Lee M, Hirokawa M, Miura A B
Third Department of Internal Medicine, Akita University School of Medicine, Japan.
Leuk Res. 1993 Jan;17(1):89-95. doi: 10.1016/0145-2126(93)90145-b.
We investigated the mechanisms of allogeneic stimulation induced TNF-alpha production in vitro by using human peripheral blood mononuclear cells (PBMC) and Daudi lymphoblastoid B-cells. PBMC produced TNF-alpha in response to mitomycin C-treated or paraformaldehyde-fixed Daudi cells, reaching a peak level after 4-6 h of culture. Monocytes were identified as the major source of TNF-alpha produced during allogeneic cell interaction. The second potent producer of TNF-alpha was E-rosette non-forming natural killer cells. Purified T-cells did not produce significant levels of TNF-alpha, even in the presence of IL-1 and IL-6. Interleukin-4 (IL-4) down-regulated TNF-alpha production by monocytes, but in contrast interferon-gamma (IFN-gamma) moderately enhanced TNF-alpha production. Our results indicate that monocytes are mainly responsible for the production of TNF-alpha in response to allogeneic stimulation, and T-cells modulate monocyte function by their soluble factors.
