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Venom immunotherapy induces monocyte activation
Author(s) -
Magnan A.,
Marin V.,
Mély L.,
Birnbaum J.,
Romanet S.,
Bongrand P.,
Vervloet D.
Publication year - 2001
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.1365-2222.2001.01171.x
Subject(s) - monocyte , tumor necrosis factor alpha , lipopolysaccharide , immunology , cytokine , immunotherapy , interleukin , interleukin 10 , allergy , medicine , immune system
Background Venom immunotherapy (VIT) is an efficient treatment of hymenoptera venom allergy. The mechanism of VIT is based on the induction of tolerance of allergen‐specific Th2 cells. The mechanisms of this T cell modulation are unknown, and could depend on cytokines produced by other cell types such as interleukin (IL)‐12, tumour necrosis factor (TNF)‐α and IL‐10 by monocytes. Objective To assess if VIT modifies the monocyte production of IL‐12, TNF‐α and IL‐10 during the 45 first days of treatment. Methods Fourteen patients and seven controls were included. Blood samples were taken once in controls and at day (D)1, D30 and D45 of VIT in patients. Monocytes were isolated, cultured with and without lipopolysaccharide (LPS), and the culture supernatant was harvested. IL‐10, IL‐12 and TNF‐α were assayed in supernatants by ELISA. Results Baseline cytokine levels were not statistically different between patients and controls. During treatment, an increase of spontaneous monocyte production of IL‐12 and TNF‐α was observed at D15 and D45. The production of IL‐10 increased at D15 and D45 but not significantly. After LPS‐stimulation, IL‐12, TNF‐α and IL‐10 monocyte production was not modified by VIT. Conclusion VIT induces a monocyte activation characterized by a delayed overproduction of IL‐12 and TNF‐α. These cytokines could be relevant to the inhibition of Th2 cells during VIT. Therefore, VIT‐induced tolerance could depend not only on the specific action of venom antigens on T cells, but also on a secondary non‐specific action of monocytes.