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Venom immunotherapy induces monocyte activation.

A Magnan1, V Marin, L Mély

  • 1UPRES 2050, Groupe de Recherche Clinique 'Pathologie respiratoire liée à l'environnement', Service de Pneumo-Allergologie, INSERM, Assistance Publique Hôpitaux de Marseille, Hôpital Ste Marguerite, Marseilles, France. amagnan@mail.ap-hm.fr

Clinical and Experimental Allergy : Journal of the British Society for Allergy and Clinical Immunology
|September 1, 2001
PubMed
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Venom immunotherapy (VIT) boosts monocyte production of IL-12 and TNF-alpha, potentially inhibiting allergic Th2 cells. This suggests a non-specific monocyte role in VIT-induced tolerance for hymenoptera venom allergy.

Area of Science:

  • Immunology
  • Allergy Research
  • Cellular Biology

Background:

  • Venom immunotherapy (VIT) is effective for hymenoptera venom allergy.
  • VIT induces tolerance by modulating allergen-specific Th2 cells.
  • Mechanisms of T cell modulation by VIT are unclear, potentially involving monocyte-derived cytokines like IL-12, TNF-alpha, and IL-10.

Purpose of the Study:

  • To investigate if VIT alters monocyte production of IL-12, TNF-alpha, and IL-10 within the initial 45 days of treatment.
  • To explore the role of monocytes in the immunological changes induced by VIT.

Main Methods:

  • Monocytes were isolated from 14 VIT patients and 7 controls.
  • Cytokine production (IL-10, IL-12, TNF-alpha) was measured in monocytes cultured with and without LPS at various time points during VIT.

Related Experiment Videos

  • Enzyme-linked immunosorbent assay (ELISA) was used to quantify cytokine levels.

    • Main Results:

    • No significant baseline differences in cytokine levels between patients and controls.
    • VIT led to increased spontaneous monocyte production of IL-12 and TNF-alpha at days 15 and 45.
    • IL-10 production showed a non-significant increase, and LPS-stimulated cytokine production remained unchanged.

    Conclusions:

    • VIT activates monocytes, causing delayed overproduction of IL-12 and TNF-alpha.
    • These cytokines may contribute to Th2 cell inhibition during VIT.
    • VIT-induced tolerance might involve both specific antigen effects and non-specific monocyte actions.