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Next Article 
The role of calcium in lymphocyte proliferation. (An interpretive review)
AH Lichtman, GB Segel and MA Lichtman
A small quantity of extracellular calcium is required for the stimulation
of lymphocytes by mitogens such as plant lectins. Lectin binding to the
lymphocyte surface and early postbinding events that eventually lead to DNA
synthesis are calcium dependent. Mitogenic lectins such as PHA and Con-A
rapidly increase the size of an exchangeable pool of cell calcium and cause
a smaller rise in intracellular ionized calcium. The increase in ionized
calcium is so small (100-200 nM), however, that no increase in total cell
calcium is measurable. When lymphocytes are stimulated by a lectin, the
rate of calcium entry into the cell increases, but the plasma membrane
calcium extrusion pump can prevent the total cell calcium from increasing
measurably. The calcium ionophore A23187 is a lymphocyte mitogen and causes
an increase in the exchangeable, ionized, and total cell calcium. The
former two effects may be causal in mitogenesis; the latter effect is
cytotoxic. With A23187 treatment, the rate of calcium influx exceeds the
maximum rate of the plasma membrane extrusion pump and cell calcium
increases in proportion to the concentration of A23187. The mitochondria,
by virtue of their high membrane potential, provide a sink for the
buffering of cytoplasmic calcium after A23187 treatment. Thus, the plasma
membrane or mitochondria regulate the distribution of lymphocyte calcium
when the cell is stimulated by mitogenic lectins or ionophores. The
evidence strongly suggests that an alteration in calcium pools or an
increase in cytoplasmic ionized calcium plays a role in the initiation of
the biochemical reactions that lead to mitogen-induced lymphocyte
proliferation in vitro and, perhaps, to the immune response.
Volume 61,
Issue 3,
pp. 413-422,
03/01/1983
Copyright © 1983 by The American Society of Hematology
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