A subset of type 2, but not type 1, CD4 T cell clones expresses IL-3R
and can be stimulated by IL-3. Expression of IL-3R on these type 2 T c
ell clones is induced by TCR stimulation, and subsequent stimulation b
y IL-3 augmented the proliferation of and IL-4 production by these cel
ls. This augmented response is inhibited by anti-IL-4 mAb, suggesting
the involvement of IL-4 in this response. In place of TCR stimulation,
treatment of these type 2 CD4 T cell clones with PMA rendered them re
sponsive to further stimulation of proliferation by IL-3, indicating t
he cooperation between thr IL-SR-elicited signals and PKC-mediated sig
nals in stimulating proliferation. Although the augmentation of the TC
R-mediated proliferative response by IL-3 was mainly due to the increa
sed production of IL-4, we also demonstrated the presence of IL-4-inde
pendent mechanism mediating the response to IL-3. In situ, we found th
at splenic T cells could be induced to respond to IL-3 by TCR stimulat
ion. Thus, IL-3 can stimulate a specific population of T cells and inf
luence the immune response.