Bibliographic Details
| Title: |
Btn2a2 Regulates ILC2–T Cell Cross Talk in Type 2 Immune Responses. |
| Authors: |
Frech, Michael, Omata, Yasunori, Schmalzl, Angelika, Wirtz, Stefan, Taher, Leila, Schett, Georg, Zaiss, Mario M., Sarter, Kerstin |
| Source: |
Frontiers in Immunology; 1/25/2022, Vol. 13, p1-14, 14p |
| Subject Terms: |
IMMUNE response, HELMINTHIASIS, T cells, INNATE lymphoid cells, CELLULAR control mechanisms |
| Abstract: |
Innate lymphoid cells (ILC) not only are responsible for shaping the innate immune response but also actively modulate T cell responses. However, the molecular processes regulating ILC-T cell interaction are not yet completely understood. The protein butyrophilin 2a2 (Btn2a2), a co-stimulatory molecule first identified on antigen-presenting cells, has a pivotal role in the maintenance of T cell homeostasis, but the main effector cell and the respective ligands remain elusive. We analyzed the role of Btn2a2 in the ILC-T cell cross talk. We found that the expression of Btn2a2 is upregulated in ILC2 following stimulation with IL-33/IL-25/TSLP. In vitro and in vivo experiments indicated that lack of Btn2a2 expression on ILC2 resulted in elevated T cell responses. We observed an enhanced proliferation of T cells as well as increased secretion of the type 2 cytokines IL-4/IL-5/IL-13 following cocultures with Btn2a2-deficient ILC2. In vivo transfer experiments confirmed the regulatory role of Btn2a2 on ILC2 as Btn2a2-deficient ILC2 induced stronger T cell responses and prevented chronic helminth infections. Taken together, we identified Btn2a2 as a significant player in the regulation of ILC2–T cell interactions. [ABSTRACT FROM AUTHOR] |
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| Database: |
Complementary Index |
