Ogawa K, Kaminuma O, Kikkawa H, Kameda R, Ikezawa K, Suko M, Okudaira H, Akiyama K, Mori A
Department of Medicine and Physical Therapy, Faculty of Medicine, University of Tokyo, Japan.
Int Arch Allergy Immunol. 1999;120 Suppl 1:15-8. doi: 10.1159/000053586.
We have recently demonstrated that allergic eosinophilic inflammation is transferred to unprimed mice by infusing IL-5-producing CD4+ T cells. The contribution of mast cells to the development of eosinophilic inflammation is controversial.
To clarify the possible different roles of CD4+ T cells and mast cells in eosinophilic inflammation, we compared antigen-induced airway eosinophilia between mast-cell-deficient mice (WBB6F1-W/W(v)) and their congenic normal littermates (WBB6F1-+/+).
The time course study indicated that equivalent numbers of eosinophils were recruited into the airway of both +/+ and W/W(v) mice 6, 24, 96, and 216 h after antigen challenge, whereas the number of eosinophils 48 h after antigen challenge was significantly lower in W/W(v) compared to +/+ mice. Administration of either anti-CD4 or anti-IL-5 monoclonal antibody almost completely inhibited antigen-induced eosinophil recruitment in W/W(v) mice 48 h after antigen challenge. In contrast, the inhibitory effect of these antibodies in +/+ mice were partial (approximately 50% inhibition). Anti-CD4 and anti-IL-5 antibodies equally suppressed airway eosinophilia in both +/+ and W/W(v) mice 96 h after antigen challenge.
Our study indicates that CD4+ T cells are crucially involved in the development of allergic eosinophilic inflammation, while mast cells may play a supplemental role depending on the kinetics of the response.
