Cryptococcus neoformans Evades Pulmonary Immunity by Modulating Xylose Precursor Transport

Author:

Li Lucy X.1,Hole Camaron R.1,Rangel-Moreno Javier2,Khader Shabaana A.1,Doering Tamara L.1ORCID

Affiliation:

1. Department of Molecular Microbiology, Washington University School of Medicine, St. Louis, Missouri, USA

2. Department of Medicine, Allergy/Immunology, and Rheumatology, University of Rochester School of Medicine, Rochester, New York, USA

Abstract

Cryptococcus neoformans is a fungal pathogen that kills almost 200,000 people each year and is distinguished by abundant and unique surface glycan structures that are rich in xylose. A mutant strain of C. neoformans that cannot transport xylose precursors into the secretory compartment is severely attenuated in virulence in mice yet surprisingly is not cleared. We found that this strain failed to induce the nonprotective T helper cell type 2 (Th2) responses characteristic of wild-type infection, instead promoting sustained interleukin 12p40 (IL-12p40) induction and increased IL-17A (IL-17) production.

Funder

HHS | National Institutes of Health

HHS | NIH | National Institute of Allergy and Infectious Diseases

Washington University in St. Louis

Publisher

American Society for Microbiology

Subject

Infectious Diseases,Immunology,Microbiology,Parasitology

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