| Literature DB >> 30799037 |
Petra Bacher1, Thordis Hohnstein2, Eva Beerbaum2, Marie Röcker3, Matthew G Blango3, Svenja Kaufmann4, Jobst Röhmel4, Patience Eschenhagen4, Claudia Grehn4, Kathrin Seidel5, Volker Rickerts5, Laura Lozza6, Ulrik Stervbo7, Mikalai Nienen8, Nina Babel7, Julia Milleck9, Mario Assenmacher9, Oliver A Cornely10, Maren Ziegler11, Hilmar Wisplinghoff11, Guido Heine12, Margitta Worm12, Britta Siegmund13, Jochen Maul14, Petra Creutz15, Christoph Tabeling16, Christoph Ruwwe-Glösenkamp15, Leif E Sander17, Christoph Knosalla18, Sascha Brunke19, Bernhard Hube20, Olaf Kniemeyer3, Axel A Brakhage21, Carsten Schwarz4, Alexander Scheffold22.
Abstract
Th17 cells provide protection at barrier tissues but may also contribute to immune pathology. The relevance and induction mechanisms of pathologic Th17 responses in humans are poorly understood. Here, we identify the mucocutaneous pathobiont Candida albicans as the major direct inducer of human anti-fungal Th17 cells. Th17 cells directed against other fungi are induced by cross-reactivity to C. albicans. Intestinal inflammation expands total C. albicans and cross-reactive Th17 cells. Strikingly, Th17 cells cross-reactive to the airborne fungus Aspergillus fumigatus are selectively activated and expanded in patients with airway inflammation, especially during acute allergic bronchopulmonary aspergillosis. This indicates a direct link between protective intestinal Th17 responses against C. albicans and lung inflammation caused by airborne fungi. We identify heterologous immunity to a single, ubiquitous member of the microbiota as a central mechanism for systemic induction of human anti-fungal Th17 responses and as a potential risk factor for pulmonary inflammatory diseases.Entities:
Keywords: Aspergillus fumigatus; Candida albicans; T cell cross-reactivity; Th17; airway inflammation; allergic bronchopulmonary aspergillosis (ABPA); anti-fungal immunity; antigen-reactive T cell enrichment (ARTE); cystic fibrosis; heterologous immunity; microbiota
Mesh:
Year: 2019 PMID: 30799037 DOI: 10.1016/j.cell.2019.01.041
Source DB: PubMed Journal: Cell ISSN: 0092-8674 Impact factor: 41.582