E proteins control the development of NKγδT cells through their invariant T cell receptor

Ariana Mihai, Sang-Yun Lee, Susan Shinton, Mitchell I. Parker, Alejandra V. Contreras, Baojun Zhang, Michele Rhodes, Roland L. Dunbrack, Juan-Carlos Zúñiga-Pflücker, Maria Ciofani, Yuan Zhuang and David L. Wiest ()
Additional contact information
Ariana Mihai: Duke University
Sang-Yun Lee: Fox Chase Cancer Center
Susan Shinton: Fox Chase Cancer Center
Mitchell I. Parker: Fox Chase Cancer Center
Alejandra V. Contreras: Fox Chase Cancer Center
Baojun Zhang: Duke University
Michele Rhodes: Fox Chase Cancer Center
Roland L. Dunbrack: Fox Chase Cancer Center
Juan-Carlos Zúñiga-Pflücker: University of Toronto
Maria Ciofani: Duke University
Yuan Zhuang: Duke University
David L. Wiest: Fox Chase Cancer Center

Nature Communications, 2024, vol. 15, issue 1, 1-14

Abstract: Abstract T cell receptor (TCR) signaling regulates important developmental transitions, partly through induction of the E protein antagonist, Id3. Although normal γδ T cell development depends on Id3, Id3 deficiency produces different phenotypes in distinct γδ T cell subsets. Here, we show that Id3 deficiency impairs development of the Vγ3+ subset, while markedly enhancing development of NKγδT cells expressing the invariant Vγ1Vδ6.3 TCR. These effects result from Id3 regulating both the generation of the Vγ1Vδ6.3 TCR and its capacity to support development. Indeed, the Trav15 segment, which encodes the Vδ6.3 TCR subunit, is directly bound by E proteins that control its expression. Once expressed, the Vγ1Vδ6.3 TCR specifies the innate-like NKγδT cell fate, even in progenitors beyond the normally permissive perinatal window, and this is enhanced by Id3-deficiency. These data indicate that the paradoxical behavior of NKγδT cells in Id3-deficient mice is determined by its stereotypic Vγ1Vδ6.3 TCR complex.

Date: 2024
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DOI: 10.1038/s41467-024-49496-3

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