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Modified T‐cell activation pattern during specific immunotherapy (SIT) in cat‐allergic patients
Author(s) -
Nicole Meissner,
S Kochs,
J. Coutelle,
Fatimah Kussebi,
C Baumgarten,
Henning Løwenstein,
G. Kunkel,
Harald Renz
Publication year - 1999
Publication title -
clinical and experimental allergy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.462
H-Index - 154
eISSN - 1365-2222
pISSN - 0954-7894
DOI - 10.1046/j.1365-2222.1999.00562.x
Subject(s) - immunotherapy , medicine , immunology , allergic reaction , allergy , immune system
Objective The aim of the study was to analyse early effects of specific immunotherapy (SIT) on immune functions in cat‐allergic patients. Methods Immunological responses of peripheral blood mononuclear cells from eight cat‐allergic patients were analysed before and after SIT in comparison with 11 nonallergic controls. Cells were stimulated in vitro with either bacterial superantigen, mitogen, or cat allergen. Production of IL‐12 and TH1/TH2 cytokines was analysed by ELISA and lymphocyte subset distribution was assessed by flow‐cytometry. Results We found a significantly reduced secretion of IL‐12 ( P < 0.05) from cells of allergic individuals compared with the controls. This finding was associated with significantly lower IFN‐γ production after stimulation with allergen ( P < 0.05) that did not increase during SIT. However, no significant differences were seen after stimulation with mitogen indicating an allergen specific IFN‐γ secretion response in allergic individuals. Prior to SIT IL‐5 production was significantly higher in cells of allergic donors stimulated with allergen < 0.005 or mitogen (< 0.05). After reaching the maintenance dose for SIT, allergen‐induced IL‐5 production returned to normal levels, whereas it remained elevated after stimulation with mitogen. These changes were associated with a reduced frequency of CD45 RO T cells following SIT. Conclusion These results suggest that SIT exerts early effects on allergen‐specific T‐cell responses with selective inhibition of the up‐regulated TH2 immune response.