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T helper-2 (Th2) lymphocytes in chronic rhinitis
S28 Abstracts
SATURDAY
T Helper-2 (Th2) Lymphocytes in Chronic Rhinitis: Initiators of the IL-4 Response but Superceded by Mast Cells D. Powe1, C. Jagger1, M. Sisson1, N. S. Jones2; 1School of Molecular Medical Sciences, Queen’s Medical Centre, Nottingham, UNITED KINGDOM, 2Department of Medical and Surgical Sciences, Queen’s Medical Centre, Nottingham, UNITED KINGDOM. RATIONALE: We tested the hypothesis that idiopathic rhinitis (IR) resembles persistent localized allergic rhinitis (PAR) in showing a Th2driven pathophysiology, characterized by increased interleukin (IL)-4 gene transcripts in nasal mucosa and increased IL-4+ peripheral blood mononuclear cells (PBMC). METHODS: IL-4 and IFNgamma; gene transcripts in PAR (12), IR (13) and normal control (10) nasal mucosa were quantified using realtime comparative PCR. A subset of each group underwent PBMC stimulation with anti-CD3 followed by FACS analysis to immunophenotype the proportion of Th1 and Th2 lymphocytes. RESULTS: Realtime PCR: IL-4 (P=0.02) and IFNgamma; (P=0.04) gene levels were significantly increased in the mucosa of PAR compared to the control group, but not to IR (P=0.6). IR showed a trend towards increased IL-4 mRNA levels (P=0.058). Anti-CD3 PBMC stimulation: PAR showed an increase in the IFNgamma+ PBMC population compared to control PBMC (P=0.006). CONCLUSIONS: Anti-CD3 stimulation is a good indicator of allergenstimulated PBMC response. The Th1 (IFNgamma) response seen in PAR mucosa is probably attributable to PBMC. Importantly, our results suggest that mucosal IL-4 gene up-regulation seen in PAR and IR is not due to T lymphocytes. Previously, we showed that IL-4+ mast cells are a feature of PAR and IR, and most probably account for the increased IL-4 levels seen in nasal mucosa. We propose that T cells are not inflammatory protagonists in the on-going inflammation in chronic rhinitis. Funding: University Monies
13
J ALLERGY CLIN IMMUNOL FEBRUARY 2004
SATURDAY
T Helper-2 (Th2) Lymphocytes in Chronic Rhinitis: Initiators of the IL-4 Response but Superceded by Mast Cells D. Powe1, C. Jagger1, M. Sisson1, N. S. Jones2; 1School of Molecular Medical Sciences, Queen’s Medical Centre, Nottingham, UNITED KINGDOM, 2Department of Medical and Surgical Sciences, Queen’s Medical Centre, Nottingham, UNITED KINGDOM. RATIONALE: We tested the hypothesis that idiopathic rhinitis (IR) resembles persistent localized allergic rhinitis (PAR) in showing a Th2driven pathophysiology, characterized by increased interleukin (IL)-4 gene transcripts in nasal mucosa and increased IL-4+ peripheral blood mononuclear cells (PBMC). METHODS: IL-4 and IFNgamma; gene transcripts in PAR (12), IR (13) and normal control (10) nasal mucosa were quantified using realtime comparative PCR. A subset of each group underwent PBMC stimulation with anti-CD3 followed by FACS analysis to immunophenotype the proportion of Th1 and Th2 lymphocytes. RESULTS: Realtime PCR: IL-4 (P=0.02) and IFNgamma; (P=0.04) gene levels were significantly increased in the mucosa of PAR compared to the control group, but not to IR (P=0.6). IR showed a trend towards increased IL-4 mRNA levels (P=0.058). Anti-CD3 PBMC stimulation: PAR showed an increase in the IFNgamma+ PBMC population compared to control PBMC (P=0.006). CONCLUSIONS: Anti-CD3 stimulation is a good indicator of allergenstimulated PBMC response. The Th1 (IFNgamma) response seen in PAR mucosa is probably attributable to PBMC. Importantly, our results suggest that mucosal IL-4 gene up-regulation seen in PAR and IR is not due to T lymphocytes. Previously, we showed that IL-4+ mast cells are a feature of PAR and IR, and most probably account for the increased IL-4 levels seen in nasal mucosa. We propose that T cells are not inflammatory protagonists in the on-going inflammation in chronic rhinitis. Funding: University Monies
13
J ALLERGY CLIN IMMUNOL FEBRUARY 2004