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Pulmonary Center and Evans Memorial Department of Medicine, Boston University School of Medicine, Boston, MA 02118
IL-16, in a CD4-dependent manner, induces high affinity IL-2R
(CD25) selectively on CD4+ T cells. Based on this
observation, we determined the relative effects of IL-16 on IL-2R
,
ß, and 
expression on CD4+ T cells and of IL-16/IL-2
cotreatment of resting human PBMC obtained from normal individuals on
CD4+ T cell proliferation and cytokine production, in
vitro. IL-16 increased CD4+ T cell IL-2R and ß
expression, but had no effect on expression of IL-2R. There was
marked synergy of thymidine uptake and expansion of CD4+ T
cell numbers in the presence of IL-16 and IL-2 or IL-16 and IL-15
compared with the responses to any of the cytokines alone. By 4 wk,
IL-16/IL-2-cotreated PBMC cultures were predominantly CD4+,
CD25+ CD45RO T cells. Of the cytokines measured, IL-16
treatment alone was sufficient to induce synthesis of
granulocyte-macrophage CSF by 2 wk. IL-16/IL-2 cotreatment did not
appear to induce selective proliferation of any Th subset, as cytokines
of both Th1 (e.g., IFN-) and Th2 (e.g., IL-5) types were synthesized
by the expanded cell populations at 2 and 4 wk. These results suggest
that IL-16 can prime CD4+ T cells for IL-2 responsiveness,
and therefore may be a useful adjunct to IL-2 therapy for immune
reconstitution in disease or therapeutic conditions resulting in
CD4+ T cell depletion.
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