We studied the in vivo antibody responses of three H-2b strains, BALB/b, C57BL/6 and BALB/B x C57BL/6 F1 to various lysozymes, REL and HEL, after priming with HEL, REL or the HEL N-terminal peptide. It was confirmed that C57BL/6 is a non-responder strain to HEL and that BALB/b is responder strain. The C57BL/6 non-responder trait was associated with HEL or peptide induction of suppressor cells, as shown by adoptive transfer experiments. We further demonstrated that the suppressor/non-responder trait is dominant in BALB/b x C57BL/6 F1 hybrids and that appropriately pulsed macrophages of BALB/b mice can bypass such suppression in these F1 mice. Possible mechanisms are discussed.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1016/0923-2494(91)90125-3 | DOI Listing |
Blood Adv
September 2020
Blood and Marrow Transplantation.
Graft-versus-host disease (GVHD) is a complication of hematopoietic cell transplantation (HCT) caused by alloreactive T cells. Murine models of HCT are used to understand GVHD and T-cell reconstitution in GVHD target organs, most notably the gastrointestinal (GI) tract where the disease contributes most to patient mortality. T-cell receptor (TCR) repertoire sequencing was used to measure T-cell reconstitution from the same donor graft (C57BL/6 H-2b) in the GI tract of different recipients across a spectrum of matching, from syngeneic (C57BL/6), to minor histocompatibility (MHC) antigen mismatch BALB.
View Article and Find Full Text PDFAm J Transplant
March 2021
Section of Transplantation Immunology, Department of Surgery, Medical University of Vienna, Vienna, Austria.
Eliminating cytoreductive conditioning from chimerism-based tolerance protocols would facilitate clinical translation. Here we investigated the impact of major histocompatibility complex (MHC) and minor histocompatibility antigen (MiHA) barriers on mechanisms of tolerance and rejection in this setting. Transient depletion of natural killer (NK) cells at the time of bone marrow (BM) transplantation (BMT) (20 × 10 BALB/c BM cells → C57BL/6 recipients under costimulation blockade [CB] and rapamycin) prevented BM rejection.
View Article and Find Full Text PDFFront Cell Infect Microbiol
June 2021
Institute for Virology and Research Center for Immunotherapy (FZI) at the University Medical Center of the Johannes Gutenberg-University of Mainz, Mainz, Germany.
Hematoablative treatment followed by hematopoietic cell transplantation (HCT) for reconstituting the co-ablated immune system is a therapeutic option to cure aggressive forms of hematopoietic malignancies. In cases of family donors or unrelated donors, immunogenetic mismatches in major histocompatibility complex (MHC) and/or minor histocompatibility (minor-H) loci are unavoidable and bear a risk of graft-vs.-host reaction and disease (GvHR/D).
View Article and Find Full Text PDFBiol Blood Marrow Transplant
December 2019
Division of Blood and Marrow Transplantation, Department of Medicine, Stanford University School of Medicine, Stanford, California; Division of Pediatric Blood and Marrow Transplantation, Stanford University School of Medicine, Stanford, California.
Graft-versus-host disease (GVHD) remains a major complication of allogeneic hematopoietic cell transplantation. Acute GVHD (aGVHD) results from direct damage by donor T cells, whereas the biology of chronic GVHD (cGVHD) with its autoimmune-like manifestations remains poorly understood, mainly because of the paucity of representative preclinical models. We examined over an extended time period 7 MHC-matched, minor antigen-mismatched mouse models for development of cGVHD.
View Article and Find Full Text PDFTransplantation
December 2015
1 Department of Surgery, Emory Transplant Center, Emory University School of Medicine, Atlanta, GA. 2 Department of Pediatrics, Emory University School of Medicine, Atlanta, GA. 3 Center for Cardiovascular Biology, Children's Healthcare of Atlanta, Atlanta, GA. 4 Department of Surgery, Duke Transplant Center, Duke University Medical Center, Durham, NC. 5 Department of Pathology, Emory University School of Medicine, Atlanta, GA. 6 Division of Transplantation, Department of Surgery, University of Wisconsin-Madison, Madison, WI.
Background: Blocking leukocyte function-associated antigen (LFA)-1 in organ transplant recipients prolongs allograft survival. However, the precise mechanisms underlying the therapeutic potential of LFA-1 blockade in preventing chronic rejection are not fully elucidated. Cardiac allograft vasculopathy (CAV) is the preeminent cause of late cardiac allograft failure characterized histologically by concentric intimal hyperplasia.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!