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Galectin‐3 negatively regulates the frequency and function of CD 4 + CD 25 + F oxp3 + regulatory T cells and influences the course of L eishmania major infection
Ist Teil von
European journal of immunology, 2013-07, Vol.43 (7), p.1806-1817
Erscheinungsjahr
2013
Link zum Volltext
Quelle
Free E-Journal (出版社公開部分のみ）
Beschreibungen/Notizen
Galectin‐3, an endogenous glycan‐binding protein, plays essential roles during microbial infection by modulating innate and adaptive immunity. However, the role of galectin‐3 within the CD 4 + CD 25 + F oxp3 + T regulatory ( T REG ) cell compartment has not yet been explored. Here, we found, in a model of L eishmania major infection, that galectin‐3 deficiency increases the frequency of peripheral T REG cells both in draining lymph nodes (LNs) and sites of infection. These observations correlated with an increased severity of the disease, as shown by increased footpad swelling and parasite burden. Galectin‐3‐deficient ( L gals3 −/− ) T REG cells displayed higher CD 103 expression, showed greater suppressive capacity, and synthesized higher amounts of IL ‐10 compared with their wild‐type ( WT ) counterpart. Furthermore, both T REG cells and T effector ( T EFF ) cells from L gals3 −/− mice showed higher expression of Notch1 and the N otch target gene H es‐1. Interestingly, N otch signaling components were also altered in both T REG and T EFF cells from uninfected L gals3 −/− mice. Thus, endogenous galectin‐3 regulates the frequency and function of CD 4 + CD 25 + F oxp3 + T REG cells and alters the course of L . major infection.