CIBICI   14215
CENTRO DE INVESTIGACION EN BIOQUIMICA CLINICA E INMUNOLOGIA
Unidad Ejecutora - UE
artículos
Título:
GALECTIN-1 SUPPRESSES AUTOIMMUNE RETINAL DISEASE BY PROMOTING CONCOMITANT T HELPER (TH)2- AND T REGULATORY-MEDIATED ANTI-INFLAMMATORY RESPONSES
Autor/es:
A. TOSCANO., MARTA; G. COMMODARO, ALESSANDRA; A. BIANCO, GERMÁN; M. ILARREGUI, JUAN; ANA LIBERMAN,; SERRA, HORACIO MARCELO; JUN HIRABAYASHI,; V. RIZZO, LUIZ; A. RABINOVICH, GABRIEL
Revista:
JOURNAL OF IMMUNOLOGY
Referencias:
Año: 2006 vol. 176 p. 6323 - 6332
ISSN:
0022-1767
Resumen:
Intraocular inflammatory diseases are a common cause of severe visual impairment and blindness. In this study, we investigated
the immunoregulatory role of galectin-1 (Gal-1), an endogenous lectin found at sites of T cell activation and immune privilege, in
experimental autoimmune uveitis (EAU), a Th1-mediated model of retinal disease. Treatment with rGal-1 either early or late
during the course of interphotoreceptor retinoid-binding protein-induced EAU was sufficient to suppress ocular pathology, inhibit
leukocyte infiltration, and counteract pathogenic Th1 cells. Administration of rGal-1 at the early or late phases of EAU ameliorated
disease by skewing the uveitogenic response toward nonpathogenic Th2 or T regulatory-mediated anti-inflammatory responses.
Consistently, adoptive transfer of CD4 regulatory T cells obtained from rGal-1-treated mice prevented the development
of active EAU in syngeneic recipients. In addition, increased levels of apoptosis were detected in lymph nodes from mice treated
with rGal-1 during the efferent phase of the disease. Our results underscore the ability of Gal-1 to counteract Th1-mediated
responses through different, but potentially overlapping anti-inflammatory mechanisms and suggest a possible therapeutic use of
this protein for the treatment of human uveitic diseases of autoimmune etiology. regulatory T cells obtained from rGal-1-treated mice prevented the development
of active EAU in syngeneic recipients. In addition, increased levels of apoptosis were detected in lymph nodes from mice treated
with rGal-1 during the efferent phase of the disease. Our results underscore the ability of Gal-1 to counteract Th1-mediated
responses through different, but potentially overlapping anti-inflammatory mechanisms and suggest a possible therapeutic use of
this protein for the treatment of human uveitic diseases of autoimmune etiology.