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Increased HLA‐DR expression after exposure of human monocytic cells to air particulates
Author(s) -
Don Porto Carero A.,
Hoet P. H. M.,
Nemery B.,
Schoeters G.
Publication year - 2002
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.1365-2222.2002.01266.x
Subject(s) - immunology , diesel exhaust , human leukocyte antigen , antigen , chemistry , adjuvant , hla dr , microbiology and biotechnology , biology , diesel fuel , organic chemistry
Background The expression of HLA‐DR on the cell membrane of antigen‐presenting cells is of major importance for the induction of an allergic response in the airways. Environmental particulates are thought to play an important role in inducing or enhancing allergic sensitization, possibly by increasing the expression of HLA‐DR on the cell membrane of antigen‐presenting cells. In addition, these particulates may synergize with common sensitizing agents in inducing or enhancing HLA‐DR and thus antigen presentation. Objective In this study, we investigated the potential of three particle types, namely carbon black, diesel exhaust particles and urban air particulates (0.1–1000 ng/cm 2 ), to induce the expression of HLA‐DR on differentiated THP‐1 cells, taken as a model for alveolar macrophages. We also assessed the ‘adjuvant’ potential of the particles on interferon (IFN)‐γ, a known enhancer of HLA‐DR. Results By themselves, the particles (0.1–1000 ng/cm 2 ) were not able to induce HLA‐DR on the THP‐1 cells after an incubation of 48 h. However, even at very low concentrations, carbon black (from 1 ng/cm 2 on) and diesel exhaust particles (from 0.1 ng/cm 2 on), interacted with IFN‐γ (100 U/mL) to enhance HLA‐DR expression (up to 2.5‐fold increase). Conclusion This finding may reflect in vitro one of the mechanisms by which pollutant particles exert an ‘adjuvant’ activity and may partially explain how exposure to particles can be related to the enhancement of allergic sensitization.