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IgA Potentiates NETosis in Response to Viral Infection

Hannah D. Stacey, Diana Golubeva, Alyssa Posca, Jann C. Ang, Kyle E. Novakowski, Muhammad Atif Zahoor, Charu Kaushic, Ewa Cairns, Dawn M. E. Bowdish, Caitlin E. Mullarkey, Matthew S. Miller
doi: https://doi.org/10.1101/2021.01.04.424830
Hannah D. Stacey
1Michael G. DeGroote Institute for Infectious Diseases Research, McMaster University, Hamilton, ON, Canada
2McMaster Immunology Research Centre, McMaster University, Hamilton, ON, Canada
3Department of Biochemistry and Biomedical Sciences, McMaster University, Hamilton, ON, Canada
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Diana Golubeva
1Michael G. DeGroote Institute for Infectious Diseases Research, McMaster University, Hamilton, ON, Canada
2McMaster Immunology Research Centre, McMaster University, Hamilton, ON, Canada
3Department of Biochemistry and Biomedical Sciences, McMaster University, Hamilton, ON, Canada
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Alyssa Posca
1Michael G. DeGroote Institute for Infectious Diseases Research, McMaster University, Hamilton, ON, Canada
2McMaster Immunology Research Centre, McMaster University, Hamilton, ON, Canada
3Department of Biochemistry and Biomedical Sciences, McMaster University, Hamilton, ON, Canada
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Jann C. Ang
1Michael G. DeGroote Institute for Infectious Diseases Research, McMaster University, Hamilton, ON, Canada
2McMaster Immunology Research Centre, McMaster University, Hamilton, ON, Canada
3Department of Biochemistry and Biomedical Sciences, McMaster University, Hamilton, ON, Canada
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Kyle E. Novakowski
1Michael G. DeGroote Institute for Infectious Diseases Research, McMaster University, Hamilton, ON, Canada
2McMaster Immunology Research Centre, McMaster University, Hamilton, ON, Canada
4Department of Medicine, McMaster University, Hamilton, ON, Canada
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Muhammad Atif Zahoor
2McMaster Immunology Research Centre, McMaster University, Hamilton, ON, Canada
4Department of Medicine, McMaster University, Hamilton, ON, Canada
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Charu Kaushic
2McMaster Immunology Research Centre, McMaster University, Hamilton, ON, Canada
4Department of Medicine, McMaster University, Hamilton, ON, Canada
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Ewa Cairns
5Department of Microbiology and Immunology, Schulich School of Medicine and Dentistry, Western University, London, ON, Canada
6Department of Medicine, Division of Rheumatology, Schulich School of Medicine and Dentistry, Western University, London, ON, Canada
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Dawn M. E. Bowdish
1Michael G. DeGroote Institute for Infectious Diseases Research, McMaster University, Hamilton, ON, Canada
2McMaster Immunology Research Centre, McMaster University, Hamilton, ON, Canada
4Department of Medicine, McMaster University, Hamilton, ON, Canada
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Caitlin E. Mullarkey
1Michael G. DeGroote Institute for Infectious Diseases Research, McMaster University, Hamilton, ON, Canada
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Matthew S. Miller
1Michael G. DeGroote Institute for Infectious Diseases Research, McMaster University, Hamilton, ON, Canada
2McMaster Immunology Research Centre, McMaster University, Hamilton, ON, Canada
3Department of Biochemistry and Biomedical Sciences, McMaster University, Hamilton, ON, Canada
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  • For correspondence: mmiller@mcmaster.ca
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ABSTRACT

IgA is the second most abundant antibody present in circulation and is enriched at mucosal surfaces. As such, IgA plays a key role in protection against a variety of mucosal pathogens, including viruses. In addition to neutralizing viruses directly, IgA can also stimulate Fc-dependent effector functions via engagement of Fc alpha receptors (FcαRI) expressed on the surface of certain immune effector cells. Neutrophils are the most abundant leukocyte, express FcαRI, and are often the first to respond to sites of injury and infection. Here, we describe a novel function for IgA:virus immune complexes (ICs) during viral infections. We show that IgA:virus ICs potentiate NETosis – the programmed cell death pathway through which neutrophils release neutrophil extracellular traps (NETs). Mechanistically, IgA:virus ICs potentiated a suicidal NETosis pathway via engagement of FcαRI on neutrophils through a toll-like receptor (TLR)-independent, NADPH oxidase complex-dependent pathway. NETs also were capable of trapping and inactivating viruses, consistent with an antiviral function.

Competing Interest Statement

The authors have declared no competing interest.

Copyright 
The copyright holder for this preprint is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under a CC-BY-NC-ND 4.0 International license.
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Posted January 05, 2021.
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IgA Potentiates NETosis in Response to Viral Infection
Hannah D. Stacey, Diana Golubeva, Alyssa Posca, Jann C. Ang, Kyle E. Novakowski, Muhammad Atif Zahoor, Charu Kaushic, Ewa Cairns, Dawn M. E. Bowdish, Caitlin E. Mullarkey, Matthew S. Miller
bioRxiv 2021.01.04.424830; doi: https://doi.org/10.1101/2021.01.04.424830
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IgA Potentiates NETosis in Response to Viral Infection
Hannah D. Stacey, Diana Golubeva, Alyssa Posca, Jann C. Ang, Kyle E. Novakowski, Muhammad Atif Zahoor, Charu Kaushic, Ewa Cairns, Dawn M. E. Bowdish, Caitlin E. Mullarkey, Matthew S. Miller
bioRxiv 2021.01.04.424830; doi: https://doi.org/10.1101/2021.01.04.424830

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