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Malassezia Enhances Natural Killer Cell‐Induced Dendritic Cell Maturation
Human natural killer (NK) cells can induce cell death in autologous dendritic cells (DCs), though an interaction between these two cell types can also lead to a reciprocal activation. We have recently shown cell contact between NK cells and DCs in vivo, in Malassezia‐induced lesional skin of patient...
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Published in: | Scandinavian journal of immunology 2004-05, Vol.59 (5), p.511-516 |
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Main Authors: | , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | Human natural killer (NK) cells can induce cell death in autologous dendritic cells (DCs), though an interaction between these two cell types can also lead to a reciprocal activation. We have recently shown cell contact between NK cells and DCs in vivo, in Malassezia‐induced lesional skin of patients with atopic eczema, where the yeast acts as an allergen although it is part of the normal skin microflora. Here we characterize the interaction of human NK cells and monocyte‐derived DCs (MDDCs) by using an in vitro system where short‐term activated polyclonal NK cells are cocultured with autologous, immature, Malassezia‐stimulated or lipopolysaccharide‐matured MDDCs. We found that the number of CD83+ MDDCs increased in the immature and Malassezia‐stimulated MDDCs upon coculture with NK cells, while an increased number of CD86+ cells was detected in the Malassezia‐stimulated MDDCs. NK cell–MDDC interaction induced the production of interleukin‐8 (IL‐8). In conclusion, our results imply that NK cells provide maturation signals and may play a role in inducing IL‐8 production in DCs. Furthermore, the increased expression of CD86 on Malassezia‐stimulated MDDCs might have a function in subsequent T‐cell activation by DCs, and indicate a role for NK cell–DC interaction in modulating the immune responses to microbial stimuli. |
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ISSN: | 0300-9475 1365-3083 |
DOI: | 10.1111/j.0300-9475.2004.01416.x |