Mechanisms of deficient interferon-γ production in atopic diseases
| Autor: | R Moessner, Heidrich S, Dieckhoff K, T. Jung, C. Neumann |
|---|---|
| Rok vydání: | 1999 |
| Předmět: |
0303 health sciences
Interferon-gamma production business.industry medicine.medical_treatment T cell Immunology Priming (immunology) Atopic dermatitis T lymphocyte medicine.disease 03 medical and health sciences 0302 clinical medicine Cytokine medicine.anatomical_structure Immune system medicine Immunology and Allergy Interferon gamma business 030304 developmental biology 030215 immunology medicine.drug |
| Zdroj: | Clinical & Experimental Allergy. 29:912-919 |
| ISSN: | 0954-7894 |
| DOI: | 10.1046/j.1365-2222.1999.00619.x |
| Popis: | Background The mechanisms responsible for an imbalanced cytokine response in atopic diseases are still not understood. While impaired interferon-gamma (IFN-γ) production may be the result of a pathological T-cell/antigen-presenting cell (APC) interaction, evidence was provided that the T cell itself may have an intrinsic defect to produce IFN-γ. Objective To clarify whether impaired IFN-γ production by T cells from patients with atopic dermatitis (AD) represents an intrinsic defect in producing IFN-γ. Methods Effector T cells were generated from CD4+ CD45RA+-naive precursors from patients with AD and healthy control individuals by activation with anti-CD3+ anti-CD28 MoAbs. Following restimulation, IFN-γ production was measured by ELISA and flow cytometry. Results IFN-γ production by atopic T cells was decreased compared with healthy T cells. IL-12 present at priming or high doses of IL-2 during the culture period, even in the absence of IL-12, completely restored IFN-γ production. Conversion of naive CD45RA+ to CD45R0+ effector cells did not differ between atopic and healthy donors' T cells. Conclusion Impaired IFN-γ production by T cells from atopic individuals is not the result of an intrinsic, genetically fixed, defect to produce sufficient amounts of IFN-γ. The data provides evidence that correction of an impaired TH1 response in AD may be successful at the precursor T cell level. |
| Databáze: | OpenAIRE |
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