Article ID Journal Published Year Pages File Type
2794458 Cytokine 2012 6 Pages PDF
Abstract

Background and aimsMeasles infection causes immune suppression that contributes to morbidity and mortality of the patients; the mechanism is poorly understood. Regulatory T cells (Treg) play a critical role in immune suppression. Integrin alphavbeta6 (avb6) is associated with Treg’s function. This study aims to investigate into the mechanism by which measles C protein (MVP)-induced avb6 contributes the generation of Tregs in the lung.MethodMVP was introduced to mouse lung by nasal drops. The expression of avb6 by lung tissue was examined by reverse transcription polymerase chain reaction and Western blotting. The development of tolerogenic dendritic cells (DC) and Tregs in the lung and their functions was examined by flow cytometry. The suppressor function of MVP-induced Tregs was examined by cell culture models.ResultsThe exposure to MVP markedly increased the expression of avb6 in the lung epithelial cells. Administration of MVP significantly suppressed the levels of IL-4 and IFNγ as well as increases in Tregs in lung tissue. DCs captured the MVP in the lung and differentiate into tolerogenic DCs; the latter has the ability to induce Treg development in the lung. Activation of MVP-induced Tregs powerfully suppressed polarized CD4+ T cells.ConclusionsExposure to MVP can induce Treg development in the lung that plays an important role in the suppression of CD4+ T cell function.

► Measles viral protein (MVP) increases integrin alphavbeta6 (avb6) by airway epithelial cells. ► Exposure to MVP markedly suppresses the levels of IL-4 and IFNγ. ► Exposure to MVP markedly increases in Tregs in lung tissue. ► Dendritic cells capture avb6 to differentiate into tolerogenic DCs. ► Activation of MVP-induced Tregs suppresses polarized CD4+ T cells.

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Life Sciences Biochemistry, Genetics and Molecular Biology Endocrinology
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