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Publication Date

Summer 2017

Degree Type

Thesis - Campus Access Only

Degree Name

Master of Science (MS)

Department

Biological Sciences

Advisor

Tzvia Abramson

Subject Areas

Biology; Immunology; Molecular biology

Abstract

Whooping cough, also known as pertussis, is a highly contagious and prolonged respiratory disease caused by the Bordetella pertussis bacterium. Lymphocytes such as T helper 17 (Th17) cells, which cause inflammation, are critical for resolving the infection. In the early stages of the pertussis infection in mice, there is a reduced number of Th17 cells. Conventional dendritic cells (cDCs) interact with naïve T helper cells to activate and promote their differentiation into functional Th17 lymphocytes. Dendritic cells are divided into subgroups characterized by the expression of cell surface markers CD11b and CD103. Integrin alpha v beta 8 (αvβ8) expressed on the surface of cDCs appears to activate transforming growth factor β (TGF-β) that modulates differentiation of Th17 cells. In this study, we tested the hypothesis that in early post B. pertussis infection in mice, there was a pertussis toxin (PTX)-dependent inhibition of αvβ8 expression on cDCs that limits Th17 differentiation. Using the peripheral blood mononuclear cells from mice infected with the B. pertussis bacterium, we analyzed the cell expression markers using multicolor flow cytometry. Early in infection, there was a PTX-dependent inhibition of αvβ8 on conventional dendritic cells. The reduced frequency of αvβ8 expression may inhibit that activation of TGF-β, resulting in decreased differentiation and proliferation of Th17 cells, thus prolonging the duration of pertussis.

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