BIOMAT Database Logo BIOMAT Database Logo

Interleukin-11 promotes T cell polarization and prevents acute graft-versus-host disease after allogeneic bone marrow transplantation. 1998

G R Hill, and K R Cooke, and T Teshima, and J M Crawford, and J C Keith, and Y S Brinson, and D Bungard, and J L Ferrara
Department of Pediatric Oncology, Dana Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts 02115, USA.

Administration of IL-11 prevented lethal graft-versus-host disease (GVHD) in a murine bone marrow transplant (BMT) model (B6 --> B6D2F1) across MHC and minor H antigen barriers (survival at day 50: 90 vs 20%, P < 0.001). Surpisingly, IL-11 administration polarized the donor T cell cytokine responses to host antigen after BMT with a 50% reduction in IFNgamma and IL-2 secretion and a 10-fold increase in IL-4. This polarization of T cell responses was associated with reduced IFNgamma serum levels and decreased IL-12 production in mixed lymphocyte cultures (MLC). In addition, IL-11 prevented small bowel damage and reduced serum endotoxin levels by 80%. Treatment with IL-11 also reduced TNFalpha serum levels and suppressed TNFalpha secretion by macrophages to LPS stimulation in vitro. IL-11 thus decreased GVHD morbidity and mortality by three mechanisms: (a) polarization of donor T cells; (b) protection of the small bowel; and (c) suppression of inflammatory cytokines such as TNFalpha. We conclude that brief treatment with IL-11 may represent a novel strategy to prevent T cell-mediated inflammatory processes such as GVHD.

UI MeSH Term Description Entries
D007371 Interferon-gamma The major interferon produced by mitogenically or antigenically stimulated LYMPHOCYTES. It is structurally different from TYPE I INTERFERON and its major activity is immunoregulation. It has been implicated in the expression of CLASS II HISTOCOMPATIBILITY ANTIGENS in cells that do not normally produce them, leading to AUTOIMMUNE DISEASES. Interferon Type II,Interferon, Immune,gamma-Interferon,Interferon, gamma,Type II Interferon,Immune Interferon,Interferon, Type II
D007421 Intestine, Small The portion of the GASTROINTESTINAL TRACT between the PYLORUS of the STOMACH and the ILEOCECAL VALVE of the LARGE INTESTINE. It is divisible into three portions: the DUODENUM, the JEJUNUM, and the ILEUM. Small Intestine,Intestines, Small,Small Intestines
D008070 Lipopolysaccharides Lipid-containing polysaccharides which are endotoxins and important group-specific antigens. They are often derived from the cell wall of gram-negative bacteria and induce immunoglobulin secretion. The lipopolysaccharide molecule consists of three parts: LIPID A, core polysaccharide, and O-specific chains (O ANTIGENS). When derived from Escherichia coli, lipopolysaccharides serve as polyclonal B-cell mitogens commonly used in laboratory immunology. (From Dorland, 28th ed) Lipopolysaccharide,Lipoglycans
D008810 Mice, Inbred C57BL One of the first INBRED MOUSE STRAINS to be sequenced. This strain is commonly used as genetic background for transgenic mouse models. Refractory to many tumors, this strain is also preferred model for studying role of genetic variations in development of diseases. Mice, C57BL,Mouse, C57BL,Mouse, Inbred C57BL,C57BL Mice,C57BL Mice, Inbred,C57BL Mouse,C57BL Mouse, Inbred,Inbred C57BL Mice,Inbred C57BL Mouse
D002478 Cells, Cultured Cells propagated in vitro in special media conducive to their growth. Cultured cells are used to study developmental, morphologic, metabolic, physiologic, and genetic processes, among others. Cultured Cells,Cell, Cultured,Cultured Cell
D005260 Female Females
D006086 Graft vs Host Disease The clinical entity characterized by anorexia, diarrhea, loss of hair, leukopenia, thrombocytopenia, growth retardation, and eventual death brought about by the GRAFT VS HOST REACTION. Graft-Versus-Host Disease,Homologous Wasting Disease,Runt Disease,Graft-vs-Host Disease,Disease, Graft-Versus-Host,Disease, Graft-vs-Host,Disease, Homologous Wasting,Disease, Runt,Diseases, Graft-Versus-Host,Diseases, Graft-vs-Host,Graft Versus Host Disease,Graft-Versus-Host Diseases,Graft-vs-Host Diseases
D000208 Acute Disease Disease having a short and relatively severe course. Acute Diseases,Disease, Acute,Diseases, Acute
D000818 Animals Unicellular or multicellular, heterotrophic organisms, that have sensation and the power of voluntary movement. Under the older five kingdom paradigm, Animalia was one of the kingdoms. Under the modern three domain model, Animalia represents one of the many groups in the domain EUKARYOTA. Animal,Metazoa,Animalia
D013601 T-Lymphocytes Lymphocytes responsible for cell-mediated immunity. Two types have been identified - cytotoxic (T-LYMPHOCYTES, CYTOTOXIC) and helper T-lymphocytes (T-LYMPHOCYTES, HELPER-INDUCER). They are formed when lymphocytes circulate through the THYMUS GLAND and differentiate to thymocytes. When exposed to an antigen, they divide rapidly and produce large numbers of new T cells sensitized to that antigen. T Cell,T Lymphocyte,T-Cells,Thymus-Dependent Lymphocytes,Cell, T,Cells, T,Lymphocyte, T,Lymphocyte, Thymus-Dependent,Lymphocytes, T,Lymphocytes, Thymus-Dependent,T Cells,T Lymphocytes,T-Cell,T-Lymphocyte,Thymus Dependent Lymphocytes,Thymus-Dependent Lymphocyte

