Interleukin-22 protects intestinal stem cells from immune-mediated tissue damage and regulates sensitivity to graft versus host disease

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 defic...

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Podrobná bibliografie
Vydáno v:	Immunity (Cambridge, Mass.) Ročník 37; číslo 2; s. 339
Hlavní autoři:	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
Médium:	Journal Article
Jazyk:	angličtina
Vydáno:	United States 24.08.2012
Témata:	Animals Bone Marrow Transplantation - adverse effects Bone Marrow Transplantation - immunology Disease Models, Animal Flow Cytometry Graft vs Host Disease - immunology Graft vs Host Disease - mortality Immunohistochemistry Interleukin-22 Interleukin-23 - metabolism Interleukins - genetics Interleukins - immunology Interleukins - metabolism Intestine, Small - cytology Intestine, Small - immunology Mice Mice, Inbred BALB C Mice, Inbred C57BL Mice, Knockout Receptors, Interleukin - metabolism Stem Cells - metabolism
ISSN:	1097-4180, 1097-4180
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Shrnutí:	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.
Bibliografie:	ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23
ISSN:	1097-4180 1097-4180
DOI:	10.1016/j.immuni.2012.05.028