Physiology of IL3

An extremely potent molecule, IL-3 is detectable in in vitro bioassays in concentrations of 0.1 pM or less. The sensitivity of various target cells to the action of IL-3 varies considerably, probably due to differences in receptor levels. Thus, whereas certain IL-3-depen-dent mast cell lines, particularly those that have been in culture for many years, are sensitive to subpico-molar concentrations of IL-3 progenitor cells and stem cells may require 10-50-fold higher concentrations for maximal effects and some mature cells, such as macrophages, even higher concentrations.

As is the case with many peptide regulatory factors, it is likely that in many physiological circumstances IL-3 acts in the vicinity of the cell that has produced it. However, when there is relatively massive activation of T lymphocytes, for example in graft-versus-host disease, IL-3 can appear in the bloodstream and act systemically. IL-3 has a relatively short half-life in the blood, of the order of 40 minutes, and is destroyed at sites such as the renal tubule and liver.

Physiologically, IL-3 links activation of T lymphocytes and mast cells to stimulation of the generation of the accessory cells - granulocytes, phagocytes and platelets - which carry out defense and repair responses. It is thus an important participant in the response of the hematopoietic system to stress.

There is no good evidence that 11.-3 is normally-present in the blood or indeed is produced in a normal animal that is not undergoing some immunological stimulation. In particular, there is no evidence that bone marrow stromal cells produce IL-3. Thus there are no data to support the view that IL-3 is involved in regulating normal, steady-state hemato-poiesis. Mice lacking functional II.-3 genes have no overt phenotype and the hematopoietic system appears to develop normally.

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