Role of CD4+ T lymphocytes and interleukin-5 in antigen-induced eosinophil recruitment into the site of cutaneous late-phase reaction in mice.
Previous studies suggested that the eosinophil recruitment into the site of cutaneous late-phase reaction (LPR) was dependent on IgE antibody and mast cells. In this study, we determined the role of CD4+ T cells and CD8+ T cells in causing antigen-induced eosinophil recruitment of LPR in mouse skin. Eosinophil infiltration into the subcutaneous tissue of ovalbumin (OVA)-sensitized BALB/c mice was biphasic, reaching the first peak at 6 h after the subcutaneous challenge with OVA and the second peak at 24 to 48 h. The in vivo depletion of CD4+ T cells by pretreatment with anti-L3T4 monoclonal antibody (mAb) significantly decreased the second peak (at 24 h and 48 h), but not the first peak (at 6 h), of OVA-induced eosinophil infiltration into the skin of OVA-sensitized mice. However, the depletion of CD8+ T cells by pretreatment with anti-Lyt-2 mAb had no significant effect on either the first peak or second peak of OVA-induced cutaneous eosinophilia. Pretreatment with anti-murine interleukin-5 (IL-5) mAb also decreased the second peak, but not the first peak, of OVA-induced cutaneous eosinophilia. In contrast to the inhibitory effects of depletion of CD4+ T cells and of anti-IL-5 mAb on the second peak of antigen-induced cutaneous eosinophilia, disodium cromoglycate and a selective antagonist for platelet activating factor (PAF) CV-6209 decreased the first peak of OVA-induced cutaneous eosinophilia in the mouse. These results indicate that CD4+ T cells, but not CD8+ T cells, cause the second peak of antigen-induced eosinophil recruitment of cutaneous LPR and that IL-5 mediates this eosinophil recruitment. In contrast, the first peak of antigen-induced eosinophil recruitment of cutaneous LPR is mediated by mast cells and PAF.
Second Department of Internal Medicine, Chiba University School of Medicine, Japan.
I
I
Iwamoto
S
S
Tomoe
H
H
Tomioka
K
K
Takatsu
S
S
Yoshida
D000818:Animals; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology*; D015550:Cell Degranulation; D002465:Cell Movement; D004205:Cromolyn Sodium / Q000494:pharmacology; D004804:Eosinophils / Q000502:physiology*; D006967:Hypersensitivity / Q000276:immunology*; D015848:Interleukin-5 / Q000502:physiology*; D008212:Lymphocyte Depletion; D008407:Mast Cells / Q000502:physiology; D051379:Mice; D008807:Mice, Inbred BALB C; D010972:Platelet Activating Factor / Q000037:antagonists & inhibitors / Q000502:physiology; D012867:Skin / Q000276:immunology*; D013997:Time Factors
D015848:Interleukin-5; D010972:Platelet Activating Factor; D004205:Cromolyn Sodium