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T Cell Antifungal Immunity and the Role of C-Type Lectin Receptors
Fungi can cause disease in humans, from mucocutaneous to life-threatening systemic infections. Initiation of antifungal immunity involves fungal recognition by pattern recognition receptors such as C-type lectin receptors (CLRs). These germline-encoded receptors trigger a multitude of innate respons...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Elsevier Science Ltd
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7427322/ https://www.ncbi.nlm.nih.gov/pubmed/31813764 http://dx.doi.org/10.1016/j.it.2019.11.007 |
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author | Speakman, Emily A. Dambuza, Ivy M. Salazar, Fabián Brown, Gordon D. |
author_facet | Speakman, Emily A. Dambuza, Ivy M. Salazar, Fabián Brown, Gordon D. |
author_sort | Speakman, Emily A. |
collection | PubMed |
description | Fungi can cause disease in humans, from mucocutaneous to life-threatening systemic infections. Initiation of antifungal immunity involves fungal recognition by pattern recognition receptors such as C-type lectin receptors (CLRs). These germline-encoded receptors trigger a multitude of innate responses including phagocytosis, fungal killing, and antigen presentation which can also shape the development of adaptive immunity. Recently, studies have shed light on how CLRs directly or indirectly modulate lymphocyte function. Moreover, CLR-mediated recognition of commensal fungi maintains homeostasis and prevents invasion from opportunistic commensals. We present an overview of current knowledge of antifungal T cell immune responses, with emphasis on the role of C-type lectins, and discuss how these receptors modulate these responses at different levels. |
format | Online Article Text |
id | pubmed-7427322 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | Elsevier Science Ltd |
record_format | MEDLINE/PubMed |
spelling | pubmed-74273222020-08-16 T Cell Antifungal Immunity and the Role of C-Type Lectin Receptors Speakman, Emily A. Dambuza, Ivy M. Salazar, Fabián Brown, Gordon D. Trends Immunol Article Fungi can cause disease in humans, from mucocutaneous to life-threatening systemic infections. Initiation of antifungal immunity involves fungal recognition by pattern recognition receptors such as C-type lectin receptors (CLRs). These germline-encoded receptors trigger a multitude of innate responses including phagocytosis, fungal killing, and antigen presentation which can also shape the development of adaptive immunity. Recently, studies have shed light on how CLRs directly or indirectly modulate lymphocyte function. Moreover, CLR-mediated recognition of commensal fungi maintains homeostasis and prevents invasion from opportunistic commensals. We present an overview of current knowledge of antifungal T cell immune responses, with emphasis on the role of C-type lectins, and discuss how these receptors modulate these responses at different levels. Elsevier Science Ltd 2020-01 /pmc/articles/PMC7427322/ /pubmed/31813764 http://dx.doi.org/10.1016/j.it.2019.11.007 Text en © 2019 The Author(s) http://creativecommons.org/licenses/by/4.0/ This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Article Speakman, Emily A. Dambuza, Ivy M. Salazar, Fabián Brown, Gordon D. T Cell Antifungal Immunity and the Role of C-Type Lectin Receptors |
title | T Cell Antifungal Immunity and the Role of C-Type Lectin Receptors |
title_full | T Cell Antifungal Immunity and the Role of C-Type Lectin Receptors |
title_fullStr | T Cell Antifungal Immunity and the Role of C-Type Lectin Receptors |
title_full_unstemmed | T Cell Antifungal Immunity and the Role of C-Type Lectin Receptors |
title_short | T Cell Antifungal Immunity and the Role of C-Type Lectin Receptors |
title_sort | t cell antifungal immunity and the role of c-type lectin receptors |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7427322/ https://www.ncbi.nlm.nih.gov/pubmed/31813764 http://dx.doi.org/10.1016/j.it.2019.11.007 |
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