Immune tolerance to self-MHC class II antigens after bone marrow transplantation

1999 ◽  
Vol 31 (1-2) ◽  
pp. 688-689 ◽  
Author(s):  
A Hess ◽  
L Horwitz ◽  
C Thoburn
Keyword(s):  
Bone Marrow ◽  
Bone Marrow Transplantation ◽  
Mhc Class Ii ◽  
Immune Tolerance ◽  
Marrow Transplantation ◽  
Class Ii ◽  
Mhc Class Ii Antigens ◽  
Class Ii Antigens

scholarly journals The importance of MHC class II in allogeneic bone marrow transplantation and chimerism-based solid organ tolerance in a rat model

PLoS ONE ◽  
2020 ◽  
Vol 15 (5) ◽  
pp. e0233497
Author(s):  
Kai Timrott ◽  
Oliver Beetz ◽  
Felix Oldhafer ◽  
Jürgen Klempnauer ◽  
Florian W. R. Vondran ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Bone Marrow Transplantation ◽  
Mhc Class Ii ◽  
Rat Model ◽  
Marrow Transplantation ◽  
Allogeneic Bone Marrow Transplantation ◽  
Class Ii ◽  
Allogeneic Bone Marrow ◽  
Solid Organ ◽  
Allogeneic Bone

Sirolimus promotes tolerance for donor and recipient antigens after MHC class II disparate bone marrow transplantation in rats

2007 ◽  
Vol 35 (1) ◽  
pp. 164-170 ◽  
Author(s):  
Mark D. Jäger ◽  
Jian Y. Liu ◽  
Kai F. Timrott ◽  
Felix C. Popp ◽  
Oliver Stoeltzing ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Bone Marrow Transplantation ◽  
Mhc Class Ii ◽  
Marrow Transplantation ◽  
Class Ii

scholarly journals Enhancement of the proliferation of human marrow erythroid (BFU-E) progenitor cells by prostaglandin E requires the participation of OKT8- positive T lymphocytes and is associated with the density expression of major histocompatibility complex class II antigens on BFU-E

Blood ◽  
1986 ◽  
Vol 68 (1) ◽  
pp. 126-133
Author(s):  
L Lu ◽  
LM Pelus ◽  
HE Broxmeyer ◽  
MA Moore ◽  
M Wachter ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Mhc Class Ii ◽  
Colony Formation ◽  
Class Ii ◽  
Low Density ◽  
Mhc Class Ii Antigens ◽  
Class Ii Antigen ◽  
Mhc Class Ii Antigen ◽  
Class Ii Antigens ◽  
Marrow Cells

The relationship between major histocompatibility complex class II antigens (MHC class II, eg, HLA-DR, Ia), T lymphocytes, and the enhancement of erythroid colony formation from BFU-E by prostaglandin E was analyzed using normal bone marrow cells. In primary methylcellulose culture, the addition of prostaglandin E1 (PGE1) to unseparated buffy coat, low-density, or nonadherent low-density (NAL) marrow cells resulted in an enhancement of the total number of erythroid (BFU-E) colonies observed. Treatment of bone marrow cells with a monoclonal antihuman MHC class II antibody plus complement (C') resulted in a reduction of the total number of colonies by approximately 50% and abrogation of the enhancing effect of PGE1. Analysis of accessory cell requirements by depletion of both adherent cells and sheep erythrocyte rosetting lymphocytes (E+ cells) and reconstitution using C' or anti- MHC class II antibody plus C'-treated T cell-depleted NAL (NALT-) marrow cells and E+ cell populations treated with C' or anti-MHC class II antibody plus C' demonstrated a requirement for MHC class II antigen- T cells, but not adherent cells, and a requirement for MHC class II antigen + BFU-E in order to observe the enhancing effect of PGE1 on erythroid colony formation. Positive selection of BFU-E in NALT- bone marrow expressing differing density distributions of MHC class II antigens was accomplished with monoclonal anti-MHC class II antibodies and sorting with a fluorescence-activated cell sorter (FACS). Addition of E+ cells to the different populations of MHC class II antigen+ NALT- cells demonstrated that the PGE-enhancing effects on erythroid colony formation were directly related to increasing density distributions of MHC class II antigens on BFU-E. Colony formation by BFU-E expressing a low density distribution of MHC class II antigens or having no detectable MHC class II antigens, as determined by FACS analysis, was not enhanced by PGE1 in the presence of MHC class II antigen-positive or -negative T cells.

