wqHiSHhr5fXvpvgtAu4DPAJD_Xto4LUqygDaAZjSCjsPo1J2SANp17xhjSUFlHgxhIQQHTDbQ3bttO13429GaoOj3hzbDWSgpfG-220ZrijZM7y-cWerq6fLy4iW7vrscXo9tIJJj6iAuR00rxopJJCTQRKU6AA-ZlzGNSFKIUWfhKnKlKSCEgAaHykkgFqcp5IFvoeNH3xZrXTjrP2toJ2TRcS9M5loc8BeTpP2SSZzkGSoI8-CWfTWd1iDFHlKQkzgI6XKCQW7IQ3HjLxbwlG8UJIThJs_mmZ3-oMCrZ1sJoqerwvrfgtLcgGC_f_IR3zrHxw33fHv2wU8kbP3Wm6T4OoA-X0YU1zlmp2IutW25nDDCb3wK2vAVB7i-jd2Urqy_3eewBnCyACyU9kfb73_zu9Q78mbUL</recordid><startdate>20110401</startdate><enddate>20110401</enddate><creator>Romani, Luigina</creator><general>Nature Publishing Group UK</general><general>Nature Publishing Group</general><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>ISR</scope><scope>3V.</scope><scope>7QR</scope><scope>7RV</scope><scope>7T5</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB0</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>NAPCQ</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>7X8</scope></search><sort><creationdate>20110401</creationdate><title>Immunity to fungal infections</title><author>Romani, Luigina</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c504t-acc84dfa9de5b145c6051a10ab2a2399cbc703807fdcecc151cf8b3ef16f8aa23</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>631/250/255/1672</topic><topic>631/250/516</topic><topic>631/326/193/2544</topic><topic>692/700/565</topic><topic>Animals</topic><topic>Antifungal Agents - 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Academic</collection><jtitle>Nature reviews. Immunology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Romani, Luigina</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Immunity to fungal infections</atitle><jtitle>Nature reviews. Immunology</jtitle><stitle>Nat Rev Immunol</stitle><addtitle>Nat Rev Immunol</addtitle><date>2011-04-01</date><risdate>2011</risdate><volume>11</volume><issue>4</issue><spage>275</spage><epage>288</epage><pages>275-288</pages><issn>1474-1733</issn><eissn>1474-1741</eissn><abstract>Key Points
Fungi can interact with humans in multiple ways, establishing symbiotic, commensal, latent or pathogenic relationships. Although the burdens of fungal diseases may rival those of many of the best-known bacterial diseases, humans have evolved with ubiquitous or commensal fungi in host–fungus relationships that for the most part are positive or neutral.
The co-evolution of humans and fungi suggests that complex mechanisms exist to allow the host immune system to respond to fungi and, likewise, that fungi have developed sophisticated mechanisms to antagonize immune responses. Indeed, fungal diseases represent an important paradigm in immunology, as they can result either from lack of recognition or from overactivation of the inflammatory response.
We are entering an exciting period of transition from studying the molecular and cellular bases of the virulence of fungal pathogens to determining the mechanisms of immune adaptations that maintain homeostasis with fungi.
As the immune system cannot ignore fungi, a fine balance between pro- and anti-inflammatory signals is required for a stable host–fungus relationship, the disruption of which leads to pathological consequences. Thus, the challenge for future studies is to gain a better understanding of the control of inflammation, the molecular bases of regulation and rupture, and the way in which innocuous but opportunistic fungal pathogens maintain 'friendly' relationships, or evade or subvert host inflammation.
The use of multidisciplinary approaches, including functional genomics, proteomics and bioinformatics, will have important biomedical implications. These may include the identification of new susceptibility genes, the identification of more accurate biomarkers that predict inflammatory fungal disorders, and the development of multi-pronged therapeutic approaches that target specific inflammatory or metabolic end points in fungal infections and diseases.
In this article, Luigina Romani describes the immune mechanisms that have evolved to recognize and respond to fungi. She explains how the failure of either pro-inflammatory or tolerogenic immune responses can lead to the development of fungal diseases.
Fungal diseases represent an important paradigm in immunology, as they can result from either a lack of recognition by the immune system or overactivation of the inflammatory response. Research in this field is entering an exciting period of transition from studying the molecular and cellular bases of fungal virulence to determining the cellular and molecular mechanisms that maintain immune homeostasis with fungi. The fine line between these two research areas is central to our understanding of tissue homeostasis and its possible breakdown in fungal infections and diseases. Recent insights into immune responses to fungi suggest that functionally distinct mechanisms have evolved to achieve optimal host−fungus interactions in mammals.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>21394104</pmid><doi>10.1038/nri2939</doi><tpages>14</tpages></addata></record> |
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subjects | 631/250/255/1672 631/250/516 631/326/193/2544 692/700/565 Animals Antifungal Agents - immunology Asthma Asthma - immunology Asthma - microbiology Biomedical and Life Sciences Biomedicine Dermatitis Development and progression Disease Drug resistance Fungal infections Fungi Fungi - immunology Fungi - pathogenicity Health aspects Homeostasis Homeostasis - immunology Hormone replacement therapy Humans Immune response Immune system Immunity Immunity, Innate Immunology Inflammatory bowel disease Mammals Mice Mycoses Mycoses - immunology Mycoses - microbiology Pathogens Physiological aspects review-article Skin Skin Diseases - immunology Skin Diseases - microbiology T-Lymphocytes - immunology T-Lymphocytes - microbiology Virulence Yeast |
title | Immunity to fungal infections |
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