Lung effector memory and activated CD4+ T cells display enhanced proliferation in surfactant protein A-deficient mice during allergen-mediated inflammation.

Lung effector memory and activated CD4+ T cells display enhanced proliferation in surfactant protein A-deficient mice during allergen-mediated inflammation.
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DOI:
10.4049/jimmunol.0904190
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发表时间:
2011-03-01
期刊:
Journal of immunology (Baltimore, Md. : 1950)
影响因子:
--
通讯作者:
Wright JR
Wright JR
中科院分区:
其他
文献类型:
--
作者:
Pastva AM;Mukherjee S;Giamberardino C;Hsia B;Lo B;Sempowski GD;Wright JR

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Although many studies show that pulmonary Surfactant Protein A (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 ovalbumin (OVA) model of allergic hypersensitivity, SP-A deficient (SP-A−/−) mice had greater eosinophilia, Th2-associated cytokine levels, and IgE levels compared to wild-type (WT) 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 (TA) and effector memory (TEM) T cells in their lungs compared to WT mice. Ex vivo recall stimulation of CD4+ T cell pools demonstrate that the 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 TA and TEM cells expand to the greatest extent in the lungs of SP-A−/− OVA mice. Taken together, our data suggest that SP-A influences the prevalence, types, and functions of CD4+ T cells in the lungs during allergic inflammation and that surfactant protein deficiency modifies the severity of inflammation in allergic hypersensitivity conditions like asthma.
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