{'fraction_non_alphanumeric': 0.03335318642048839, 'fraction_numerical': 0.02084574151280524, 'mean_word_length': 4.915492957746479, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Allergen-Mediated Inflammation Surfactant Protein A-Deficient Mice during T Cells Display Enhanced Proliferation in + Lung Effector Memory and Activated CD4

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 2 / 2 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 2 / 2 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 2 / 2 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 2 / 2 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.