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A Novel Function for Galectin-1 at the Crossroad of Innate and Adaptive Immunity: Galectin-1 Regulates Monocyte/Macrophage Physiology through a Nonapoptotic ERK-Dependent Pathway¹

Paula Barrionuevo^2,*,, Macarena Beigier-Bompadre^2,, Juan M. Ilarregui^*, Marta A. Toscano^*, Germán A. Bianco^*, Martín A. Isturiz and Gabriel A. Rabinovich^3,*

^* División Inmunogenética. Hospital de Clínicas "José de San Martín," Facultad de Medicina, Universidad de Buenos Aires, Buenos Aires, Argentina; and Departamento de Inmunología, Instituto de Investigaciones Hematológicas, Academia Nacional de Medicina, Buenos Aires, Argentina

Several environmental factors can differentially regulate monocyte and macrophage response patterns, resulting in the display of distinct functional phenotypes. Galectin-1, an endogenous lectin found at peripheral lymphoid organs and inflammatory sites, has shown immunoregulatory activity in vivo in experimental models of autoimmunity and cancer. Whereas compelling evidence has been accumulated regarding the effects of galectin-1 on T cell fate, limited information is available on how galectin-1 may impact other immune cell types. In the present study, we report a novel role for galectin-1 in the regulation of monocyte and macrophage physiology. Treatment with galectin-1 in vitro differentially regulates constitutive and inducible FcRI expression on human monocytes and FcRI-dependent phagocytosis. In addition, galectin-1 inhibits IFN--induced MHC class II (MHC-II) expression and MHC-II-dependent Ag presentation in a dose-dependent manner. These regulatory effects were also evident in mouse macrophages recruited in response to inflammatory stimuli following treatment with recombinant galectin-1 and further confirmed in galectin-1-deficient mice. Investigation of the mechanisms involved in these functions showed that galectin-1 does not affect survival of human monocytes, but rather influences FcRI- and MHC-II-dependent functions through active mechanisms involving modulation of an ERK1/2-dependent pathway. Our results provide evidence of a novel unrecognized role for galectin-1 in the control of monocyte/macrophage physiology with potential implications at the crossroad of innate and adaptive immunity.

The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ This work was supported by grants from the Cancer Research Institute (USA), Mizutani Foundation for Glycoscience (Japan), Agencia de Promoción Científica y Tecnológica (PICT 2003-05-13787), Fundación Sales/Consejo Nacional de Investigaciones Científicas y Técnicas de Argentina Program, Wellcome Trust (U.K.), Fundación Florencio Fiorini, Fundación Bunge & Born, and University of Buenos Aires (UBACYT-M091; to G.A.R.), and by grants from Agencia Nacional de Promoción Científica y Tecnológica (PICT 05-14061; to M.A.I.). P.B., J.M.I., M.A.T., and G.A.B. thank Consejo Nacional de Investigaciones Científicas y Técnicas de Argentina for the fellowships granted.

² P.B. and M.B.-B. contributed equally to this work.

³ Address correspondence and reprint requests to Dr. Gabriel A. Rabinovich, División Inmunogenética, Hospital de Clínicas "José de San Martín," Facultad de Medicina, Universidad de Buenos Aires, Avenue Córdoba 2351, 3^er Piso, (C1120) Ciudad de Buenos Aires, Argentina. E-mail address: gabyrabi{at}ciudad.com.ar

⁴ Abbreviation used in this paper: MHC-II, MHC class II; MFI, median of fluorescence intensity; SRBC, sheep RBC; WT, wild type.

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