Immunity (Cambridge, Mass.), 2012-08, Vol.37 (2), p.339-350
- Hanash, Alan M.
- Dudakov, Jarrod A.
- Hua, Guoqiang
- O’Connor, Margaret H.
- Young, Lauren F.
- Singer, Natalie V.
- West, Mallory L.
- Jenq, Robert R.
- Holland, Amanda M.
- Kappel, Lucy W.
- Ghosh, Arnab
- Tsai, Jennifer J.
- Rao, Uttam K.
- Yim, Nury L.
- Smith, Odette M.
- Velardi, Enrico
- Hawryluk, Elena B.
- Murphy, George F.
- Liu, Chen
- Fouser, Lynette A.
- Kolesnick, Richard
- Blazar, Bruce R.
- van den Brink, Marcel R.M.
2012
Details
- Autor(en) / Beteiligte
- Hanash, Alan M.
- Dudakov, Jarrod A.
- Hua, Guoqiang
- O’Connor, Margaret H.
- Young, Lauren F.
- Singer, Natalie V.
- West, Mallory L.
- Jenq, Robert R.
- Holland, Amanda M.
- Kappel, Lucy W.
- Ghosh, Arnab
- Tsai, Jennifer J.
- Rao, Uttam K.
- Yim, Nury L.
- Smith, Odette M.
- Velardi, Enrico
- Hawryluk, Elena B.
- Murphy, George F.
- Liu, Chen
- Fouser, Lynette A.
- Kolesnick, Richard
- Blazar, Bruce R.
- van den Brink, Marcel R.M.
- Titel
- Interleukin-22 Protects Intestinal Stem Cells from Immune-Mediated Tissue Damage and Regulates Sensitivity to Graft versus Host Disease
- Ist Teil von
- Immunity (Cambridge, Mass.), 2012-08, Vol.37 (2), p.339-350
- Ort / Verlag
- United States: Elsevier Inc
- Erscheinungsjahr
- 2012
- Link zum Volltext
- Quelle
- MEDLINE
- Beschreibungen/Notizen
- Little is known about the maintenance of intestinal stem cells (ISCs) and progenitors during immune-mediated tissue damage or about the susceptibility of transplant recipients to tissue damage mediated by the donor immune system during graft versus host disease (GVHD). We demonstrate here that deficiency of recipient-derived IL-22 increased acute GVHD tissue damage and mortality, that ISCs were eliminated during GVHD, and that ISCs as well as their downstream progenitors expressed the IL-22 receptor. Intestinal IL-22 was produced after bone marrow transplant by IL-23-responsive innate lymphoid cells (ILCs) from the transplant recipients, and intestinal IL-22 increased in response to pretransplant conditioning. However, ILC frequency and IL-22 amounts were decreased by GVHD. Recipient IL-22 deficiency led to increased crypt apoptosis, depletion of ISCs, and loss of epithelial integrity. Our findings reveal IL-22 as a critical regulator of tissue sensitivity to GVHD and a protective factor for ISCs during inflammatory intestinal damage. [Display omitted] ► Intestinal stem cells (ISCs) and progenitors express the IL-22 receptor ► Intestinal IL-22 increases after radiation injury but is decreased in GVHD ► Recipient innate lymphoid cells make IL-22 post-BMT, but they are eliminated by GVHD ► Recipient IL-22 deficiency increases crypt apoptosis, loss of ISC, and GVHD mortality
- Sprache
- Englisch
- Identifikatoren
- ISSN: 1074-7613eISSN: 1097-4180DOI: 10.1016/j.immuni.2012.05.028Titel-ID: cdi_proquest_miscellaneous_1113217082
- Format
- –
- Schlagworte
- Animals, Apoptosis, Bone marrow, Bone Marrow Transplantation - adverse effects, Bone Marrow Transplantation - immunology, Disease Models, Animal, Donors, Flow Cytometry, Graft vs Host Disease - immunology, Graft vs Host Disease - mortality, Graft-versus-host reaction, Immune system, Immunohistochemistry, Inflammation, Inflammatory bowel disease, Interleukin 22, Interleukin-23 - metabolism, Interleukins - genetics, Interleukins - immunology, Interleukins - metabolism, Intestine, Intestine, Small - cytology, Intestine, Small - immunology, Lymphoid cells, Medical research, Mice, Mice, Inbred BALB C, Mice, Inbred C57BL, Mice, Knockout, Mortality, Receptors, Interleukin - metabolism, Rodents, Stem cells, Stem Cells - metabolism, Transplants & implants