Resting human T cells are known to express significant numbers of intermedi
ate but none or barely detectable low and high affinity IL-2 receptors (IL-
2R). IL-2 alone failed to induce proliferation In these cells. However, in
presence of small proportion of autologous monocytes, as low as 22 pM, IL-2
induced high levels of proliferation in resting T cells. Introduction of a
semi permeable membrane between the two cell types or addition of an anti-
CD11b mAb inhibited such induction of proliferation by IL-2. Neither recomb
inant IL-1 nor IL-1-containing cell-free extracts from activated monocytes
substituted for intact monocytes. Autologous B cells failed to replace mono
cytes. Using antigen-specific cloned human T cells we have shown a lack of
requirement for antigen. The proliferation was inhibited by anti-IL-2R alph
a mAb. IL-2 appears to be unique since neither IL-4 nor IL-6, alone or in p
resence of monocytes, led to induction of proliferation in resting T cells.
Combination of IL-2 and monocytes induced proliferation in all T cell subp
opulations (CD4(+), CD8(+), CD45RA(+) and CD45RO(+)) and antigen-specific c
lones examined. It also induces mRNA and surface expression of IL-2R alpha,
appearance of high affinity IL-2R and induction of proliferation in large
proportions of T cells. As in humans, the IL-2 induction of proliferation i
n murine resting T cells required contact with syngeneic monocytes, suggest
ing that such a mechanism of T cells activation is highly conserved.