S2e). Gal-1, gal-3 and gal-9 were also explored by their effect on anti-CD3/anti-CD28-induced cytokines in peripheral T lymphocytes. Lymphocytes were stimulated during 24 h

with anti-CD3 and anti-CD28 in the presence or not of gal-1, gal-3 and gal-9 as indicated in Material and methods. Cytokine production was determined using a bead-based immunoassay. Our results showed that the presence of gal-1 during T cell receptor (TCR) stimulation induces a high production of IL-10, P = 0·02 (Fig. 4c). An augmented IL-4 production was also observed in those lymphocytes co-incubated with gal-3 and anti-CD3/anti-CD28; however, this difference was not statistically significant (data not shown). Most published studies on the immunopathogenesis of asthma and other inflammatory diseases focus on proinflammatory mediators. However, in recent years the study of cells and selleckchem molecules with immunoregulatory activity has Selleckchem Doxorubicin begun to gain importance. The data presented here show that airway cells obtained from induced sputum samples of asthma patients express lower levels of gal-1 and gal-9 and higher levels of IL-5 and IL-13 compared with cells from healthy subjects. In addition, we have identified macrophages as the cells from sputum expressing gal-1 and gal-9. A recent study analysed

the presence of galectin-bound proteins in broncoalveolar lavage (BAL) from patients with mild asthma, and a different profile of galectin-bound proteins was observed between patients and healthy subjects. In parallel, authors describe that BAL contains galectins at low concentrations, suggesting that functional interactions with galectins occur at sites where airway cells are present [24]. Numerous studies have highlighted the immunomodulatory

properties of galectins [7]. Lck The anti-inflammatory properties of gal-1 have been evaluated in animal models of chronic inflammation [13, 25-27]. However, the role of gal-1 in asthma has not been explored previously. Published data highlight the ability of gal-1 to counteract Th1 and Th17-mediated responses through a number of anti-inflammatory mechanisms. One reported mechanism is a skewing of the balance from Th1 towards Th2 polarized immune responses, mainly through the induction of Th1 cell apoptosis. The numerous anti-inflammatory effects of gal-1 include induction of IL-10 release [28, 29], down-regulation of the secretion of TNF-α and IFN-γ [30, 31] and inhibition of transendothelial migration as well as chemotaxis of neutrophils [32]. Disruption of all these processes could contribute to exacerbated inflammatory responses in an environment with defective expression of this lectin. In the context of asthma, IL-10 plays a key role in the control of inflammatory process, able to down-modulate the Th2 response [33-35]. Decreased IL-10 expression has been linked recently to the impaired ability of natural regulatory T cells from allergic asthma patients to induce a tolerogenic phenotype in dendritic cells [36].