| First Author | Nkyimbeng-Takwi EH | Year | 2012 |
| Journal | Mucosal Immunol | Volume | 5 |
| Issue | 4 | Pages | 409-19 |
| PubMed ID | 22472774 | Mgi Jnum | J:323164 |
| Mgi Id | MGI:6843238 | Doi | 10.1038/mi.2012.18 |
| Citation | Nkyimbeng-Takwi EH, et al. (2012) Neuroimmune semaphorin 4A downregulates the severity of allergic response. Mucosal Immunol 5(4):409-19 |
| abstractText | To define the role of semaphorin 4A (Sema4A) in allergic response, we employed Sema4A(-)/(-) and wild-type (WT) mice in the experimental model of ovalbumin (OVA)-induced allergic airway inflammation. We observed a selective increase in eosinophilic airway infiltration accompanied by bronchial epithelial cell hyperplasia in allergen-treated Sema4A(-)/(-) mice relative to WT mice. This enhanced inflammatory response was associated with a selective increase in bronchoalveolar lavage (BAL) interleukin 13 (IL-13) content, augmented airway hyperreactivity, and lower regulatory T cell (Treg) numbers. In vivo allergen-primed Sema4A(-)/(-) CD4+ T cells were more effective in transferring T helper type 2 (Th2) response to naive mice as compared with WT CD4+ T cells. T-cell proliferation and IL-13 productions in OVA(3)(2)(3)(-)(3)(3)(9)-restimulated Sema4A(-)/(-) cell cultures were upregulated. Generated bone marrow chimeras showed an equal importance of both lung-resident cell and inflammatory cell Sema4A expression in optimal disease regulation. These data provide a new insight into Sema4A biology and define Sema4A as an important regulator of Th2-driven lung pathophysiology. |
