scholarly journals The Role of the Class II Transactivator (CIITA) in MHC Class I and II Regulation and Graft Rejection in Kidney

2001 ◽  
Vol 1 (3) ◽  
pp. 211-221 ◽  
Author(s):  
Tasha N. Sims ◽  
Marjan Afrouzian ◽  
Joan Urmson ◽  
Lin-Fu Zhu ◽  
Philip F. Halloran
Keyword(s):  
Mhc Class I ◽  
Graft Rejection ◽  
Class Ii ◽  
Class I ◽  
Class Ii Transactivator

Prevention of allogeneic marrow graft rejection by donor T cells that do not recognize recipient alloantigens: potential role of a veto mechanism

Blood ◽  
1996 ◽  
Vol 88 (3) ◽  
pp. 962-969 ◽  
Author(s):  
PJ Martin
Keyword(s):  
T Cells ◽  
Mhc Class I ◽  
Graft Rejection ◽  
Class Ii ◽  
Class I ◽  
Marrow Graft ◽  
Cd8 Cells ◽  
Donor T Cells ◽  
Veto Mechanism ◽  
Allogeneic Marrow

Clinical trials and experimental studies have demonstrated that donor T cells can play a critical role in preventing allogeneic marrow graft rejection. Results of a previous study showed that donor T cells were most effective for preventing rejection when they recognize an alloantigen expressed by recipient T cells and can cause graft-versus- host disease (GVHD). The present study examined models where marrow graft rejection can be prevented by donor T cells that do not recognize host alloantigens and cannot cause GVHD. Donor T cells prevented rejection of major histocompatibility complex (MHC) class I and II- disparate F1 marrow in parental recipients prepared with > or = 800 cGy total body irradiation (TBI) but not in those prepared with < or = 750 cGy TBI. In recipients prepared with high TBI exposures, rejection was mediated entirely by host CD8 cells. With lower TBI exposures, rejection was mediated by host CD4 cells and CD8 cells. These observations suggested the hypothesis that donor T cells prevent rejection mediated by host effectors that recognize donor MHC class I alloantigens but do not prevent rejection mediated by host effectors that recognize donor class II alloantigens. Consistent with this hypothesis, further experiments showed that F1 donor T cells can prevent rejection of MHC class I-disparate marrow in irradiated parental recipients but have no detectable effect on rejection of MHC class II-disparate marrow. We propose that the expression of MHC class I molecules on donor T cells makes it possible for these cells to inactivate the host response against donor class I alloantigens through a veto mechanism, whereas the absence of MHC class II molecules on murine T cells explains why these cells cannot inactivate the host response against donor class II alloantigens. Finally, donor CD4 cells and CD8 cells were equivalently effective for preventing rejection of F1 marrow in parental recipients, suggesting that veto activity is not restricted solely to the CD8 subset of murine T cells. A veto mechanism could enable donor T cells to prevent allogeneic marrow graft rejection without causing GVHD.

scholarly journals Induction of MHC Class I Expression by the MHC Class II Transactivator CIITA

Immunity ◽  
1997 ◽  
Vol 6 (5) ◽  
pp. 591-600 ◽  
Author(s):  
Brian K Martin ◽  
Keh-Chuang Chin ◽  
John C Olsen ◽  
Cheryl A Skinner ◽  
Anup Dey ◽  
...  
Keyword(s):  
Mhc Class I ◽  
Mhc Class Ii ◽  
Class Ii ◽  
Class I ◽  
Class Ii Transactivator ◽  
Mhc Class Ii Transactivator

scholarly journals Rapamycin, a potent inhibitor of T-cell function, prevents graft rejection in murine recipients of allogeneic T-cell-depleted donor marrow [published erratum appears in Blood 1994 Jun 1;83(11):3424-5]

Blood ◽  
1994 ◽  
Vol 83 (2) ◽  
pp. 600-609 ◽  
Author(s):  
BR Blazar ◽  
PA Taylor ◽  
SN Sehgal ◽  
DA Vallera
Keyword(s):  
T Cell ◽  
Mhc Class I ◽  
Graft Rejection ◽  
Cell Function ◽  
Class Ii ◽  
Class I ◽  
Therapeutic Modality ◽  
Hematopoietic Recovery ◽  
Cell Subpopulations ◽  
T Cell Subpopulations

