| 1. |
|
|
| 2. |
- Matricardi, PM, et al.
(author)
-
EAACI Molecular Allergology User's Guide
- 2016
-
In: Pediatric allergy and immunology : official publication of the European Society of Pediatric Allergy and Immunology. - : Wiley. - 1399-3038. ; 2727 Suppl 23, s. 1-250
-
Journal article (peer-reviewed)
|
|
| 3. |
|
|
| 4. |
|
|
| 5. |
- Akdis, M, et al.
(author)
-
Immune responses in healthy and allergic individuals are characterized by a fine balance between allergen-specific T regulatory 1 and T helper 2 cells
- 2004
-
In: Journal of Experimental Medicine. - : Rockefeller University Press. - 0022-1007 .- 1540-9538. ; 199:11, s. 1567-1575
-
Journal article (peer-reviewed)abstract
- The mechanisms by which immune responses to nonpathogenic environmental antigens lead to either allergy or nonharmful immunity are unknown. Single allergen-specific T cells constitute a very small fraction of the whole CD4(+) T cell repertoire and can be isolated from the peripheral blood of humans according to their cytokine profile. Freshly purified interferon-gamma-, interleukin (IL)-4-, and IL-10-producing allergen-specific CD4(+) T cells display characteristics of T helper cell (Th)1-, Th2, and T regulatory (Tr)1-like cells, respectively. Tr1 cells consistently represent the dominant subset specific for common environmental allergens in healthy individuals; in contrast, there is a high frequency of allergen-specific IL-4-secreting T cells in allergic individuals. Tr1 cells use multiple suppressive mechanisms, IL-10 and TGF-beta as secreted cytokines, and cytotoxic T lymphocyte antigen 4 and programmed death 1 as surface molecules. Healthy and allergic individuals exhibit all three allergen-specific subsets in different proportions, indicating that a change in the dominant subset may lead to allergy development or recovery. Accordingly, blocking the suppressor activity of Tr1 cells or increasing Th2 cell frequency enhances allergen-specific Th2 cell activation ex vivo. These results indicate that the balance between allergen-specific Tr1 cells and Th2 cells may be decisive in the development of allergy.
|
|
| 6. |
|
|
| 7. |
|
|
| 8. |
|
|
| 9. |
|
|
| 10. |
|
|
| 11. |
|
|
| 12. |
|
|
| 13. |
|
|
| 14. |
|
|
| 15. |
|
|
| 16. |
|
|
| 17. |
|
|
| 18. |
|
|
| 19. |
|
|
| 20. |
|
|
| 21. |
|
|
| 22. |
|
|
| 23. |
|
|
| 24. |
|
|
| 25. |
|
|
| 26. |
|
|
| 27. |
|
|
| 28. |
|
|
| 29. |
|
|
| 30. |
|
|
| 31. |
|
|
| 32. |
|
|
| 33. |
|
|
| 34. |
|
|
| 35. |
|
|
| 36. |
|
|
| 37. |
- Vilhelmsson, M, et al.
(author)
-
The Malassezia sympodialis allergen Mala s 11 induces human dendritic cell maturation, in contrast to its human homologue manganese superoxide dismutase
- 2007
-
In: International archives of allergy and immunology. - : S. Karger AG. - 1018-2438 .- 1423-0097. ; 143:2, s. 155-162
-
Journal article (peer-reviewed)abstract
- <i>Background:</i> Recently, we identified a major <i>Malassezia sympodialis</i> allergen, Mala s 11, which displays a high degree of DNA sequence homology to human manganese superoxide dismutase (hMnSOD). In atopic eczema patients sensitized to <i>M. sympodialis</i>, hMnSOD can elicit eczematous reactions and positive skin prick tests, suggesting cross- reactivity to Mala s 11 based on molecular mimicry. The objective of the current study was to compare the influence of Mala s 11 and hMnSOD on human dendritic antigen-presenting cells. <i>Methods:</i> Monocyte-derived dendritic cells (MDDCs) from healthy blood donors were co-cultured with recombinant Mala s 11 (rMala s 11), recombinant hMnSOD (rhMnSOD), lipopolysaccharide or cultured in medium alone. Phenotypic changes were analysed using flow cytometry and allogeneic lymphocyte proliferation assays. Cytokine release into culture supernatants was investigated using cytometric bead array. <i>Results:</i> Whereas rhMnSOD did not affect the MDDC phenotype, rMala s 11 up-regulated the maturation marker CD83, the co-stimulatory molecules CD40, CD80, CD86 and HLA-DR to a similar extent as lipopolysaccharide. Furthermore, rMala s 11, but not rhMnSOD, induced significantly higher levels of TNF-α, IL-6, IL-8, IL-10 and IL-12p70 in the culture supernatants at 24 h in comparison with MDDCs cultured in medium alone. Finally, MDDCs pre-incubated with rMala s 11 induced a significantly higher proliferation of allogeneic CD14-depleted peripheral blood monocytes than MDDCs pre-incubated with rhMnSOD. <i>Conclusion:</i> Our results suggest that Mala s 11, but not hMnSOD, affects the immune response of healthy individuals through dendritic cell maturation and cytokine release. This indicates that dendritic cells possess the ability to distinguish between Mala s 11 and its human homologue MnSOD.
|
|
| 38. |
|
|
| 39. |
- Zeller, S, et al.
(author)
-
Immunoglobulin-E-mediated reactivity to self antigens: a controversial issue
- 2008
-
In: International archives of allergy and immunology. - : S. Karger AG. - 1423-0097 .- 1018-2438. ; 145:2, s. 87-93
-
Journal article (peer-reviewed)abstract
- Immunoglobulin E (IgE) reactivity to self antigens is well established in vitro by ELISA, inhibition ELISA, Western blot analyses and T cell proliferation experiments. In vivo, IgE-binding self antigens are able to elicit strong type I reactions in sensitized individuals and, in the case of human manganese superoxide dismutase, to elicit eczematous reactions on healthy skin areas of patients suffering from atopic eczema. The reactions against self antigens sharing structural homology with environmental allergens can be plausibly explained by molecular mimicry between common B cell epitopes. For the second class of IgE-binding self antigens without sequence homology to known allergens, it is still unclear if the structures are able to induce a B cell switch to IgE production, or if the reactivity is due to sequence similarity shared with not yet detected environmental allergens. However, in all cases, cross-reactivity is never complete, indicating either a lower affinity of IgE antibodies to self allergens than to the homologous environmental allergens or the presence of additional B cell epitopes on the surface of the environmental allergens, or both. Increasing evidence shows that self allergens could play a decisive role in the exacerbation of long-lasting atopic diseases. However, the only observation supporting a clinical role of IgE-mediated autoreactivity is confined to the fact that IgE levels against self antigens correlate with disease severity.
|
|
