Magic™ Anti-LGALS3 polyclonal antibody [HRP]

Here, we report the identification of the ubiquitin-like gene UBD as a downstream element of FOXP3 in human activated regulatory CD4(+)CD25(hi) T cells (T-reg). Retroviral transduction of UBD in human allo-reactive effector CD4(+) T helper (T-h) cells upregulates CD25 and mediates downregulation of IL4 and IL5 expression similar to overexpression of FOXP3. Moreover, UBD impairs T-h cell proliferation without upregulation of FOXP3 and impairs calcium mobilization. In the presence of ionomycin, overexpression of UBD in T-h cells leads to the induction of IL1R2 that resemble FOXP3-transduced T-h cells and naturally derived T-reg cells. A comparison of the transcriptome of FOXP3- and UBD-transduced T-h cells with T-reg cells allowed the identification of the gene LGALS3. However, high levels of LGALS3 protein expression were observed only in human CD4(+)CD25(hi) derived T-reg cells and FOXP3- transduced T-h cells, whereas little was induced in UBD-transduced T-h cells. Thus, UBD contributes to the anergic phenotype of human regulatory T cells and acts downstream in FOXP3 induced regulatory signaling pathways, including regulation of LGALS3 expression. High levels of LGALS3 expression represent a FOXP3- signature of human antigen-stimulated CD4(+)CD25(hi) derived regulatory T cells.

LGALS3, a member of the lectin family, has an important role in tumor progression through inhibition of apoptosis. LGALS3 shares several significant structural properties with BCL2. In this study, we examined the prognostic significance of LGALS3 and BCL2 in uniformly treated classical Hodgkin's lymphoma. Diagnostic tissues from 110 patients with uniformly treated classical Hodgkin's lymphoma were evaluated retrospectively by immunohistochemical analysis of LGALS3 and BCL2 expression. The median follow-up time was 6.2 years (range, 0.2-17.3 years). Twenty-seven patients (25%) expressed LGALS3 protein in Hodgkin/Reed-Sternberg cells, which was associated with poor overall survival and event-free survival (P=0.007 and P<0.001). Fifteen patients (14%) expressed BCL2 protein in Hodgkin/Reed-Sternberg cells, which was not associated with overall survival and event-free survival (P=0.928 and P=0.900). There was no correlation between LGALS3 and BCL2 expression (P=0.193). Multivariate analysis identified LGALS3 protein as an independent prognostic factor for event-free survival (P=0.007). Subgroup analysis according to the Ann Arbor stage of classical Hodgkin's lymphoma showed that LGALS3 protein expression had a prognostic value in limited-stage classical Hodgkin's lymphoma (P<0.001). The results of this study suggest that LGALS3 is an independent prognostic factor in classical Hodgkin's lymphoma, and may allow the identification of a subgroup of patients with limited-stage classical Hodgkin's lymphoma who require more intensive therapy.