نتایج جستجو برای: gvhd

تعداد نتایج: 4940  

Journal: :Pediatric blood & cancer 2013
Kody R Crowell Raza A Patel Mark Fluchel Amy Lowichik Staci Bryson John F Pohl

BACKGROUND Graft-versus-host disease (GvHD) causes morbidity and mortality in recipients of hematopoietic stem cell transplantation (SCT). This study assessed the distribution of GvHD in gastrointestinal (GI) biopsies from the upper and lower GI tract in pediatric patients who had undergone SCT and evaluated if there was correlation between biopsy findings and possible extra-intestinal manifest...

Journal: :Journal of immunology 2012
Hongmei Li Anthony J Demetris Jennifer McNiff Catherine Matte-Martone Hung Sheng Tan David M Rothstein Fadi G Lakkis Warren D Shlomchik

The efficacy of allogeneic hematopoietic stem cell transplantation is limited by graft-versus-host disease (GVHD). Host hematopoietic APCs are important initiators of GVHD, making them logical targets for GVHD prevention. Conventional dendritic cells (DCs) are key APCs for T cell responses in other models of T cell immunity, and they are sufficient for GVHD induction. However, we report in this...

Journal: :Blood 2015
Dawn K Reichenbach Vincent Schwarze Benjamin M Matta Victor Tkachev Elisabeth Lieberknecht Quan Liu Brent H Koehn Dietmar Pfeifer Patricia A Taylor Gabriele Prinz Heide Dierbach Natalie Stickel Yvonne Beck Max Warncke Tobias Junt Annette Schmitt-Graeff Susumu Nakae Marie Follo Tobias Wertheimer Lukas Schwab Jason Devlin Simon C Watkins Justus Duyster James L M Ferrara Heth R Turnquist Robert Zeiser Bruce R Blazar

Interleukin (IL)-33 binding to the receptor suppression of tumorigenicity 2 (ST2) produces pro-inflammatory and anti-inflammatory effects. Increased levels of soluble ST2 (sST2) are a biomarker for steroid-refractory graft-versus-host disease (GVHD) and mortality. However, whether sST2 has a role as an immune modulator or only as a biomarker during GVHD was unclear. We show increased IL-33 prod...

Journal: :Blood 1995
L D Fast C R Valeri J P Crowley

Graft-versus-host disease (GVHD) is currently encountered after bone marrow transplantation and transfusion. GVHD associated with transfusion (TA-GVHD) in apparently immunocompetent recipients has been recently reported with increasing frequency. A consistent finding in many of these cases is that the recipient received blood from a donor homozygous for one of the recipient's HLA haplotypes. Ho...

Journal: :Haematologica 2006
Federico Sizzano Paola Magistroni Franco Locatelli Alessandro Busca Michele Falda Paola Affaticati Gina Mazzola Anna Maria Dall'omo Antonio Amoroso

We investigated the prognostic value of cytotoxic T-lymphocyte precursor frequencies (CTL-p-f) for the development of graft-versus-host disease (GvHD) in a cohort of 92 recipients of a hematopoietic stem cell transplantation from HLA-matched sibling donors. CTL-p-f and clinical variables were correlated with acute GvHD and chronic GvHD in univariate and multivariate analyses. CTL-p-f resulted a...

Journal: :Blood 2015
Anne-Kathrin Hechinger Benjamin A H Smith Ryan Flynn Kathrin Hanke Cameron McDonald-Hyman Patricia A Taylor Dietmar Pfeifer Björn Hackanson Franziska Leonhardt Gabriele Prinz Heide Dierbach Annette Schmitt-Graeff Jiri Kovarik Bruce R Blazar Robert Zeiser

The common γ chain (CD132) is a subunit of the interleukin (IL) receptors for IL-2, IL-4, IL-7, IL-9, IL-15, and IL-21. Because levels of several of these cytokines were shown to be increased in the serum of patients developing acute and chronic graft-versus-host disease (GVHD), we reasoned that inhibition of CD132 could have a profound effect on GVHD. We observed that anti-CD132 monoclonal ant...

Journal: :Blood 2008
Britt E Anderson Patricia A Taylor Jennifer M McNiff Dhanpat Jain Anthony J Demetris Angela Panoskaltsis-Mortari Ann Ager Bruce R Blazar Warren D Shlomchik Mark J Shlomchik

Graft-versus-host disease (GVHD) remains a major cause of morbidity and mortality in allogeneic stem cell transplantation. Effector memory T cells (T(EM)) do not cause GVHD but engraft and mount immune responses, including graft-versus-tumor effects. One potential explanation for the inability of T(EM) to cause GVHD is that T(EM) lack CD62L and CCR7, which are instrumental in directing naive T ...

2009
Jo Nadine Fleming Howard M. Shulman Richard A. Nash Pamela Y. Johnson Thomas N. Wight Allen Gown Stephen M. Schwartz

BACKGROUND The clinical and histologic appearance of fibrosis in cutaneous lesions in chronic graft-versus -host disease (c-GVHD) resembles the appearance of fibrosis in scleroderma (SSc). Recent studies identified distinctive structural changes in the superficial dermal microvasculature and matrix of SSc skin. We compared the dermal microvasculature in human c-GVHD to SSc to determine if c-GVH...

Journal: :Blood 1991
M L Cohn R A Cahill H J Deeg

We investigated in a murine model whether UVB irradiation of lymphohemopoietic cells would prevent the development of graft-versus-host disease (GVHD). Preliminary experiments showed that spleen colony (CFU-S) formation by hemopoietic cells was preserved at UVB doses that eliminated lymphocyte proliferation. In a parent into F1 model, UVB irradiation (5 to 15 mJ/cm2) of spleen cells added to no...

Journal: :Blood 1993
T Nierle D Bunjes R Arnold H Heimpel M Theobald

Recent studies in mice and humans have emphasized an important contribution of host-reactive minor histocompatibility antigen (mH)-specific lymphokine-secreting donor T-helper cells (Th) for the induction of acute graft-versus-host disease (GVHD) after allogeneic bone marrow transplantation (BMT). By using limiting dilution (LD) and clonal specificity analyses, we investigated in 14 patients wi...

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