Erika Garner-Spitzer1, Claudia Seidl-Friedrich2, Ines Zwazl3, Michael Hofer4, Tamar Kinaciyan5, Reinhart Jarisch6, Karin Stiasny7, Gerhard J Zlabinger8, Michael Kundi9, Ursula Wiedermann10. 1. Institute of Specific Prophylaxis and Tropical Medicine, Medical University of Vienna Kinderspitalgasse 15, A-1090 Vienna, Austria. Electronic address: erika.garner-spitzer@meduniwien.ac.at. 2. Institute of Specific Prophylaxis and Tropical Medicine, Medical University of Vienna Kinderspitalgasse 15, A-1090 Vienna, Austria. Electronic address: claudia.seidl-friedrich@meduniwien.ac.at. 3. Institute of Specific Prophylaxis and Tropical Medicine, Medical University of Vienna Kinderspitalgasse 15, A-1090 Vienna, Austria. Electronic address: ines.zwazl@meduniwien.ac.at. 4. Institute of Specific Prophylaxis and Tropical Medicine, Medical University of Vienna Kinderspitalgasse 15, A-1090 Vienna, Austria. Electronic address: michael.hofer@meduniwien.ac.at. 5. Department of Dermatology, Division of Immunology, Allergy and Infectious Diseases, Medical University of Vienna, Währinger Gürtel 18-20, A-1090 Vienna, Austria. Electronic address: tamar.kinaciyan@meduniwien.ac.at. 6. FAZ - Floridsdorf Allergy Center, Franz-Jonas-Platz 8/6, A-1210 Vienna, Austria. Electronic address: reinhart.jarisch@outlook.com. 7. Department of Virology, Medical University of Vienna, Kinderspitalgasse 15, A-1090 Vienna, Austria. Electronic address: karin.stiasny@meduniwien.ac.at. 8. Institute for Immunology, Medical University of Vienna, Lazarettgasse 19, A-1090 Vienna, Austria. Electronic address: gerhard.zlabinger@meduniwien.ac.at. 9. Center for Public Health, Medical University of Vienna, Kinderspitalgasse 15, A-1090 Vienna, Austria. Electronic address: michael.kundi@meduniwien.ac.at. 10. Institute of Specific Prophylaxis and Tropical Medicine, Medical University of Vienna Kinderspitalgasse 15, A-1090 Vienna, Austria. Electronic address: ursula.wiedermann@meduniwien.ac.at.
Abstract
BACKGROUND: Allergic diseases are caused by Th2-driven immune responses and their treatment with specific immunotherapy (SIT) leads to immunomodulation via IL10, TGF-ß and Th1/Tr1 shift. This phase IV, open-label clinical trial investigated whether allergies and SIT treatment influenced immune responses to routine vaccination. METHODS: We studied three groups: 49 allergic patients (allergic group), 21 allergic patients receiving maintenance doses of SIT (SIT group), and 49 non-allergic controls. All subjects received tick-borne encephalitis (TBE) booster vaccines and humoral and cellular immune responses were evaluated after one week, four weeks and six months. RESULTS: The levels and kinetics of neutralizing TBE-specific antibodies, reflecting protection against TBE, were not significantly different in the three groups. The allergic group showed Th2 polarization pre-booster as indicated by increased TBE-specific IgG1 and elevated mitogen-induced IL5 production. Alum-adjuvanted TBE vaccine led to Th2 biased immune responses in the controls, but to no further enhancement of Th2 polarization in the allergic and SIT group. Furthermore, in the SIT group cellular parameters reflected the induction of immunomodulation due to increased Tregs, elevated baseline IL10 and lack of TBE-specific IL5. Importantly, these cellular regulatory responses did not limit the ability to mount sufficient TBE-specific antibodies after the booster. All groups tolerated the vaccine well with no exacerbation of allergic symptoms. CONCLUSION: TBE booster vaccinations were immunogenic and safe in both the allergic and SIT group and contributed to balanced immune responses. Our data indicate that all allergic patients, even when undergoing SIT, should be vaccinated without hesitation and at regular intervals according to standard recommendations. ClinicalTrials.gov (NCT02511535).
BACKGROUND:Allergic diseases are caused by Th2-driven immune responses and their treatment with specific immunotherapy (SIT) leads to immunomodulation via IL10, TGF-ß and Th1/Tr1 shift. This phase IV, open-label clinical trial investigated whether allergies and SIT treatment influenced immune responses to routine vaccination. METHODS: We studied three groups: 49 allergicpatients (allergic group), 21 allergicpatients receiving maintenance doses of SIT (SIT group), and 49 non-allergic controls. All subjects received tick-borne encephalitis (TBE) booster vaccines and humoral and cellular immune responses were evaluated after one week, four weeks and six months. RESULTS: The levels and kinetics of neutralizing TBE-specific antibodies, reflecting protection against TBE, were not significantly different in the three groups. The allergic group showed Th2 polarization pre-booster as indicated by increased TBE-specific IgG1 and elevated mitogen-induced IL5 production. Alum-adjuvanted TBE vaccine led to Th2 biased immune responses in the controls, but to no further enhancement of Th2 polarization in the allergic and SIT group. Furthermore, in the SIT group cellular parameters reflected the induction of immunomodulation due to increased Tregs, elevated baseline IL10 and lack of TBE-specific IL5. Importantly, these cellular regulatory responses did not limit the ability to mount sufficient TBE-specific antibodies after the booster. All groups tolerated the vaccine well with no exacerbation of allergic symptoms. CONCLUSION: TBE booster vaccinations were immunogenic and safe in both the allergic and SIT group and contributed to balanced immune responses. Our data indicate that all allergicpatients, even when undergoing SIT, should be vaccinated without hesitation and at regular intervals according to standard recommendations. ClinicalTrials.gov (NCT02511535).
Authors: Marek Jutel; Maria J Torres; Oscar Palomares; Cezmi A Akdis; Thomas Eiwegger; Eva Untersmayr; Domingo Barber; Magdalena Zemelka-Wiacek; Anna Kosowska; Elizabeth Palmer; Stefan Vieths; Vera Mahler; Walter G Canonica; Kari Nadeau; Mohamed H Shamji; Ioana Agache Journal: Allergy Date: 2022-03-18 Impact factor: 14.710