Innate-like self-reactive B cells infiltrate human renal allografts during transplant rejection

Yuta Asano, Joe Daccache, Dharmendra Jain, Kichul Ko, Andrew Kinloch, Margaret Veselits, Donald Wolfgeher, Anthony Chang, Michelle Josephson, Patrick Cunningham, Anat Tambur, Aly A. Khan, Shiv Pillai, Anita S. Chong and Marcus R. Clark ()
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Yuta Asano: Section of Rheumatology and The Knapp Center for Lupus and Immunology Research, Department of Medicine, The University of Chicago
Joe Daccache: Transplantation Research Center, Renal Division, Brigham and Women’s Hospital, Harvard Medical School
Dharmendra Jain: Section of Transplant, Department of Surgery, The University of Chicago
Kichul Ko: Section of Rheumatology and The Knapp Center for Lupus and Immunology Research, Department of Medicine, The University of Chicago
Andrew Kinloch: Section of Rheumatology and The Knapp Center for Lupus and Immunology Research, Department of Medicine, The University of Chicago
Margaret Veselits: Section of Rheumatology and The Knapp Center for Lupus and Immunology Research, Department of Medicine, The University of Chicago
Donald Wolfgeher: The University of Chicago
Anthony Chang: The University of Chicago
Michelle Josephson: Section of Nephrology, Department of Medicine, The University of Chicago
Patrick Cunningham: Section of Nephrology, Department of Medicine, The University of Chicago
Anat Tambur: Transplant Immunology Laboratory, Northwestern University
Aly A. Khan: The University of Chicago
Shiv Pillai: Ragon Institute of Massachusetts General Hospital, Massachusetts Institute of Technology, and Department of Medicine, Harvard Medical School
Anita S. Chong: Section of Transplant, Department of Surgery, The University of Chicago
Marcus R. Clark: Section of Rheumatology and The Knapp Center for Lupus and Immunology Research, Department of Medicine, The University of Chicago

Nature Communications, 2021, vol. 12, issue 1, 1-15

Abstract: Abstract Intrarenal B cells in human renal allografts indicate transplant recipients with a poor prognosis, but how these cells contribute to rejection is unclear. Here we show using single-cell RNA sequencing that intrarenal class-switched B cells have an innate cell transcriptional state resembling mouse peritoneal B1 or B-innate (Bin) cells. Antibodies generated by Bin cells do not bind donor-specific antigens nor are they enriched for reactivity to ubiquitously expressed self-antigens. Rather, Bin cells frequently express antibodies reactive with either renal-specific or inflammation-associated antigens. Furthermore, local antigens can drive Bin cell proliferation and differentiation into plasma cells expressing self-reactive antibodies. These data show a mechanism of human inflammation in which a breach in organ-restricted tolerance by infiltrating innate-like B cells drives local tissue destruction.

Date: 2021
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DOI: 10.1038/s41467-021-24615-6

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