We have examined the role of endogenously produced interleukin-4 (IL-4) in
the contact hypersensitivity (CH) reaction to the haptene trinitrochloroben
zene (TNCB). The CH reaction was abolished in IL-4 genetically deficient mi
ce (IL-4 KO), when compared to wild-type (wt) mice. The CH reaction was res
tored by treatment with IL-4 and further analysis revealed that IL-4 exerte
d its action both at the induction and effector stages of the CH reaction.
Despite failure to develop a CH reaction, IL-4 KO mice developed a T helper
type 1 (Th1) response to TNCB, in terms of lymphokine production in vitro.
Furthermore, the number of V gamma 3(+) cells accumulating in the lymph no
des of TNCB-immune IL-4 KO mice was normal. The recruitment of mononuclear
cells and vascular leakage at the challenge site were consistently reduced
in IL04 KO mice and were restored by injection of IL-4. This suggests that
IL-4 acts as a proinflammatory mediator in CH, perhaps favouring the accumu
lation of mononuclear cells at the site of inflammation. Among Th2-type cyt
okines, IL-13, but not IL-10, was shown to restore the CH reaction to TNCB
in IL-4 KO mice. However, IL-4 KO mice developed a normal CH response to ox
azolone, indicating that IL-4 was required for the CH reaction to TNCB, but
not for that to oxazolone.