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Clinical and Diagnostic Laboratory Immunology, November 2002, p. 1169-1174, Vol. 9, No. 6
1071-412X/02/$04.00+0 DOI: 10.1128/CDLI.9.6.1169-1174.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.
Department of Microbiology and Immunology and Division of Bacterial Toxins, Research Center for Infectious Disease, Aichi Medical University, Nagakute, Aichi 480-1195,1 Department of Medicine, Hyogo College of Medicine, Nishinomiya, Hyogo 663-8501, Japan2
Received 19 February 2002/ Returned for modification 8 May 2002/ Accepted 17 July 2002
The in vitro effects of gamma interferon (IFN-
) 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-
, 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-
. 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-
-induced phosphorylation of p38 MAP kinase and the appearance of macrophage-like cells. IFN-
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-
, a Th1 cytokine, and IL-4, a Th2 cytokine, may have clear immunological significance.
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