ANTIGEN-INDUCED RECRUITMENT OF EOSINOPHILS - IMPORTANCE OF CD4(-CELLS, IL5, AND MAST-CELLS() T)

Authors
Citation
Jt. Hom et T. Estridge, ANTIGEN-INDUCED RECRUITMENT OF EOSINOPHILS - IMPORTANCE OF CD4(-CELLS, IL5, AND MAST-CELLS() T), Clinical immunology and immunopathology, 73(3), 1994, pp. 305-311
Citations number
33
Categorie Soggetti
Pathology,Immunology
ISSN journal
00901229
Volume
73
Issue
3
Year of publication
1994
Pages
305 - 311
Database
ISI
SICI code
0090-1229(1994)73:3<305:AROE-I>2.0.ZU;2-1
Abstract
Eosinophils of sensitized mice readily recruit to the site of antigen challenge. In the present study, experiments were performed to determi ne the involvement of different cell types in the antigen-induced recr uitment of eosinophils. We demonstrated that a single treatment with a nti-L3T4 monoclonal antibody (mAb) on the day of allergen challenge si gnificantly decreased antigen-induced recruitment of eosinophils. Trea tments with anti-L3T4 mAb during the sensitization period also caused a substantial reduction in the migration of eosinophils into the site of challenge with antigen. Thus, it appears that both stages of eosino phil recruitment, sensitization and antigen-challenge, are dependent u pon the presence of L3T4(+) T cells, Moreover, while treatments with a nti-IL5 mAb blocked eosinophil migration, anti-IL2 mAb failed to alter the antigen-induced recruitment of eosinophils. In addition, signific ant numbers of eosinophils from the mast-cell-deficient mice were foun d to migrate into the peritoneal cavities upon allergen challenge. Eos inophil migration was also observed in several mouse strains of differ ent H-2 haplotypes. The present findings suggest that CD4(+) T cells a nd IL5 but not IL2 may play important roles in modulating the recruitm ent of eosinophils. Moreover, the involvement of mast cells does not a ppear to be essential for eosinophil migration. Finally, the developme nt of antigen-induced recruitment of eosinophils is probably not under the immunogenetic regulation by genes within the H-2 complex. (C) 199 4 Academic Press, Inc.