Forskningsoutput per år
Forskningsoutput per år
Julia Westerlund, Sandra Askman, Åsa Pettersson, Thomas Hellmark, Åsa C M Johansson, Markus Hansson
Forskningsoutput: Tidskriftsbidrag › Artikel i vetenskaplig tidskrift › Peer review
Normal density granulocytes (NDGs) can suppress T-cell responses in a similar way as myeloid-derived suppressor cells (MDSCs). In this study, we tested the hypothesis that NDGs from healthy donors preferentially inhibit T helper 1 (Th1) cells and investigated the myeloid-derived suppressive effect in different T-cell populations. We found that NDG-induced suppression of T-cell proliferation was contact dependent, mediated by integrin CD11b, and dependent on NDG-production of reactive oxygen species (ROS). The suppression was rapid and occurred within the first few hours of coculture. The suppression did not influence the CD8 +/CD4 + ratio indicating an equal sensitivity in these populations. We further analyzed the CD4 + T helper subsets and found that NDGs induced a loss of Th1 surface marker, CD183, that was unrelated to ligand-binding to CD183. In addition, we analyzed the Th1, Th2, and Th17 cytokine production and found that all cytokine groups were suppressed when T-cells were incubated with NDGs. We therefore concluded that NDGs do not preferentially suppress Th1-cells. Instead, NDGs generally suppress Th cells and cytotoxic T-cells but specifically downregulate the Th1 marker CD183.
Originalspråk | engelska |
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Artikelnummer | 8077281 |
Tidskrift | Journal of Immunology Research |
Volym | 2022 |
DOI | |
Status | Published - 2022 |
Forskningsoutput: Avhandling › Doktorsavhandling (sammanläggning)