Related Publications

G R Hill, and K R Cooke, and T Teshima, and J M Crawford, and J C Keith, and Y S Brinson, and D Bungard, and J L Ferrara
Acute graft-versus-host disease after allogeneic bone marrow transplantation.
November 1983, Canadian Medical Association journal,
G R Hill, and K R Cooke, and T Teshima, and J M Crawford, and J C Keith, and Y S Brinson, and D Bungard, and J L Ferrara
Oligoclonal T-cell repertoire and graft-versus-host disease after allogeneic bone marrow transplantation.
July 1995, Annals of the New York Academy of Sciences,
G R Hill, and K R Cooke, and T Teshima, and J M Crawford, and J C Keith, and Y S Brinson, and D Bungard, and J L Ferrara
[Acute and chronic graft-versus-host disease after allogeneic bone marrow transplantation].
January 1985, [Rinsho ketsueki] The Japanese journal of clinical hematology,
G R Hill, and K R Cooke, and T Teshima, and J M Crawford, and J C Keith, and Y S Brinson, and D Bungard, and J L Ferrara
[Acute graft-versus-host disease in allogeneic bone marrow transplantation].
July 1984, [Rinsho ketsueki] The Japanese journal of clinical hematology,
G R Hill, and K R Cooke, and T Teshima, and J M Crawford, and J C Keith, and Y S Brinson, and D Bungard, and J L Ferrara
Interferon-gamma prevents graft-versus-host disease after allogeneic bone marrow transplantation in mice.
December 1993, Journal of immunology (Baltimore, Md. : 1950),
G R Hill, and K R Cooke, and T Teshima, and J M Crawford, and J C Keith, and Y S Brinson, and D Bungard, and J L Ferrara
Elevated interleukin (IL)-18 levels during acute graft-versus-host disease after allogeneic bone marrow transplantation.
June 2000, British journal of haematology,
G R Hill, and K R Cooke, and T Teshima, and J M Crawford, and J C Keith, and Y S Brinson, and D Bungard, and J L Ferrara
Cytokine serum levels and acute graft versus host disease after allogeneic bone marrow transplantation.
January 1992, Haematologica,
G R Hill, and K R Cooke, and T Teshima, and J M Crawford, and J C Keith, and Y S Brinson, and D Bungard, and J L Ferrara
Host MyD88 signaling protects against acute graft-versus-host disease after allogeneic bone marrow transplantation.
January 2019, Clinical and experimental immunology,
G R Hill, and K R Cooke, and T Teshima, and J M Crawford, and J C Keith, and Y S Brinson, and D Bungard, and J L Ferrara
T-cell depletion of allogeneic bone marrow prevents acceleration of graft-versus-host disease induced by exogenous interleukin 2.
December 1986, Cellular immunology,
G R Hill, and K R Cooke, and T Teshima, and J M Crawford, and J C Keith, and Y S Brinson, and D Bungard, and J L Ferrara
Graft versus host disease following allogeneic bone marrow transplantation.
October 1992, Current opinion in immunology,
Copied contents to your clipboard!