Blocking of LFA-1 enhances expansion of Th17 cells induced by human CD14(+) CD16(++) nonclassical monocytes
© 2015 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim..
Among human peripheral blood (PB) monocyte (Mo) subsets, the classical CD14(++) CD16(-) (cMo) and intermediate CD14(++) CD16(+) (iMo) Mos are known to activate pathogenic Th17 responses, whereas the impact of nonclassical CD14(+) CD16(++) Mo (nMo) on T-cell activation has been largely neglected. The aim of this study was to obtain new mechanistic insights on the capacity of Mo subsets from healthy donors (HDs) to activate IL-17(+) T-cell responses in vitro, and assess whether this function was maintained or lost in states of chronic inflammation. When cocultured with autologous CD4(+) T cells in the absence of TLR-2/NOD2 agonists, PB nMos from HDs were more efficient stimulators of IL-17-producing T cells, as compared to cMo. These results could not be explained by differences in Mo lifespan and cytokine profiles. Notably, however, the blocking of LFA-1/ICAM-1 interaction resulted in a significant increase in the percentage of IL-17(+) T cells expanded in nMo/T-cell cocultures. As compared to HD, PB Mo subsets of patients with rheumatoid arthritis were hampered in their T-cell stimulatory capacity. Our new insights highlight the role of Mo subsets in modulating inflammatory T-cell responses and suggest that nMo could become a critical therapeutic target against IL-17-mediated inflammatory diseases.
| Medienart: |
E-Artikel |
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| Erscheinungsjahr: |
2015 |
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| Erschienen: |
2015 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:45 |
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| Enthalten in: |
European journal of immunology - 45(2015), 5 vom: 05. Mai, Seite 1414-25 |
| Sprache: |
Englisch |
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| Beteiligte Personen: |
Traunecker, Emmanuel [VerfasserIn] |
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| Links: |
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| Anmerkungen: |
Date Completed 03.08.2015 Date Revised 16.11.2017 published: Print-Electronic Citation Status MEDLINE |
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| doi: |
10.1002/eji.201445100 |
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| funding: |
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| Förderinstitution / Projekttitel: |
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| PPN (Katalog-ID): |
NLM246203455 |
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| 100 | 1 | |a Traunecker, Emmanuel |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a Blocking of LFA-1 enhances expansion of Th17 cells induced by human CD14(+) CD16(++) nonclassical monocytes |
| 264 | 1 | |c 2015 | |
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| 500 | |a Date Revised 16.11.2017 | ||
| 500 | |a published: Print-Electronic | ||
| 500 | |a Citation Status MEDLINE | ||
| 520 | |a © 2015 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim. | ||
| 520 | |a Among human peripheral blood (PB) monocyte (Mo) subsets, the classical CD14(++) CD16(-) (cMo) and intermediate CD14(++) CD16(+) (iMo) Mos are known to activate pathogenic Th17 responses, whereas the impact of nonclassical CD14(+) CD16(++) Mo (nMo) on T-cell activation has been largely neglected. The aim of this study was to obtain new mechanistic insights on the capacity of Mo subsets from healthy donors (HDs) to activate IL-17(+) T-cell responses in vitro, and assess whether this function was maintained or lost in states of chronic inflammation. When cocultured with autologous CD4(+) T cells in the absence of TLR-2/NOD2 agonists, PB nMos from HDs were more efficient stimulators of IL-17-producing T cells, as compared to cMo. These results could not be explained by differences in Mo lifespan and cytokine profiles. Notably, however, the blocking of LFA-1/ICAM-1 interaction resulted in a significant increase in the percentage of IL-17(+) T cells expanded in nMo/T-cell cocultures. As compared to HD, PB Mo subsets of patients with rheumatoid arthritis were hampered in their T-cell stimulatory capacity. Our new insights highlight the role of Mo subsets in modulating inflammatory T-cell responses and suggest that nMo could become a critical therapeutic target against IL-17-mediated inflammatory diseases | ||
| 650 | 4 | |a Journal Article | |
| 650 | 4 | |a Research Support, Non-U.S. Gov't | |
| 650 | 4 | |a LFA-1 | |
| 650 | 4 | |a Monocyte | |
| 650 | 4 | |a Rheumatoid arthritis | |
| 650 | 4 | |a TLR-2 | |
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| 650 | 7 | |a Lymphocyte Function-Associated Antigen-1 |2 NLM | |
| 650 | 7 | |a NOD2 protein, human |2 NLM | |
| 650 | 7 | |a Nod2 Signaling Adaptor Protein |2 NLM | |
| 650 | 7 | |a Receptors, IgG |2 NLM | |
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| 650 | 7 | |a TLR2 protein, human |2 NLM | |
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| 700 | 1 | |a Gardner, Rui |e verfasserin |4 aut | |
| 700 | 1 | |a Fonseca, João Eurico |e verfasserin |4 aut | |
| 700 | 1 | |a Polido-Pereira, Joaquim |e verfasserin |4 aut | |
| 700 | 1 | |a Seitz, Michael |e verfasserin |4 aut | |
| 700 | 1 | |a Villiger, Peter M |e verfasserin |4 aut | |
| 700 | 1 | |a Iezzi, Giandomenica |e verfasserin |4 aut | |
| 700 | 1 | |a Padovan, Elisabetta |e verfasserin |4 aut | |
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