Transferrin is an essential requirement for lymphocyte proliferation, because it supplies activated lymphocytes with iron needed for cell proliferation. However, during inflammation or an immune response, the iron content of circulating transferrin, which is of hepatic origin, decreases. It is hypothesized that activated lymphocytes may therefore obtain transferrin-iron from an alternative source, and we have investigated the possibility that transferrin is synthesized locally in lymphoid tissues. It was found that lymph node cells from mice stimulated in vivo with Freund's complete adjuvant were able to synthesize transferrin, and this was because of the macrophage rather than the lymphocyte population. Transferrin synthesized by mouse lymph node or peritoneal macrophages contained iron and was able to promote mouse lymphocyte proliferation. Peritoneal macrophages activated in vivo synthesized more transferrin, released more transferrin-bound iron, and were more effective than resident macrophages at enhancing lymphocyte proliferation. These results suggest that transferrin synthesized by macrophages acts in a paracrine manner to support lymphocyte proliferation, thus eliminating possible detrimental effect of hypoferremia on the immune system.
We have investigated transferrin synthesis by human and mouse lymphoid and myeloid cells. It was found that transferrin synthesis is a property of mouse but not human macrophages, whereas in man T lymphocytes synthesised transferrin. Synthesis by mouse macrophages showed a dose‐dependent increase in response to γ‐interferon (γ‐IFN), but iron added as ferric nitrilotriacetate had no effect. Macrophage‐derived transferrin was found to contain iron already bound to it and was able to support Con A‐stimulated mouse lymphocyte proliferation.
Transferrin is an essential requirement for lymphocyte proliferation, because it supplies activated lymphocytes with iron needed for cell proliferation. However, during inflammation or an immune response, the iron content of circulating transferrin, which is of hepatic origin, decreases. It is hypothesized that activated lymphocytes may therefore obtain transferrin-iron from an alternative source, and we have investigated the possibility that transferrin is synthesized locally in lymphoid tissues. It was found that lymph node cells from mice stimulated in vivo with Freund's complete adjuvant were able to synthesize transferrin, and this was because of the macrophage rather than the lymphocyte population. Transferrin synthesized by mouse lymph node or peritoneal macrophages contained iron and was able to promote mouse lymphocyte proliferation. Peritoneal macrophages activated in vivo synthesized more transferrin, released more transferrin-bound iron, and were more effective than resident macrophages at enhancing lymphocyte proliferation. These results suggest that transferrin synthesized by macrophages acts in a paracrine manner to support lymphocyte proliferation, thus eliminating possible detrimental effect of hypoferremia on the immune system.
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