ILC3 GM-CSF production and mobilisation orchestrate acute intestinal inflammation.
Innate lymphoid cells (ILCs) contribute to host defence and tissue repair but can induce immunopathology. Recent work has revealed tissue-specific roles for ILCs; however, the question of how a small population has large effects on immune homeostasis remains unclear. We identify two mechanisms that...
| Main Authors: | , , , , , , , , , , |
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| Format: | Journal article |
| Language: | English |
| Published: |
eLife Sciences Publications
2016
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| _version_ | 1797059455472369664 |
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| author | Pearson, C Thornton, E McKenzie, B Schaupp, A Huskens, N Griseri, T West, N Tung, S Seddon, B Uhlig, H Powrie, F |
| author_facet | Pearson, C Thornton, E McKenzie, B Schaupp, A Huskens, N Griseri, T West, N Tung, S Seddon, B Uhlig, H Powrie, F |
| author_sort | Pearson, C |
| collection | OXFORD |
| description | Innate lymphoid cells (ILCs) contribute to host defence and tissue repair but can induce immunopathology. Recent work has revealed tissue-specific roles for ILCs; however, the question of how a small population has large effects on immune homeostasis remains unclear. We identify two mechanisms that ILC3s utilise to exert their effects within intestinal tissue. ILC-driven colitis depends on production of granulocyte macrophage-colony stimulating factor (GM-CSF), which recruits and maintains intestinal inflammatory monocytes. ILCs present in the intestine also enter and exit cryptopatches in a highly dynamic process. During colitis, ILC3s mobilize from cryptopatches, a process that can be inhibited by blocking GM-CSF, and mobilization precedes inflammatory foci elsewhere in the tissue. Together these data identify the IL-23R/GM-CSF axis within ILC3 as a key control point in the accumulation of innate effector cells in the intestine and in the spatio-temporal dynamics of ILCs in the intestinal inflammatory response. |
| first_indexed | 2024-03-06T20:04:31Z |
| format | Journal article |
| id | oxford-uuid:287bd319-c33f-4ea6-8612-5f3524484dd2 |
| institution | University of Oxford |
| language | English |
| last_indexed | 2024-03-06T20:04:31Z |
| publishDate | 2016 |
| publisher | eLife Sciences Publications |
| record_format | dspace |
| spelling | oxford-uuid:287bd319-c33f-4ea6-8612-5f3524484dd22022-03-26T12:13:04ZILC3 GM-CSF production and mobilisation orchestrate acute intestinal inflammation.Journal articlehttp://purl.org/coar/resource_type/c_dcae04bcuuid:287bd319-c33f-4ea6-8612-5f3524484dd2EnglishSymplectic Elements at OxfordeLife Sciences Publications2016Pearson, CThornton, EMcKenzie, BSchaupp, AHuskens, NGriseri, TWest, NTung, SSeddon, BUhlig, HPowrie, FInnate lymphoid cells (ILCs) contribute to host defence and tissue repair but can induce immunopathology. Recent work has revealed tissue-specific roles for ILCs; however, the question of how a small population has large effects on immune homeostasis remains unclear. We identify two mechanisms that ILC3s utilise to exert their effects within intestinal tissue. ILC-driven colitis depends on production of granulocyte macrophage-colony stimulating factor (GM-CSF), which recruits and maintains intestinal inflammatory monocytes. ILCs present in the intestine also enter and exit cryptopatches in a highly dynamic process. During colitis, ILC3s mobilize from cryptopatches, a process that can be inhibited by blocking GM-CSF, and mobilization precedes inflammatory foci elsewhere in the tissue. Together these data identify the IL-23R/GM-CSF axis within ILC3 as a key control point in the accumulation of innate effector cells in the intestine and in the spatio-temporal dynamics of ILCs in the intestinal inflammatory response. |
| spellingShingle | Pearson, C Thornton, E McKenzie, B Schaupp, A Huskens, N Griseri, T West, N Tung, S Seddon, B Uhlig, H Powrie, F ILC3 GM-CSF production and mobilisation orchestrate acute intestinal inflammation. |
| title | ILC3 GM-CSF production and mobilisation orchestrate acute intestinal inflammation. |
| title_full | ILC3 GM-CSF production and mobilisation orchestrate acute intestinal inflammation. |
| title_fullStr | ILC3 GM-CSF production and mobilisation orchestrate acute intestinal inflammation. |
| title_full_unstemmed | ILC3 GM-CSF production and mobilisation orchestrate acute intestinal inflammation. |
| title_short | ILC3 GM-CSF production and mobilisation orchestrate acute intestinal inflammation. |
| title_sort | ilc3 gm csf production and mobilisation orchestrate acute intestinal inflammation |
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