Abstract
Lipocalin allergens form a notable group of proteins, as they contain most of the significant respiratory allergens from mammals. The basis for the allergenic capacity of allergens in the lipocalin family, that is, the development of T-helper type 2 immunity against them, is still unresolved. As immunogenicity has been proposed to be a decisive feature of allergens, the purpose of this work was to examine human CD4+ T cell responses to the major dog allergen Can f 1 and to compare them with those to its human homologue, tear lipocalin (TL). For this, specific T cell lines were induced in vitro from the peripheral blood mononuclear cells of Can f 1-allergic and healthy dog dust-exposed subjects with peptides containing the immunodominant T cell epitopes of Can f 1 and the corresponding TL peptides. We found that the frequency of Can f 1 and TL-specific T cells in both subject groups was low and close to each other, the difference being about two-fold. Importantly, we found that the proliferative responses of both Can f 1 and TL-specific T cell lines from allergic subjects were stronger than those from healthy subjects, but that the strength of the responses within the subject groups did not differ between these two antigens. Moreover, the phenotype of the Can f 1 and TL-specific T cell lines, determined by cytokine production and expression of cell surface markers, resembled each other. The HLA system appeared to have a minimal role in explaining the allergenicity of Can f 1, as the allergic and healthy subjects' HLA background did not differ, and HLA binding was very similar between Can f 1 and TL peptides. Along with existing data on lipocalin allergens, we conclude that strong antigenicity is not decisive for the allergenicity of Can f 1.
Highlights
Type I allergic immune response is known to be mediated by CD4+ T-helper type 2 (Th2) lymphocytes that, through the production of cytokines, such as interleukin (IL)-4, IL-5 and IL-13, orchestrate allergen-specific IgE synthesis and eventually eosinophilic inflammation in the target organs [1]
The stimulatory capacity of the dog major allergen Can f 1 and its human homologue tear lipocalin (TL) was first assessed by determining the frequency of peptide-recognizing T cells by generating peptidespecific T cell lines (TCLs) from the peripheral-blood mononuclear cells (PBMCs) of allergic and nonallergic subjects
We have previously proposed that the allergenicity of lipocalin allergens may be associated with the presence of homologous endogenous lipocalin proteins in humans resulting in the absence of highavidity lipocalin allergen-reactive CD4+ T cells due to thymic deletion [6,40,41,42]
Summary
Type I allergic immune response is known to be mediated by CD4+ T-helper type 2 (Th2) lymphocytes that, through the production of cytokines, such as interleukin (IL)-4, IL-5 and IL-13, orchestrate allergen-specific IgE synthesis and eventually eosinophilic inflammation in the target organs [1]. It is reasonable to hypothesize, though, that allergens possess specific allergenic properties because allergic sensitization is mostly manifested by the production of IgE specific to only a few selected proteins present in the allergen source [2,3,4]. Especially indoors, the allergens of the lipocalin family are of great importance, as they contain most of the significant respiratory allergens from dog, cat, mouse, rat, guinea pig, rabbit, horse and cow [5,6,7]. Many of the mammalian lipocalin allergens are classified as major allergens These include, for example, dog allergen Can f 1 [8], horse allergen Equ c 1 [9], and cow allergen Bos d 2 [10]. Several other lipocalin allergens are known to exhibit homologies of 30–60% with human endogenous lipocalins [5,17]
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