T‐cell migration: Kruppeled T cells move again

Abstract

Kruppel-like transcription factors are a large family of proteins that can both activate and repress genes and regulate a wide variety of biological processes in multiple organ systems. In T lymphocytes, Kruppel-like factor 2 (KLF2) is an essential gene, as very few T cells are found in the spleen and lymph nodes of mice with targeted deficiency of KLF2.1 This was initially thought to reflect a requirement for KLF2 in T-cell survival and homeostasis. However, subsequent studies showed that KLF2 was required for thymic emigration and lymph node homing by regulating cell surface receptors required for these processes, namely S1P1 and CD62L.2 Now Mark Kahn's group3 adds a new twist to the story. They show that KLF2 also represses chemokine-receptor gene expression. Thus KLF2-deficient T cells aberrantly express multiple chemokine receptors that can cause T cells to home to various tissues in the body. Altogether, these studies establish KLF2 as a ‘master regulator’ that coordinates expression of multiple different types of cell surface receptors to control T-cell trafficking during an immune response.