| First Author | Kawashima S | Year | 2012 |
| Journal | J Immunol | Volume | 189 |
| Issue | 12 | Pages | 5713-21 |
| PubMed ID | 23136202 | Mgi Jnum | J:190879 |
| Mgi Id | MGI:5449821 | Doi | 10.4049/jimmunol.1201521 |
| Citation | Kawashima S, et al. (2012) beta-Glucan Curdlan Induces IL-10-Producing CD4+ T Cells and Inhibits Allergic Airway Inflammation. J Immunol 189(12):5713-21 |
| abstractText | A number of studies have suggested a correlation between a decreased incidence in infectious diseases and an increased incidence of allergic diseases, including asthma. Although several pathogen-derived products have been shown to possess therapeutic potential for allergic diseases, it remains largely unknown whether beta-glucan, a cell wall component of a variety of fungi, yeasts, and bacteria, has a regulatory potential for allergic diseases. In this study, we examined the effect of curdlan, a linear beta-(1-3)-glucan, on the development of allergic airway inflammation. We found that i.p. injection of curdlan significantly inhibited Ag-induced eosinophil recruitment and Th2 cytokine production in the airways. The activation of CD4(+) T cells in the presence of curdlan induced IL-10-producing CD4(+) T cells with high levels of c-Maf expression. Curdlan-induced development of IL-10-producing CD4(+) T cells required the presence of APCs and ICOS/ICOS ligand interaction. Curdlan-induced development of IL-10-producing CD4(+) T cells also required intrinsic expression of STAT6. Furthermore, the transfer of Ag-specific CD4(+) T cells that were stimulated in the presence of curdlan inhibited Ag-induced eosinophil recruitment into the airways. Taken together, these results suggest that curdlan is capable of inducing IL-10-producing CD4(+) T cells and inhibiting the development of eosinohilic airway inflammation, underscoring the therapeutic potential of curdlan for allergic diseases. |
