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The Journal of Immunology, Vol 140, Issue 4 1168-1174, Copyright © 1988 by American Association of Immunologists
ARTICLES |
K Nakanishi, T Yoshimoto, Y Katoh, S Ono, K Matsui, K Hiroishi, T Noma, T Honjo, K Takatsu and K Higashino
Third Department of Internal Medicine, Hyogo College of Medicine, Japan.
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.
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