scholarly journals Bone marrow transplantation in major histocompatibility complex class II deficiency: a single-center study of 19 patients

Blood ◽  
1995 ◽  
Vol 85 (2) ◽  
pp. 580-587
Author(s):  
C Klein ◽  
M Cavazzana-Calvo ◽  
F Le Deist ◽  
N Jabado ◽  
M Benkerrou ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Major Histocompatibility Complex ◽  
Bone Marrow Transplantation ◽  
Mhc Class Ii ◽  
Marrow Transplantation ◽  
Class Ii ◽  
Combined Immunodeficiency ◽  
Major Histocompatibility ◽  
Histocompatibility Complex ◽  
Mhc Class Ii Deficiency

Major histocompatibility complex (MHC) class II deficiency (bare lymphocyte syndrome) is a rare inborn error of the immune system characterized by impaired antigen presentation and combined immunodeficiency. It causes severe and unremitting infections leading to progressive liver and lung dysfunctions and death during childhood. As in other combined immunodeficiency disorders, bone marrow transplantation (BMT) is considered the treatment of choice for MHC class II deficiency. We analyzed the files of 19 patients who have undergone BMT in our center. Of the 7 patients who underwent HLA- identical BMT, 3 died in the immediate posttransplant period of severe viral infections, whereas the remaining 4 were cured, with recovery of normal immune functions. Of the 12 patients who underwent HLA-haplo- identical BMT, 3 were cured, 1 was improved by partial engraftment, 7 died of infectious complications due to graft failure or rejection, and 1 is still immunodeficient because of engraftment failure. A favorable outcome in the HLA-non-identical BMT group was associated with an age of less than 2 years at the time of transplantation. All the patients with stable long-term engraftment had persistently low CD4 counts after transplantation (105 to 650/microL at last follow up), but no clear susceptibility to opportunistic infections despite persisting MHC class II deficiency on thymic epithelium and other nonhematopoietic cells. We conclude that HLA-identical and -haploidentical BMT can cure MHC class II deficiency, although the success rate of haploidentical BMT is lower than that in other combined immunodeficiency syndromes. HLA- haploidentical BMT should preferably be performed in the first 2 years of life, before the acquisition of chronic virus carriage and sequelae of infections.

scholarly journals Bone marrow transplantation in major histocompatibility complex class II deficiency: a single-center study of 19 patients

Blood ◽  
1995 ◽  
Vol 85 (2) ◽  
pp. 580-587 ◽  
Author(s):  
C Klein ◽  
M Cavazzana-Calvo ◽  
F Le Deist ◽  
N Jabado ◽  
M Benkerrou ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Major Histocompatibility Complex ◽  
Bone Marrow Transplantation ◽  
Mhc Class Ii ◽  
Marrow Transplantation ◽  
Class Ii ◽  
Combined Immunodeficiency ◽  
Major Histocompatibility ◽  
Histocompatibility Complex ◽  
Mhc Class Ii Deficiency

Abstract Major histocompatibility complex (MHC) class II deficiency (bare lymphocyte syndrome) is a rare inborn error of the immune system characterized by impaired antigen presentation and combined immunodeficiency. It causes severe and unremitting infections leading to progressive liver and lung dysfunctions and death during childhood. As in other combined immunodeficiency disorders, bone marrow transplantation (BMT) is considered the treatment of choice for MHC class II deficiency. We analyzed the files of 19 patients who have undergone BMT in our center. Of the 7 patients who underwent HLA- identical BMT, 3 died in the immediate posttransplant period of severe viral infections, whereas the remaining 4 were cured, with recovery of normal immune functions. Of the 12 patients who underwent HLA-haplo- identical BMT, 3 were cured, 1 was improved by partial engraftment, 7 died of infectious complications due to graft failure or rejection, and 1 is still immunodeficient because of engraftment failure. A favorable outcome in the HLA-non-identical BMT group was associated with an age of less than 2 years at the time of transplantation. All the patients with stable long-term engraftment had persistently low CD4 counts after transplantation (105 to 650/microL at last follow up), but no clear susceptibility to opportunistic infections despite persisting MHC class II deficiency on thymic epithelium and other nonhematopoietic cells. We conclude that HLA-identical and -haploidentical BMT can cure MHC class II deficiency, although the success rate of haploidentical BMT is lower than that in other combined immunodeficiency syndromes. HLA- haploidentical BMT should preferably be performed in the first 2 years of life, before the acquisition of chronic virus carriage and sequelae of infections.

