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Decrease of allergen‐specific T‐cell response induced by local nasal immunotherapy
Author(s) -
L Giannarini,
Enrico Maggi
Publication year - 1998
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.1365-2222.1998.00265.x
Subject(s) - immunoglobulin e , immunology , allergen , immunotherapy , medicine , allergen immunotherapy , cytokine , peripheral blood mononuclear cell , antibody , allergy , immune system , biology , in vitro , biochemistry
Background The clinical efficacy and safety of local nasal immunotherapy (LNIT) with lyophilized ‘macronized’ powder has been demonstrated. However, the immunological changes possibly induced by LNIT which may account for the clinical improvement are still unclear. Objective To investigate the effects of a successful LNIT‐treatment on the allergen‐driven T cell response, cytokine secretion and IgE and IgG antibody production. Methods Three groups (untreated, subcutaneous immunotherapy‐ SIT‐ and LNIT‐treated) of grass‐sensitive patients suffering from seasonal rhinitic symptoms were ramdomized for the 2‐year study. The proliferative response of PBMC to purified Rye‐1 allergen and serum levels of grass‐specific IgE and IgG were evaluated before treatment and during the 2‐year subsequent pollination periods. The proliferative response of allergen‐specific short‐term T‐cell lines, as well as production of allergen‐driven cytokine by PBMC, were also assessed. Results Both SIT and LNIT induced a significant reduction of symptom scores during the pollination season. SIT, but not LNIT, induced a significant change in serum levels of allergen‐specific IgE and IgG antibody. By contrast, both SIT and LNIT reduced the increase of the proliferative response of allergen‐specific T cells driven by natural allergen exposure and significantly decreased T cell proliferation to low doses of allergen, as shown also by the mitogenic index of allergen‐specific T‐cell lines. A reduced IL‐4 and IFNγ production by PBMC of LNIT‐ and SIT‐treated patients was also observed in the absence of a clearcut TH 2 ‐TH 1 switch. Conclusions These data suggest that a common mechanism of both LNIT and SIT is the induction of T‐cell tolerance, thus providing a rational basis to explain why LNIT may be clinically successful in allergic patients with rhinits.