The Interleukin-17 Receptor B Subunit Is Essential for the Th2 Response to Helicobacter pylori, but Not for Control of Bacterial Burden

Open Access

Peer-reviewed

Research Article

Dennis J. Horvath Jr.,

Affiliation Departments of Medicine, Vanderbilt University School of Medicine, Nashville, Tennessee, United States of America
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Jana N. Radin,

Affiliation Departments of Medicine, Vanderbilt University School of Medicine, Nashville, Tennessee, United States of America
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Sung Hoon Cho,

Affiliation Pathology, Microbiology, and Immunology, Vanderbilt University School of Medicine, Nashville, Tennessee, United States of America
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M. Kay Washington,

Affiliation Pathology, Microbiology, and Immunology, Vanderbilt University School of Medicine, Nashville, Tennessee, United States of America
⨯
Holly M. Scott Algood

* E-mail: holly.m.algood@vanderbilt.edu

Affiliations Veterans Affairs Tennessee Valley Healthcare System, Nashville, Tennessee, United States of America, Departments of Medicine, Vanderbilt University School of Medicine, Nashville, Tennessee, United States of America, Pathology, Microbiology, and Immunology, Vanderbilt University School of Medicine, Nashville, Tennessee, United States of America
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Helicobacter pylori
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Mouse models
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Inflammation
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Helicobacter pylori infection
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B cells
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