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Alpha synuclein, the culprit in Parkinson disease, is required for normal immune function

  1. Author:
    Alam,Md Masud
    Yang,De
    Li, Xiao-Qing
    Liu, Jia
    Back, Timothy Carrel
    Trivett, Anna
    Karim, Baktiar
    Barbut, Denise
    Zasloff, Michael
    Oppenheim, Joost J
  2. Author Address

    Cellular Immunology Section, Laboratory of Cancer ImmunoMetabolism, Center for Cancer Research, National Cancer Institute, Frederick, MD 21702-1201, USA., Cellular Immunology Section, Laboratory of Cancer ImmunoMetabolism, Center for Cancer Research, National Cancer Institute, Frederick, MD 21702-1201, USA. Electronic address: yangd@mail.nih.gov., Molecular Histopathology Laboratory, Leidos Biomedical Research, Center for Cancer Research, National Cancer Institute, Frederick, MD 21702-1201, USA., Enterin Research Institute, Philadelphia, PA 19103, USA., Enterin Research Institute, Philadelphia, PA 19103, USA; MedStar Georgetown Transplant Institute, Georgetown University Hospital, Washington, DC 20007, USA., Cellular Immunology Section, Laboratory of Cancer ImmunoMetabolism, Center for Cancer Research, National Cancer Institute, Frederick, MD 21702-1201, USA. Electronic address: oppenhej@mail.nih.gov.,
    1. Year: 2022
    2. Date: Jan 11
  1. Journal: Cell Reports
    1. 38
    2. 2
  2. Type of Article: Article
  3. Article Number: 110090
  4. ISSN: 2211-1247
  1. Abstract:

    Alpha-synuclein (aS) is causally involved in the development of Parkinson disease (PD); however, its role in normal vertebrate physiology has remained unknown. Recent studies demonstrate that aS is induced by noroviral infection in the enteric nervous system of children and protects mice against lethal neurotropic viral infection. Additionally, aS is a potent chemotactic activator of phagocytes. In this report, using both wild-type and aS knockout mice, we show that aS is a critical mediator of inflammatory and immune responses. aS is required for the development of a normal inflammatory response to bacterial peptidoglycan introduced into the peritoneal cavity as well as antigen-specific and TĀ cell responses following intraperitoneal immunization. Furthermore, we show that neural cells are the sources of aS required for immune competence. Our report supports the hypothesis that aS accumulates within the nervous system of PD individuals because of an inflammatory/immune response. Published by Elsevier Inc.

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External Sources

  1. DOI: 10.1016/j.celrep.2021.110090
  2. PMID: 35021075
  3. WOS: 000747197600005
  4. PII : S2211-1247(21)01581-3

Library Notes

  1. Fiscal Year: FY2021-2022
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