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Published online before print August 18, 2006

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(Journal of Leukocyte Biology. 2006;80:1233-1241.)
© 2006 by Society for Leukocyte Biology

CD69 targeting differentially affects the course of collagen-induced arthritis

David Sancho^*,1,2, Manuel Gómez^*,1, Gloria Martinez del Hoyo^*, Amalia Lamana^*, Enric Esplugues, Pilar Lauzurica, Carlos Martinez-A and Francisco Sánchez-Madrid^*,3

^* Servicio de Inmunología, Hospital de la Princesa, Universidad Autónoma de Madrid, Madrid, Spain;
Departamento de Fisiología, Universidad de Barcelona, Barcelona, Spain; and
Department of Immunology and Oncology, Centro Nacional de Biotecnología, Consejo Superior de Investigaciones Científicas-Universidad Autónoma de Madrid, Madrid, Spain

³ Correspondence: Servicio de Inmunología, Hospital Universitario de La Princesa,C/ Diego de León, 62, Madrid E-28006, Spain. E-mail: fsanchez.hlpr{at}salud.madrid.org

ABSTRACT

CD69 expression is induced following activation of leukocytes at inflammatory sites and plays a negative regulatory role in the development of collagen-induced arthritis (CIA). To evaluate potential strategies of CD69 targeting in chronic inflammatory diseases, two different anti-CD69 mAbs were generated and their effects on CIA were studied. Administration of the IgG1 anti-CD69 mAb 2.2 to DBA/1 mice with CIA led to an exacerbation of the disease, correlated with down-modulation of CD69 from the cell surface, and reproduced the phenotype of the CD69(–/–) mouse in wild-type animals. In contrast, treatment with the IgG2a anti-CD69 mAb 2.3 was effective in ameliorating CIA when administered in the early or intermediate phases of the disease, causing a decreased production of proinflammatory cytokines in inflammatory foci. Monoclonal antibody 2.3 induces partial depletion of CD69+ cells in vivo. Moreover, adoptive transfer of type-II collagen (CII)-sensitized cells treated with mAb 2.3 to deplete CD69+ cells did not result in arthritis. The attenuation of inflammation correlates with reduced lymphocyte proliferative response in response to CII and with a reduction in the frequency of CII-specific T cells producing IFN-. We thus conclude that CD69 targeting by mAbs can either enhance or dampen the immune response.

Key Words: antibodies • autoimmunity • T cells • cytokines • chemokines

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