Deletion of the Complement Anaphylatoxin C3a Receptor Attenuates, Whereas Ectopic Expression of C3a in the Brain Exacerbates, Experimental Autoimmune Encephalomyelitis-Reference-Cited by-同舟云学术

Deletion of the Complement Anaphylatoxin C3a Receptor Attenuates, Whereas Ectopic Expression of C3a in the Brain Exacerbates, Experimental Autoimmune Encephalomyelitis

Published:2004-09-21 Issue:7 Volume:173 Page:4708-4714
ISSN:0022-1767
Container-title:The Journal of Immunology
language:en
Short-container-title:J Immunol

Author:

Boos Laura,Campbell Iain L.,Ames Robert,Wetsel Rick A.,Barnum Scott R.

Publisher

The American Association of Immunologists

Subject

Immunology,Immunology and Allergy

Reference44 articles.

1. Expression of the Complement Anaphylatoxin C3a and C5a Receptors on Bronchial Epithelial and Smooth Muscle Cells in Models of Sepsis and Asthma

2. Complement C3a and C5a Induce Different Signal Transduction Cascades in Endothelial Cells

3. Regulation by complement C3a and C5a anaphylatoxins of cytokine production in human umbilical vein endothelial cells

4. Ember, J. A., M. A. Jagels, T. E. Hugli. 1998. Characterization of complement anaphylatoxina and their biological responses. J. E. Volanakis, Jr, and M. M. Frank, Jr, eds. The Human Complement System in Health and Disease 241. Marcel Dekker, New York.

5. Functional receptor for C3a anaphylatoxin is expressed by normal hematopoietic stem/progenitor cells, and C3a enhances their homing-related responses to SDF-1

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