Seasonal changes in suppressive capacity of CD4+ CD25+ T cells from patients with hayfever are allergen-specific and may result in part from expansion of effector T cells among the CD25+ population.
BACKGROUND
Suppression of allergen-stimulated peripheral blood CD4(+) CD25(-) effector T cells by CD4(+) CD25(+) regulatory T cells obtained from subjects with allergic rhinoconjunctivitis is reduced during the pollen season when compared with out of season.


OBJECTIVE
We examined possible explanations for this effect of seasonal pollen exposure on suppression of allergen responses.


METHODS
CD4(+) CD25(-) and CD4(+) CD25(+) T cells were isolated from blood obtained from 44 volunteers with allergic rhinoconjunctivitis during and out of the UK grass pollen season. Co-cultures were performed with grass pollen extract and house dust mite (HDM) to examine allergen specificity. The frequency of IL-5 and IL-10 producing cells was determined by ELISPOT and the expression of T cell activation markers and the CD25(+) regulatory T cell-associated transcription factor Foxp3 were examined. Lactic acid stripping of IgE was used to determine IgE dependence of T cell responses.


RESULTS
The seasonal reduction in suppression by CD4(+) CD25(+) T cells was confirmed and was shown to be allergen specific because suppression of HDM-stimulated cultures was not affected significantly. The CD4(+) CD25(+) population contained IL-5 and IL-10 producing cells but increases in their frequencies with seasonal pollen exposure were not significant. Both activation marker and Foxp3 expression increased during the pollen season. IgE stripping reduced CD4(+) and CD4(+) CD25(-) T cell responses to allergen, but had no effect on suppression by CD4(+) CD25(+) T cells.


CONCLUSIONS
The seasonal reduction in suppression of grass pollen-stimulated effector T cells by CD4(+) CD25(+) T cells is allergen specific and cannot be explained by increased IgE-facilitated allergen presentation. We suggest that changes in the proportion of effector to regulatory T cells among the CD25(+) population isolated may partially explain these findings, and that trafficking to the site of allergic disease may reduce allergen-specific regulatory T cell numbers in peripheral blood.
Anderson
A E
AE
Leukocyte Biology Section, National Heart and Lung Institute Division, Imperial College, Faculty of Medicine, London, UK.
Mackerness
K J
KJ
Aizen
M
M
Carr
V A
VA
Nguyen
D
D
Du Pre
F
F
Durham
S R
SR
Robinson
D S
DS
D000328:Adult; D000485:Allergens / Q000276:immunology / Q000378:metabolism; D005260:Female; D051858:Forkhead Transcription Factors / Q000096:biosynthesis / Q000276:immunology; D005786:Gene Expression Regulation / Q000276:immunology; D006801:Humans; D007073:Immunoglobulin E / Q000097:blood* / Q000276:immunology; D016753:Interleukin-10 / Q000097:blood* / Q000276:immunology; D015848:Interleukin-5 / Q000097:blood* / Q000276:immunology; D008297:Male; D006255:Rhinitis, Allergic, Seasonal / Q000097:blood* / Q000276:immunology; D012621:Seasons; D050378:T-Lymphocytes, Regulatory / Q000276:immunology / Q000378:metabolism*; D006113:United Kingdom
D000485:Allergens; C418974:FOXP3 protein, human; D051858:Forkhead Transcription Factors; C508609:IL10 protein, human; C508599:IL5 protein, human; D015848:Interleukin-5; D016753:Interleukin-10; D007073:Immunoglobulin E