Figure 17.  Anti-IL2Ra and anti-IL2/IL15Rb mAbs inhibit the proliferation of NK cells
		20nM IL2					2nM or 0.2nM IL2
	Proliferation [percent of that in the absence of antibodies]
The finding that NK cells express IL2Ra chains raises the question of whether these can participate in the
delivery of proliferative signals.  To test this the following experiment was performed.
CD4 T cells, CD8 T cells, immature NK cells, and mature NK cells were incubated in medium containing either
high dose [20nM] or low dose [2nM for NK cells, 0.2nM for T cells] IL2 together with 7D4 and PC61 anti-IL2Ra
mAb, TMb1 anti-IL2/IL15Rb mAb, or both mAbs together.  Cells were labelled with 3H-TdR for the last 4hr of
a 48hr incubation.  Figures show the percentage thymidine uptake in each group compared to cells cultured
in the absence of mAbs.
Conclusions
1.  As shown by the top left graph, anti-IL2Ra mAbs are unable to inhibit the proliferation of NK cells [or T cells] when
growing in 20nM IL2.
2.  However, as shown by the middle left graph, their proliferation under these conditions is inhibited by anti-IL2Rb mAb.
3.  Puzzlingly, but in agreement with the observations of others, the proliferation of T cells is not inhibited by anti-IL2Rb
mAb alone, but is inhibited by a combination of anti-IL2Ra and anti-IL2Rb mAbs [bottom left graph].
4.  When IL2 concentrations are reduced, anti-IL2Ra mAbs can completely inhibit proliferation not only of T cells but
also of NK cells [top right].
5.  Thus, the limited proliferation of NK cells that occurs in the presence of 2nM IL2 is presumably dependent on high
affinity IL2 receptors involving the IL2Ra chains.  Whether the failure of anti-IL2Ra mAbs to block proliferation in the
presence of 20nM IL2 is because the high concentration of IL2 competes effectively with antibody for binding to IL2Ra,
or because most of the proliferation is being driven through low affinity receptors that involve IL2Rb but not IL2Ra chains
is unclear.