ABSTRACT
It seems tting that the scientists credited for the discovery of the rst vertebrate “galectin” also described its rst and most impressive effects on leukocytes. Levi and Tiechburg demonstrated that prophylactic administration of “electrolectin” (equivalent to galectin-1 of the electric organ tissue of Electrophorus electricus [1]) prevented the formation of experimentally induced myasthenia gravis [2]. Several years later, Offner et al. demonstrated that human galectin-1 (Gal-1) also suppressed the clinical signs and pathology associated with experimental autoimmune encephalomyelitis (EAE) in rats [3], suggesting a broad immunosuppressive spectrum for Gal-1. Interestingly, both of these authors attributed the immunomodulatory effects of Gal-1 to suppressor T cells [2-4]. However, suppressor T cells quickly fell out of vogue [5], requiring an alternative explanation for the potent immunosuppressive activities of Gal-1. In 1995, Baum and colleagues suggested that Gal-1 reduced immune responses by directly inducing apoptotic cell death in activated, but not resting, T cells [6].
