Different role of IL‐4 in the onset of hapten‐induced contact hypersensitivity in BALB/c and C57BL/6 mice

Abstract

1 To study the role of interleukin (IL)-4 in the onset of contact hypersensitivity (CH) in mice, the e ect of IL-4 gene-depletion and anti-IL-4 monoclonal antibody treatment on dinitro¯uorobenzene (DNFB)-induced CH was examined. Simultaneously, to clarify the e ect of background gene, DNFB-induced CH in BALB/c and C57BL/6 mice was compared. 2 Five repeated topical applications of DNFB to the ears of mice resulted in CH of the ears in terms of increases in ear thickness and histopathological changes. The magnitude of ear thickness increase in BALB/c mice was almost three times greater than that in C57BL/6 mice. 3 The CH in BALB/c mice was signi®cantly suppressed by IL-4 gene-depletion and anti-IL-4 monoclonal antibody treatment. In contrast, the symptoms of dermatitis in C57BL/6 mice were slightly a ected by the same treatment. These changes corresponded well to the production of speci®c IgE antibody. 4 Total IgE antibody production and the expression of productive Ce mRNA were dramatically suppressed by IL-4 gene-depletion and anti-IL-4 treatment in BALB/c and C57BL/6 mice. Neither total IgG nor IgM levels in either strain of mice was altered by depletion of IL-4. 5 The expression of IFN-g in the skin lesion was dramatically suppressed by IL-4 gene-depletion in BALB/c mice, but not in C57BL/6 mice. 6 These ®ndings indicate that IL-4 plays an important role in the onset of DNFB-induced CH in BALB/c mice, but not in C57BL/6 mice.

A targeted mutation in the IL-4Rα gene protects mice against autoimmune diabetes

“…Thus, IL-4-deficient BALB͞c mice and BALB͞c mice treated with anti-IL-4 antibody exhibit diminished contact hypersensitivity responses to dinitrofluorobenzine; IFN-␥ production was diminished at the site of challenge (35,36). IL-4Ϫ͞Ϫ mice failed to develop contact hypersensitivity to trinitrochlorobenzine, although in this instance they did develop cells capable of producing TH1 cytokines (37).…”

Dual Role of Interleukin-4 (IL-4) in Pulmonary Paracoccidioidomycosis: Endogenous IL-4 Can Induce Protection or Exacerbation of Disease Depending on the Host Genetic Pattern

“…Similar findings have been described for the development of hapten-induced contact hypersensitivity. IL-4 played an important role in the onset of hapten-induced reactions in BALB/c mice but not in C57BL/6 mice (35).…”

SH2 Domain-Containing Phosphatase 2 Is a Critical Regulator of Connective Tissue Mast Cell Survival and Homeostasis in Mice

“…IgE-mediated passive cutaneous reactions, which are dependent on mast cells (8), were performed essentially as described previously (36). Control (shp2 fl/fl ) and MC-shp2 KO mice (5 mice per genotype from 2 separate experiments) were sensitized by tail vein injection of antidinitrophenyl (anti-DNP)-IgE (2 g in 0.1 ml saline).…”