Mast Cells: A Cellular Link Between Autoantibodies and Inflammatory Arthritis-Reference-Cited by-同舟云学术

Mast Cells: A Cellular Link Between Autoantibodies and Inflammatory Arthritis

Published:2002-09-06 Issue:5587 Volume:297 Page:1689-1692
ISSN:0036-8075
Container-title:Science
language:en
Short-container-title:Science

Author:

Lee David M.¹²,Friend Daniel S.³,Gurish Michael F.¹²,Benoist Christophe¹⁴,Mathis Diane¹⁴,Brenner Michael B.¹²

Affiliation:

1. Department of Medicine and

2. Division of Rheumatology, Immunology and Allergy, Brigham and Women's Hospital; Harvard Medical School, Boston, MA 02115, USA.

3. Department of Pathology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA.

4. Section on Immunology and Immunogenetics, Joslin Diabetes Center, Harvard Medical School, One Joslin Place, Boston, MA 02215, USA.

Abstract

Previous studies have revealed that autoantibodies, complement components, and Fc receptors each participate in the pathogenesis of erosive arthritis in K/BxN mice. However, it is not known which cellular populations are responsive to these inflammatory signals. We find that two strains of mice deficient in mast cells, W/W v and Sl/Sl d , were resistant to development of joint inflammation and that susceptibility was restored in the W/W v strain by mast cell engraftment. Thus, mast cells may function as a cellular link between autoantibodies, soluble mediators, and other effector populations in inflammatory arthritis.

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Multidisciplinary

Reference34 articles.

1. Arthritis Provoked by Linked T and B Cell Recognition of a Glycolytic Enzyme

2. Organ-Specific Disease Provoked by Systemic Autoimmunity

3. From Systemic T Cell Self-Reactivity to Organ-Specific Autoimmune Disease via Immunoglobulins

4. Essential Role of Neutrophils in the Initiation and Progression of a Murine Model of Rheumatoid Arthritis

5. Arthritis Critically Dependent on Innate Immune System Players

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