Both B151-T cell replacing factor 1 and IL-5 regulate Ig secretion and IL-2 receptor expression on a cloned B lymphoma line

J Immunol. 1988 Feb 15;140(4):1168-74.

Abstract

In the present study, we have demonstrated that both B151-T cell-replacing factor 1 and rIL-5 are responsible for the activity to partially induce CL-3 cells into IgM-synthesizing cells and also to synergize with IL-2 to augment IL-2R expression on and IgM synthesis in CL-3 cells. These actions of rIL-5 on a homogeneous cloned line (BCL1-CL-3 cells) allow us to identify and characterize the two alternated B cell developmental pathways. One is an IL-2-independent, IL-5-driven differentiation pathway without preceding up-regulated IL-2R expression, and the other is an IL-5 plus IL-2-dependent augmented differentiation pathway with preceding up-regulated IL-2R expression. We have also demonstrated the functional difference of two distinct B cell growth-promoting factors, B cell-stimulating factor 1 (rIL-4) and rIL-5. CL-3 cells are equally stimulated to grow by rIL-4 and rIL-5, whereas only rIL-5 can render CL-3 cells responsive to rIL-2, indicating that these two lymphokines affect B cells in a strikingly different manner.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Antibodies, Monoclonal / metabolism
  • Antibodies, Neoplasm / metabolism
  • B-Lymphocytes / drug effects*
  • B-Lymphocytes / metabolism
  • Cell Differentiation / drug effects
  • Cell Division / drug effects
  • Clone Cells
  • Drug Synergism
  • Immunoglobulin M / metabolism*
  • Interleukin-2 / pharmacology
  • Interleukin-5
  • Interleukins / pharmacology*
  • Lymphoma, Non-Hodgkin / pathology*
  • Mice
  • Receptors, Immunologic / biosynthesis*
  • Receptors, Interleukin-2
  • Tumor Cells, Cultured / drug effects
  • Tumor Cells, Cultured / metabolism

Substances

  • Antibodies, Monoclonal
  • Antibodies, Neoplasm
  • Immunoglobulin M
  • Interleukin-2
  • Interleukin-5
  • Interleukins
  • Receptors, Immunologic
  • Receptors, Interleukin-2