The Role of Innate Immunity in Autoimmunity-Reference-Cited by-同舟云学术

The Role of Innate Immunity in Autoimmunity

Published:2004-12-20 Issue:12 Volume:200 Page:1527-1531
ISSN:1540-9538
Container-title:Journal of Experimental Medicine
language:en
Short-container-title:

Author:

Bach Jean-François¹,Bendelac Albert²,Brenner Michael B.³,Cantor Harvey⁴,De Libero Gennaro⁵,Kronenberg Mitchell⁶,Lanier Lewis L.⁷,Raulet David H.⁸,Shlomchik Mark J.⁹,von Herrath Matthias G.⁶

Affiliation:

1. INSERM U580, Hôpital Necker, Paris, France

2. Department of Pathology, University of Chicago, Chicago, IL

3. Brigham and Women's Hospital, Harvard Medical School, Boston, MA

4. Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA

5. Experimental Immunology, Department of Research, University Hospital, Basel, Switzerland

6. La Jolla Institute for Allergy and Immunology, San Diego, CA

7. Department of Microbiology and Immunology and the Cancer Research Institute, University of California, San Francisco, San Francisco, CA

8. Department of Molecular and Cell Biology, University of California, Berkeley, CA

9. Department of Medicine and Section of Immunobiology, Yale University School of Medicine, New Haven, CT

Abstract

During the 2004 International Congress of Immunology in Montreal, a panel of experts gathered for an “Ideashop” discussion on the potential role of innate immunity in autoimmunity and the ways in which this might be targeted in future therapies.

Publisher

Rockefeller University Press

Subject

Immunology,Immunology and Allergy

Link

http://rupress.org/jem/article-pdf/200/12/1527/1127451/jem200121527.pdf

Reference28 articles.

1. Chromatin–IgG complexes activate B cells by dual engagement of IgM and Toll-like receptors

2. NKG2D Blockade Prevents Autoimmune Diabetes in NOD Mice

3. Natural killer T cells: natural or unnatural regulators of autoimmunity?

4. Defective IgE production by SJL mice is linked to the absence of CD4+, NK1.1+ T cells that promptly produce interleukin 4.

5. Early quantitative and functional deficiency of NK1+-like thymocytes in the NOD mouse

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