Blockade of the C5a receptor fails to protect against experimental autoimmune encephalomyelitis in rats

Morgan, BP, Griffiths, M, Khanom, H, Taylor, SM and Neal, JW (2004) Blockade of the C5a receptor fails to protect against experimental autoimmune encephalomyelitis in rats. Clinical And Experimental Immunology, 138 3: 430-438. doi:10.1111/j.1365-2249.2004.02646.x


Author Morgan, BP
Griffiths, M
Khanom, H
Taylor, SM
Neal, JW
Title Blockade of the C5a receptor fails to protect against experimental autoimmune encephalomyelitis in rats
Journal name Clinical And Experimental Immunology   Check publisher's open access policy
ISSN 0009-9104
1365-2249
Publication date 2004
Sub-type Article (original research)
DOI 10.1111/j.1365-2249.2004.02646.x
Volume 138
Issue 3
Start page 430
End page 438
Total pages 9
Editor A. P. Weetman
Place of publication Europe
Publisher Blackwell
Collection year 2004
Language eng
Subject C1
320599 Pharmacology not elsewhere classified
730102 Immune system and allergy
Abstract Complement activation contributes to inflammation and tissue damage in human demyelinating diseases and in rodent models of demyelination. Inhibitors of complement activation ameliorate disease in the rat model antibody-dependent experimental autoimmune encephalomyelitis and rats unable to generate the membrane attack complex of complement develop inflammation without demyelination. The role of the highly active chemotactic and anaphylactic complement-derived peptide C5a in driving inflammation and pathology in rodent models of demyelination has been little explored. Here we have used a small molecule C5a receptor antagonist, AcF-[OPdChaWR], to examine the effects of C5a receptor blockade in rat models of brain inflammation and demyelination. C5a receptor antagonist therapy completely blocked neutrophil response to C5a in vivo but had no effect on clinical disease or resultant pathology in either inflammatory or demyelinating rat models. We conclude that C5a is not required for disease induction or perpetuation in these strongly complement-dependent disease models.
Keyword Rodent
Complement
Neuroimmunology
Chemokines
Experimental Allergic Encephalomyelitis
Myelin Oligodendrocyte Glycoprotein
Multiple-sclerosis Lesions
Central-nervous-system
Axonal-injury
Anaphylatoxin Receptor
Complement Activation
Monoclonal-antibodies
Demyelination
Expression
Immunology
Q-Index Code C1

 
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