Recombinant Mouse IL-7 (E. coli expressed, carrier-free)

Mouse IL-7 was initially described as a pre-B cell growth factor expressed in bone marrow stromal cells. IL-7 is essential for normal murine B cell development, and plays a key role in regulating the homeostasis and function of T-cells. The binding of IL-7 to its receptor induces dimerization of IL-7Ra and the common gamma chain (γc) which leads to activation of receptor associated tyrosine Janus kinases JAK1 (IL-7R) and JAK3 (γc). The activated JAK proteins in turn phosphorylates specific residues on the IL-7R creating docking sites for signaling molecules such as STAT5 and to a lesser extent STAT1 and STAT3. In adult mice, IL-7/IL-7R signaling up regulates expression of early B cell factor (EBF), and EBF in turn regulates expression of B cell-specific genes required for the transition from lymphoid progenitor to pro-B cells. IL-7 plays a role in the development of secondary lymphoid tissues. IL-7 is necessary to specify CD8 lineage differentiation during CD4/CD8 cell fate choice in the thymus by inducing expression of the transcription factor Runx3. IL-7 induces anti-apoptotic factors Bcl2 and Bcl-xL and inhibits pro-apoptotic factors such as Bad and Bax. In this fashion, IL-7 induces cell activation, survival, and proliferation of T lymphocytes. In addition, IL-7 controls T-cell size and metabolism through the activation of PI3 kinase-dependent pathways and regulation of glucose metabolism. IL-7 also controls T cell–dendritic cell interactions that are essential for both T-cell homeostasis and activation in vivo. CD4 T cell lymphopenia increases the expression of circulating IL-7, and TGFb induces IL-7 downregulation.