Endogenous IFNp induction

Circumstantial evidence points to a low level of IFNp production under various conditions in cell culture and in vivo in the absence of known IFN inducers, a situation which has been described as physiological, spontaneous or autocrine IFN|3 production. This endogenous IFN(3 has been implicated in control of cell growth and differentiation. Primary mouse macrophages proliferate in response to macrophage colony-stimulating factor (M-CSF). Inclusion of an antimouse IFNa/p serum further stimulates the mitogenic response and increases the susceptibility of the culture to virus infection. In mouse myeloid Ml cells, IFN|3 mRNA has been detected following differentiation by cytokines (e.g. M-CSF, TNFa, interleukin 6 (IL-6)) and differentiation was inhibited by antilFNp serum. Activities similar to those of IFNfJ have also been demonstrated in dimethyl sulfoxide (DMSO(-differentiated Friend erythroleukemia cells and in phorbol-12-mvr-istatc-13-acetate (PMA) differentiated U937 cells.

Endogenous IFN3 production is not restricted to cells of hematopoietic origin; IFN(3 RNA has been found in IE-1- and TNF-treated Hep-2 cells and is of crucial importance to the antiviral activity of TNF, whereas in FS-4 fibroblasts the mitogenic stimulus provided by TNF is enhanced by antibodies against IFN (3.

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