Early lymphocyte expansion is severely impaired in interleukin 7 receptor-deficient mice.

TLDR

Interleukin‑7 drives proliferation of B‑cell progenitors, thymocytes, and mature T cells via its high‑affinity IL‑7 receptor. The study aimed to determine IL‑7 and IL‑7R roles in B and T cell development by creating IL‑7R‑deficient mice. The authors generated IL‑7R‑deficient mice and examined lymphoid progenitor populations to map the developmental stages affected by the mutation. IL‑7R deficiency led to a profound loss of thymic and peripheral lymphoid cells, showing that early thymocyte expansion before T‑cell receptor rearrangement critically depends on IL‑7R signaling.

Abstract

Interleukin 7 (IL-7) stimulates the proliferation of B cell progenitors, thymocytes, and mature T cells through an interaction with a high affinity receptor (IL-7R) belonging to the hematopoietin receptor superfamily. We have further addressed the role of IL-7 and its receptor during B and T cell development by generating mice genetically deficient in IL-7R. Mutant mice display a profound reduction in thymic and peripheral lymphoid cellularity. Analyses of lymphoid progenitor populations in IL-7R-deficient mice define precisely those developmental stages affected by the mutation and reveal a critical role for IL-7R during early lymphoid development. Significantly, these studies indicate that the phase of thymocyte expansion occurring before the onset of T cell receptor gene rearrangement is critically dependent upon, and mediated by the high affinity receptor for IL-7.