INVESTIGADORES
RABINOVICH Gabriel Adrian
congresos y reuniones científicas
Título:
EVIDENCE OF A GALECTIN-1-MEDIATED RHEOSTAT IN THE REGULATION OF T-CELL IMMUNITY IN LYMPHOMA-BEARING RATS
Autor/es:
M ZACARIAS FLUCK; M. RICO; V. ROZADOS; G. RABINOVICH; O.G. SCHAROVSKY
Lugar:
LOS ANGELES
Reunión:
Congreso; AMERICAN ASSOCIATION OF CANCER RESEARCH- ANNUAL MEETING; 2007
Institución organizadora:
AACR
Resumen:
Evidence of a galectin-1 mediated rheostat in the regulation of T-cell immunity in lymphoma-bearing rats   Zacarías Fluck Mariano F*, Rico María J*, Rozados Viviana R, Rabinovich Gabriel A, Scharovsky O Graciela. Instituto de Genética Experimental, Facultad de Ciencias Médicas, Universidad Nacional de Rosario, Rosario, Argentina (MFZF, MJR, VRR, OGS) y Laboratorio de Inmunogenética, Hospital de Clínicas, Universidad de Buenos Aires, Buenos Aires, Argentina (GAR). *Contributed equally to this work.   We have previously demonstrated that the kinetics of galectin-1 (Gal-1) expression was different in tumors with different immunogenicity: in the immunogenic rat lymphoma L-TACB, Gal-1 expression showed a significantly increase during tumor progression; in the non-immunogenic rat sarcoma S-E100 Gal-1 expression remained unchanged; in the mouse adenocarcinoma M-234p Gal-1 showed a significantly decrease. We also showed that Gal-1-induced immunosuppression is a mechanism used by tumors to evade the immune response. We hypothesized that the kinetics of Gal-1 expression would depend on the relationship between tumor immunogenicity and host immune response. The aim of this study was to validate the postulated hypothesis. Euthymic inbred e and m rats and Balb/c mice were s.c. challenged with L-TACB, S-E100 and M-234p, respectively, on day 0. Rats and mice were sacrificed periodically until day 21 and 40 respectively. Primary tumors were excised, homogenates prepared and Gal-1 expression determined by Western Blot. Simultaneously, nude mice were s.c. challenged with each of the tumors and sacrificed on the same days. M-234p and S-E100 growth rate did not show significant variation between euthymic host and nude mice. Even though the rate of L-TACB growth was lower in nude mice with respect to e rats, the growth rate in nude mice was not different among all the tumors. Besides, Gal-1 expression in nude mice, measured at days 7, 14 and 21, did not show significant variations during tumor growth in each of the three tumor models. In M-234p mammary adenocarcinoma Gal-1 expression was significantly lower when growing in nude mice with respect to Balb/c mice, during tumor progression (p<0.05). These results demonstrate that Gal-1 expression is strongly regulated by the host immune response induced by the tumor. In the absence of a specific antitumoral immune response, in nude mice, Gal-1 expression, during tumor growth, remains unchanged. Considering our previous observations that the kinetics of Gal-1 expression is significantly different among the three tumor models, which differ in their immunogenicity, we postulate that Gal-1 would act as a potentiometer in a servomechanism with a negative feedback, where the tumor would be the motor and the immune response the executor arm.