Impaired contact hypersensitivity to trinitrochlorobenzene in interleukin-4-deficient mice

Citation
F. Dieli et al., Impaired contact hypersensitivity to trinitrochlorobenzene in interleukin-4-deficient mice, IMMUNOLOGY, 98(1), 1999, pp. 71-79
Citations number
35
Categorie Soggetti
Immunology
Journal title
IMMUNOLOGY
ISSN journal
00192805 → ACNP
Volume
98
Issue
1
Year of publication
1999
Pages
71 - 79
Database
ISI
SICI code
0019-2805(199909)98:1<71:ICHTTI>2.0.ZU;2-O
Abstract
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.