International Immunology Advance Access originally published online on November 4, 2004
International Immunology 2004 16(12):1781-1788; doi:10.1093/intimm/dxh179
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© 2004 The Japanese Society for Immunology
Negative regulatory effect of histamine in DNFB-induced contact hypersensitivity
1 Department of Dermatology and Allergology, 2 Dermatological Research Group of the Hungarian Academy of Sciences at the Department of Dermatology and Allergology, 3 Institute of Surgical Research, University of Szeged and 4 Department of Genetics, Cell and Immunobiology, Semmelweis University, Budapest, Hungary
Correspondence to: E. Garaczi; Email: egaraczi{at}yahoo.com
Histamine plays an important role in the regulation of various immunological functions. To evaluate the role of histamine in contact hypersensitivity, contact dermatitis was induced with dinitrofluorobenzene (DNFB) in histidine decarboxylase knockout (HDC–/–) histamine-deficient and wild-type mice. The DNFB-induced increase of the ear thickness was significantly higher in HDC–/– mice than in wild-type mice. Using flow cytometry, significantly lower percentages of CD4+ Th and CD8+ Tc cells, and significantly higher percentages of CD45R+ B cells were observed in the regional lymph nodes in HDC–/– mice than in wild-type mice. In the ear specimens of both groups, the majority of the infiltrating cells were neutrophils and macrophages at 24 and 48 h after challenge. Using immunohistochemistry, we observed significantly more CD45+ leukocytes in HDC–/– mice than in wild-type mice. The expression of Th1 (IL-2, IFN-
, TNF-
) and Th2 (IL-4) mRNAs was examined by quantitative real time RT–PCR in the ear samples. The levels of Th1 cytokine mRNAs both at 24 and 48 h after challenge and IL-4 mRNA at 48 h showed a significantly higher increase in HDC–/– mice than in wild-type mice. These results suggest that histamine plays a negative immunoregulatory role in DNFB-induced contact hypersensitivity.
Keywords: delayed type hypersensitivity, histidine decarboxylase, immunoregulation
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