Change of mouse CD5(+) B1 cells to a macrophage-like morphology induced by gamma interferon and inhibited by interleukin-4.
The in vitro effects of gamma interferon (IFN-gamma) on the mouse CD5(+) B1-cell line, TH2.52, a hybridoma between mouse B lymphoma and mouse splenic B cells that expresses a series of B1 markers, were investigated. A significant number of macrophage-like cells appeared in the cultures of TH2.52 cells exposed to IFN-gamma, these adhering to plastic dishes and exhibiting phagocytic activity. Positive for esterase staining, the macrophage-like cells returned to the original TH2.52 morphology upon removal of IFN-gamma. The change was prevented by treatment with SB202190, an inhibitor of p38 mitogen-activated protein (MAP) kinase and by transfection of a p38 MAP kinase dominant-negative mutant. Further, interleukin-4 (IL-4) inhibited IFN-gamma-induced phosphorylation of p38 MAP kinase and the appearance of macrophage-like cells. IFN-gamma and IL-4 exhibited contradictory actions on morphological change of CD5(+) B1 cells into macrophage-like cells. Differential regulation of CD5(+) B1 cells by IFN-gamma, a Th1 cytokine, and IL-4, a Th2 cytokine, may have clear immunological significance.
Koide
Naoki
N
Department of Microbiology and Immunology, Research Center for Infectious Disease, Aichi Medical University, Nagakute, Aichi 480-1195, Japan.
Sugiyama
Tsuyoshi
T
Mori
Isamu
I
Mu
Mya Mya
MM
Hamano
Teruaki
T
Yoshida
Tomoaki
T
Yokochi
Takashi
T
D000818:Animals; D001402:B-Lymphocytes / Q000166:cytology / Q000187:drug effects*; D018956:CD5 Antigens / Q000032:analysis*; D002460:Cell Line; D007371:Interferon-gamma / Q000494:pharmacology*; D015847:Interleukin-4 / Q000494:pharmacology*; D008264:Macrophages / Q000166:cytology* / Q000502:physiology; D051379:Mice; D020928:Mitogen-Activated Protein Kinases / Q000502:physiology; D048051:p38 Mitogen-Activated Protein Kinases
D018956:CD5 Antigens; D015847:Interleukin-4; D007371:Interferon-gamma; D020928:Mitogen-Activated Protein Kinases; D048051:p38 Mitogen-Activated Protein Kinases