Genetic Deficiency and Biochemical Inhibition of ITK Affect Human Th17, Treg, and Innate Lymphoid Cells
JOURNAL OF CLINICAL IMMUNOLOGY, vol.39, no.4, pp.391-400, 2019 (SCI-Expanded, Scopus)
- Publication Type: Article / Article
- Volume: 39 Issue: 4
- Publication Date: 2019
- Doi Number: 10.1007/s10875-019-00632-5
- Journal Name: JOURNAL OF CLINICAL IMMUNOLOGY
- Journal Indexes: Science Citation Index Expanded (SCI-EXPANDED), Scopus
- Page Numbers: pp.391-400
- Keywords: ITK, Th17, Treg, Foxp3, ILC, interleukin-2-inducible T cell kinase, ibrutinib
- Erciyes University Affiliated: Yes
Abstract
Purpose Interleukin-2-inducible T cell kinase (ITK) is an important mediator of T cell receptor signaling. Loss of function mutations in ITK results in hypogammaglobulinemia and CD4+ T cell loss in humans, and the patients often present with EBV-associated B cell lymphoproliferative syndrome. Itk-deficient mice show loss of T cell naivety, impaired cytolytic activity of CD8+ T cells, and defects in CD4+ T cell lineage choice decisions. In mice, Itk mutations were shown to affect Th17-Treg lineage choice in favor of the latter. In this study, we explored whether human ITK reciprocally regulates Th17-Treg balance as its murine ortholog.