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Oxford University Press, Precision Clinical Medicine, 1(4), p. 56-61, 2021

DOI: 10.1093/pcmedi/pbaa039

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RhoA and Cdc42 in T cells: Are they targetable for T cell-mediated inflammatory diseases?

Journal article published in 2021 by Fukun Guo
Distributing this paper is prohibited by the publisher
Distributing this paper is prohibited by the publisher

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Data provided by SHERPA/RoMEO

Abstract

Abstract Many inflammatory diseases are not curable, necessitating a better understanding of their pathobiology that may help identify novel biological targets. RhoA and Cdc42 of Rho family small GTPases regulate a variety of cellular functions such as actin cytoskeletal organization, cell adhesion, migration, proliferation, and survival. Recent characterization of mouse models of conditional gene knockout of RhoA and Cdc42 has revealed their physiological and cell type-specific roles in a number of cell types. In T lymphocytes, which play an important role in the pathogenesis of most, if not all, of the inflammatory diseases, we and others have investigated the effects of T cell-specific knockout of RhoA and Cdc42 on T cell development in the thymus, peripheral T cell homeostasis, activation, and differentiation to effector and regulatory T cells, and on T cell-mediated allergic airway inflammation and colitis. Here we highlight the phenotypes resulting from RhoA and Cdc42 deletion in T cells and discuss whether pharmacological targeting of RhoA and Cdc42 is feasible in treating asthma that is driven by allergic airway inflammation and colitis.