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Int Arch Allergy Immunol. 2007;144(1):69-78. Epub 2007 May 15.

Inductions of histidine decarboxylase in mouse tissues following systemic antigen challenge: contributions made by mast cells, non-mast cells and IL-1.

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  • 1Department of Molecular Regulation, Graduate School of Dentistry, Tohoku University, Sendai, Japan.



Previous findings suggest that antigen challenge (AC) may induce histidine decarboxylase (HDC) in cells other than mast cells (MCs) via MC-derived IL-1. We examined this hypothesis.


Mice were sensitized to ovalbumin. After the sensitization, an AC was delivered intravenously.


In control mice, AC markedly induced HDC at a postanaphylactic time in the liver, lung, spleen, and ears. In MC-deficient W/W(v) mice, AC also induced HDC, although the effect was weaker than in control mice. AC increased IL-1 in the tissues, the pattern being similar in W/W(v) and control mice. AC induced HDC similarly in IL-1-deficient and control mice. In control mice, AC decreased histamine in the tissues (except the liver) for several hours.


(1) AC induces HDC in both MC-dependent and MC-independent ways. (2) AC induces IL-1 mostly in non-MCs, but this IL-1 is not a prerequisite for the induction of HDC by AC. (3) HDC induction may contribute to the replenishment of the reduced pool of MC histamine in the anaphylactic period. (4) In the case of MC-dependent HDC induction, AC may stimulate MCs in such a way as to induce HDC within the MCs themselves, and/or AC-stimulated MCs may stimulate HDC induction in other cells, which will need to be directly identified in future studies.

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