Genetic Deficiency and Biochemical Inhibition of ITK Affect Human Th17, Treg, and Innate Lymphoid Cells


Eken A. , Cansever M., Somekh I., Mizoguchi Y., Zietara N., Okus F., ...Daha Fazla

JOURNAL OF CLINICAL IMMUNOLOGY, cilt.39, ss.391-400, 2019 (SCI İndekslerine Giren Dergi) identifier identifier identifier

  • Cilt numarası: 39 Konu: 4
  • Basım Tarihi: 2019
  • Doi Numarası: 10.1007/s10875-019-00632-5
  • Dergi Adı: JOURNAL OF CLINICAL IMMUNOLOGY
  • Sayfa Sayıları: ss.391-400

Özet

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.