| First Author | Pastva AM | Year | 2011 |
| Journal | J Immunol | Volume | 186 |
| Issue | 5 | Pages | 2842-9 |
| PubMed ID | 21257967 | Mgi Jnum | J:169410 |
| Mgi Id | MGI:4940942 | Doi | 10.4049/jimmunol.0904190 |
| Citation | Pastva AM, et al. (2011) Lung Effector Memory and Activated CD4+ T Cells Display Enhanced Proliferation in Surfactant Protein A-Deficient Mice during Allergen-Mediated Inflammation. J Immunol 186(5):2842-9 |
| abstractText | Although many studies have shown that pulmonary surfactant protein (SP)-A functions in innate immunity, fewer studies have addressed its role in adaptive immunity and allergic hypersensitivity. We hypothesized that SP-A modulates the phenotype and prevalence of dendritic cells (DCs) and CD4(+) T cells to inhibit Th2-associated inflammatory indices associated with allergen-induced inflammation. In an OVA model of allergic hypersensitivity, SP-A(-/-) mice had greater eosinophilia, Th2-associated cytokine levels, and IgE levels compared with wild-type counterparts. Although both OVA-exposed groups had similar proportions of CD86(+) DCs and Foxp3(+) T regulatory cells, the SP-A(-/-) mice had elevated proportions of CD4(+) activated and effector memory T cells in their lungs compared with wild-type mice. Ex vivo recall stimulation of CD4(+) T cell pools demonstrated that cells from the SP-A(-/-) OVA mice had the greatest proliferative and IL-4-producing capacity, and this capability was attenuated with exogenous SP-A treatment. Additionally, tracking proliferation in vivo demonstrated that CD4(+) activated and effector memory T cells expanded to the greatest extent in the lungs of SP-A(-/-) OVA mice. Taken together, our data suggested that SP-A influences the prevalence, types, and functions of CD4(+) T cells in the lungs during allergic inflammation and that SP deficiency modifies the severity of inflammation in allergic hypersensitivity conditions like asthma. |
