Newson, Justine and Stables, Melanie and Karra, Efthimia and Arce-Vargas, Frederick and Quezada, Sergio and Motwani, Madhur and Mack, Matthias and Yona, Simon and Audzevich, Tatsiana and Gilroy, Derek W. (2014) Resolution of acute inflammation bridges the gap between innate and adaptive immunity. BLOOD, 124 (11). pp. 1748-1764. ISSN 0006-4971, 1528-0020
Full text not available from this repository. (Request a copy)Abstract
Acute inflammation is traditionally characterized by polymorphonuclear leukocytes (PMN) influx followed by phagocytosing macrophage (M phi s) that clear injurious stimuli leading to resolution and tissue homeostasis. However, using the peritoneal cavity, we found that although innate immune-mediated responses to low-dose zymosan or bacteria resolve within days, these stimuli, but not hyperinflammatory stimuli, trigger a previously overlooked second wave of leukocyte influx into tissues that persists for weeks. These cells comprise distinct populations of tissue-resident M phi s (resM phi s), Ly6c(hi) monocyte-derived M phi s (moM phi s), monocyte-derived dendritic cells (moDCs), and myeloid-derived suppressor cells (MDSCs). Postresolution mononuclear phagocytes were observed alongside lymph node expansion and increased numbers of blood and peritoneal memory T and B lymphocytes. The resM phi s and moM phi s triggered FoxP3 expression within CD4 cells, whereas moDCs drive T-cell proliferation. The resM phi s preferentially clear apoptotic PMNs and migrate to lymph nodes to bring about their contraction in an inducible nitric oxide synthase-dependent manner. Finally, moM phi s remain in tissues for months postresolution, alongside altered numbers of T cells collectively dictating the magnitude of subsequent acute inflammatory reactions. These data challenge the prevailing idea that resolution leads back to homeostasis and asserts that resolution acts as a bridge between innate and adaptive immunity, as well as tissue reprogramming.
| Item Type: | Article |
|---|---|
| Uncontrolled Keywords: | EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS; OXIDE MEDIATES IMMUNOSUPPRESSION; DELAYED-TYPE HYPERSENSITIVITY; PERSISTENT LCMV INFECTION; CELL RECEPTOR PEPTIDE; MYELIN BASIC-PROTEIN; NITRIC-OXIDE; DENDRITIC CELLS; APOPTOTIC CELLS; I INTERFERON; |
| Subjects: | 600 Technology > 610 Medical sciences Medicine |
| Divisions: | Medicine > Lehrstuhl für Innere Medizin II |
| Depositing User: | Dr. Gernot Deinzer |
| Date Deposited: | 14 Aug 2019 09:11 |
| Last Modified: | 14 Aug 2019 09:11 |
| URI: | https://pred.uni-regensburg.de/id/eprint/9554 |
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