Expression of MHC Class II Antigens on Rat Bone Marrow Cells and Macrophages, and Their Modulation during Culture with Murine GM-CSF or M-CSF

Immunobiology ◽  
1995 ◽  
Vol 192 (3-4) ◽  
pp. 185-197 ◽  
Author(s):  
Alois Gessl ◽  
Walter Krugluger ◽  
Kurt Langer ◽  
Isabella Baumgartner ◽  
Andreas Spittler ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Mhc Class Ii ◽  
Bone Marrow Cells ◽  
Class Ii ◽  
Gm Csf ◽  
Mhc Class Ii Antigens ◽  
Class Ii Antigens ◽  
Rat Bone ◽  
Marrow Cells

Enhancement of the proliferation of human marrow erythroid (BFU-E) progenitor cells by prostaglandin E requires the participation of OKT8- positive T lymphocytes and is associated with the density expression of major histocompatibility complex class II antigens on BFU-E

Blood ◽  
1986 ◽  
Vol 68 (1) ◽  
pp. 126-133 ◽  
Author(s):  
L Lu ◽  
LM Pelus ◽  
HE Broxmeyer ◽  
MA Moore ◽  
M Wachter ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Mhc Class Ii ◽  
Colony Formation ◽  
Class Ii ◽  
Low Density ◽  
Mhc Class Ii Antigens ◽  
Class Ii Antigen ◽  
Mhc Class Ii Antigen ◽  
Class Ii Antigens ◽  
Marrow Cells

Abstract The relationship between major histocompatibility complex class II antigens (MHC class II, eg, HLA-DR, Ia), T lymphocytes, and the enhancement of erythroid colony formation from BFU-E by prostaglandin E was analyzed using normal bone marrow cells. In primary methylcellulose culture, the addition of prostaglandin E1 (PGE1) to unseparated buffy coat, low-density, or nonadherent low-density (NAL) marrow cells resulted in an enhancement of the total number of erythroid (BFU-E) colonies observed. Treatment of bone marrow cells with a monoclonal antihuman MHC class II antibody plus complement (C') resulted in a reduction of the total number of colonies by approximately 50% and abrogation of the enhancing effect of PGE1. Analysis of accessory cell requirements by depletion of both adherent cells and sheep erythrocyte rosetting lymphocytes (E+ cells) and reconstitution using C' or anti- MHC class II antibody plus C'-treated T cell-depleted NAL (NALT-) marrow cells and E+ cell populations treated with C' or anti-MHC class II antibody plus C' demonstrated a requirement for MHC class II antigen- T cells, but not adherent cells, and a requirement for MHC class II antigen + BFU-E in order to observe the enhancing effect of PGE1 on erythroid colony formation. Positive selection of BFU-E in NALT- bone marrow expressing differing density distributions of MHC class II antigens was accomplished with monoclonal anti-MHC class II antibodies and sorting with a fluorescence-activated cell sorter (FACS). Addition of E+ cells to the different populations of MHC class II antigen+ NALT- cells demonstrated that the PGE-enhancing effects on erythroid colony formation were directly related to increasing density distributions of MHC class II antigens on BFU-E. Colony formation by BFU-E expressing a low density distribution of MHC class II antigens or having no detectable MHC class II antigens, as determined by FACS analysis, was not enhanced by PGE1 in the presence of MHC class II antigen-positive or -negative T cells.

Sign in / Sign up

Export Citation Format

Share Document