Journal
JOURNAL OF IMMUNOLOGY
Volume 186, Issue 5, Pages 2842-2849Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.0904190
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Funding
- National Institutes of Health/National Heart, Lung, and Blood Institute [5P50HL084917, 5R01HL68072]
- National Institutes of Health/National Institute of Allergy and Infectious Diseases [1K08AI068822]
- Duke University's Center for Comparative Biology of Vulnerable Populations [5P30-ES-011961-04]
- National Institute of Aging [5R01AG025150]
- National Institutes of Health [AI-051445]
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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 Foxp(3+) 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. The Journal of Immunology, 2011, 186: 2842-2849.
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