Association between specific timothy grass antigens and changes in TH1- and TH2-cell responses following specific immunotherapy - 07/11/14
Abstract |
Background |
Different populations of T cells are involved in the pathogenesis of allergic diseases.
Objective |
We investigated changes in TH-cell populations in patients with allergies after specific immunotherapy (SIT).
Methods |
PBMCs were isolated from patients with allergies who received SIT and those who did not (controls). We tested the ability of peptides from 93 timothy grass (TG) proteins to induce T-cell responses (cytokine production). We used ELISPOT and staining assays for intracellular cytokines to measure the production of IL-4, IL-5, IL-13, IFN-γ, and IL-10.
Results |
Compared with PBMCs from controls, PBMCs from patients who received SIT produced lower levels of TH2 cytokines on incubation with several different TG peptides. These data were used to select 20 peptides to be tested in an independent cohort of 20 patients with allergies who received SIT and 20 controls. We again observed a significant decrease in the production of TH2 cytokines, and an increase in the production of the TH1 cytokine IFN-γ, in PBMCs from the validation groups. These changes correlated with improved symptoms after SIT. Immunization with this selected pool of peptides (or their associated antigens) could protect a substantial proportion of the population from TG allergy.
Conclusions |
We observed a significant decrease in the production of TH2 cytokines by PBMCs from patients who received SIT for TG allergy compared to those who did not. These changes might be used to monitor response to therapy. The decrease occurred in response to antigens that elicit little (if any) IgE responses; these antigens might be developed for use in immunotherapy.
Le texte complet de cet article est disponible en PDF.Key words : T cells, specific immunotherapy, timothy grass, cytokine
Abbreviations used : ATGA, KTGA, MNA, SFC, SIT, TG
Plan
| This project has been funded in whole or in part with federal funds from the National Institute of Allergy and Infectious Diseases, National Institutes of Health (NIH), the Department of Health and Human Services (under contract no. HHSN272200700048C and U19 grant no. U19 AI100275). This project was partially supported by the NIH (grant ULRR031980 for years 1 and 2 of Clinical and Translational Science Award [CTSA] funding and grant no. UL1TR000100 for year 3 and beyond of CTSA funding). R.A. was supported by the NIH (grant no. RO1 AI091614). |
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| Disclosure of potential conflict of interest: V. Schulten, V. Tripple, J. Sidney, J. Greenbaum, A. Frazier, B. Peters, and A. Sette have received research support from the National Institutes of Health (NIH; U19 grant nos. ALL00275 and HHSN272200700048C) and have received royalties from ALK-Abelló. R. Alam has received research support from the NIH (RO1 AI091614). D. Broide has received research support from the NIH (ULRR031980 and ULITR000100), the Immune Trial Network, and the Department of Defense. |
Vol 134 - N° 5
P. 1076-1083 - novembre 2014 Retour au numéro
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