alexa Suppression of Collagen-Induced Arthritis in Mice by Anti-Collagen Antibody Fab Fragments | OMICS International | Abstract
ISSN: 2167-7921

Journal of Arthritis
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Research Article

Suppression of Collagen-Induced Arthritis in Mice by Anti-Collagen Antibody Fab Fragments

Shin Yoshino*, Raktham Maktrirat and Nobuaki Mizutani
Department of Pharmacology, Kobe Pharmaceutical University, Kobe, Japan
Corresponding Author : Shin Yoshino
Department of Pharmacology
Kobe Pharmaceutical University
4-9-1 Motoyamakita-machi, Higashinada-ku
Kobeshi, Hyogo-ken, Japan
Tel: +81-78-441-7572
E-mail: [email protected]
Received January 29, 2014; Accepted February 27, 2014; Published March 03, 2014
Citation: Yoshino S, Maktrirat R, Mizutani N (2014) Suppression of Collagen- Induced Arthritis in Mice by Anti-Collagen Antibody Fab Fragments. J Arthritis 3:124. doi:10.4172/2167-7921.1000124
Copyright: © 2014 Yoshino S, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

Fabs fragments (Fabs) maintain binding ability to specific antigens, but lack the binding site for complements and for receptors on leukocytes that play a crucial role in Rheumatoid Arthritis (RA). In the present study, we investigated whether type II Collagen (CII)-Induced Arthritis (CIA) in mice was suppressed by anti-CII Fabs prepared by papain digestion of anti-CII antibodies. CIA was induced in DBA/1J mice by immunization with chicken CII and completes Freund’s adjuvant. To investigate the effect of anti-CII Fabs on the CIA model, mice were injected intraperitoneally with anti-CII Fabs 1 day before the first immunization. As a result, CIA was markedly inhibited by anti-CII Fabs; furthermore, the histological features of anti-CII Fabs-untreated mice included severe hyperplatic synnovium, cartilage and joint destruction, and leukocytic infiltration, whereas animals given anti-CII Fabs showed significant reduction of these histological changes. Additionally, antigen-specific suppression of CIA by anti-CII Fabs was related to the reduced levels of complement C3a in serum. Meanwhile, in vitro studies revealed that anti-CII Fabs significantly blocked the binding of intact anti-CII antibodies and also decreased complement activation. Collectively, the development of CIA was suppressed by anti-CII Fabs, which prevented the binding of anti-CII antibodies to antigen followed by the inhibition of complement activation, suggesting that autoimmune arthritic diseases such as RA may be specifically treated with pathogenic antibody Fabs.

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