ENFUMOSA (courriel: Chanez (at) montp.inserm.fr ) The European Network For Understanding Mechanisms of Severe Asthma BIOMED 2 Program - European Commission 4th quaterly meeting, with the support of INSERM and Merck Sharp & Dhome Laboratory February 13-14th 1998 in Montpellier- France (see programm, abstracts and experts comments )

Suppression of allergic airway inflammation in gd T-cell deficient mice.
C. Zuany-Amorim, C. Ruffie, P. Pereira, BB. Vargaftig and M. Pretolani.
Unite de Pharmacologie cellulaire/INSERM U285
and Unite d’Immunobiologie, Institut Pasteur, Paris, France.

gd T-cells residing primarily in epithelia-rich tissues are claimed to play a role in the emergence or the resolution of inflammatory immune processes. We examined the antigen-induced cellular rec~uitment, cytokine release and antibody titers in ovalbumin-sensitized gd T-cell-deficient mice and in control Balb/c littermates. Mice were sensitized systemically with ovalbumin (OVA) and challenged 3 times via the intra-nasal route with 20 ug OVA or saline, 3 days apart. Three days after the last challenge, Balb/c mice showed a massive eosinophil, CD4+ and CD8+ T-cell accumulation in the broncho-alveolar lavage (BAL) fluid, a rise in the levels of interleukin (L)-5 and a decrease in those of IL- 10. An increase in the number of BAL gd T-cells, mostly of the CD4- CD8- phenotype, was also detectod by flow cytometry after the challenge. Total IgE, but not IgG, increased in the serum of antigen- as opposed to saline-challenged Balb/c mice (p < 0.05). In contrast, gd T-cell deficient OVA-challenged mice showed very low numbers of CD4+ and CD8+ T-cells and eosinophils and practically no release of IL-5 in BAL fluid. In contrast, a markod increase in interferon-y production and no changes in the amounts of IL- 10 were detected in OVA-challenged gd T-cell deficient, as compared to Balb/c control mice. Total IgE in OVA-challenged y6-T-cell deficient vs Balb/c mice were decreased by 70 % (p < 0.05), while IgG were unaffectod. We conclude that gd T-cells play a major role in the initiation and progression of IgE-mediated allergic airway inflammation in sensitized mice.