The RNA editing enzyme ADAR1 has been shown to be an essential molecule for hematopoietic cell differentiation, embryonic development, and regulation of immune responses. Here, we present evidence in a T-cell-specific gene knockout mouse model that ADAR1 is required for early T cell development. Loss of ADAR1 led to cell death of the progenitors at the double negative stage and prevented T cell maturation in the thymus. Furthermore, ADAR1 deletion in pre-T cells preferentially affected TCRβ-expressing cells causing TCRβ positive cell depletion. Interruption of IFN signaling occurred in the premature T cells, indicating a role of IFN signaling in the survival of TCRβ-expressing cells regulated by ADAR1. This study demonstrated an essential role for the RNA editing enzyme ADAR1 as a potential regulator for T-cell fate determination during clonal selection, which, in turn, contributes to immunologic homeostasis.
Keywords: ADAR1; Conditional knockout; RNA editing; T cell development.
Copyright © 2020 The Authors. Published by Wolters Kluwer Health Inc., on behalf of the Chinese Association for Blood Sciences.