Abstract We investigated the ability of the macrolide antifungal agent rapamycin (RAPA) to inhibit the rejection of T-cell-depleted (TCD) donor bone marrow (BM) transplanted into major histocompatibility complex (MHC)- disparate irradiated recipients. RAPA (1.5 mg/kg) was administered for 14 days beginning on the day of transplant. In the present study, we have tested RAPA administration in two types of fully allogeneic BM transplantation (BMT) systems in which host T cells mediate the rejection of TCD BM grafts (DBA/1 transplanted into C57BL/6 and BALB/c transplanted into C57BL/6). In both instances, RAPA administration prevented the rejection of the donor graft, accelerated post-BMT hematopoietic recovery, and did not compromise recipient survival. Sequential post-BMT fluorescence-activated cell sorter analysis of the spleen showed that RAPA administration inhibited host CD4+ and CD8+ T- cell expansion that leads to graft rejection. To further investigate the effect of RAPA on T-cell subpopulations, we used two congenic donor mouse stains with isolated MHC class I (bm1) or class II (bm12) mutations. In these studies, we showed that RAPA administration can inhibit MHC class I-restricted CD8+ or class II-restricted CD4+ T-cell- mediated graft rejection without compromising recipient survival. The RAPA-facilitated alloengraftment is multilineage and durable. We have also shown that RAPA speeds hematopoietic recovery post-BMT. We conclude that RAPA represents a new therapeutic modality for promoting alloengraftment and accelerating hematopoietic recovery.

The role of MHC class I and class II molecules in susceptibility to Lyme disease in inbred B10 H-2 congenic and recombinant mice

2011 ◽  
Vol 4 (02) ◽  
pp. 88-93
Author(s):  
Sunitha Reddy ◽  
Colin Young ◽  
Regina Hokanson ◽  
Julie Rawlings ◽  
Chella David
Keyword(s):  
Lyme Disease ◽  
Mhc Class I ◽  
Class Ii ◽  
Class I ◽  
Recombinant Mice

Regulation of the expression of MHC class I and II by class II transactivator (CIITA) in hematopoietic cells

1999 ◽  
Vol 17 (4) ◽  
pp. 149-160 ◽  
Author(s):  
Aichun Liu ◽  
Masuhiro Takahashi ◽  
Ken Toba ◽  
Zhiyin Zheng ◽  
Shigeo Hashimoto ◽  
...  
Keyword(s):  
Mhc Class I ◽  
Hematopoietic Cells ◽  
Class Ii ◽  
Class I ◽  
Class Ii Transactivator

scholarly journals Prevention of allogeneic marrow graft rejection by donor T cells that do not recognize recipient alloantigens: potential role of a veto mechanism

Blood ◽  
1996 ◽  
Vol 88 (3) ◽  
pp. 962-969 ◽  
Author(s):  
PJ Martin
Keyword(s):  
T Cells ◽  
Mhc Class I ◽  
Graft Rejection ◽  
Class Ii ◽  
Class I ◽  
Marrow Graft ◽  
Cd8 Cells ◽  
Donor T Cells ◽  
Veto Mechanism ◽  
Allogeneic Marrow

Abstract Clinical trials and experimental studies have demonstrated that donor T cells can play a critical role in preventing allogeneic marrow graft rejection. Results of a previous study showed that donor T cells were most effective for preventing rejection when they recognize an alloantigen expressed by recipient T cells and can cause graft-versus- host disease (GVHD). The present study examined models where marrow graft rejection can be prevented by donor T cells that do not recognize host alloantigens and cannot cause GVHD. Donor T cells prevented rejection of major histocompatibility complex (MHC) class I and II- disparate F1 marrow in parental recipients prepared with > or = 800 cGy total body irradiation (TBI) but not in those prepared with < or = 750 cGy TBI. In recipients prepared with high TBI exposures, rejection was mediated entirely by host CD8 cells. With lower TBI exposures, rejection was mediated by host CD4 cells and CD8 cells. These observations suggested the hypothesis that donor T cells prevent rejection mediated by host effectors that recognize donor MHC class I alloantigens but do not prevent rejection mediated by host effectors that recognize donor class II alloantigens. Consistent with this hypothesis, further experiments showed that F1 donor T cells can prevent rejection of MHC class I-disparate marrow in irradiated parental recipients but have no detectable effect on rejection of MHC class II-disparate marrow. We propose that the expression of MHC class I molecules on donor T cells makes it possible for these cells to inactivate the host response against donor class I alloantigens through a veto mechanism, whereas the absence of MHC class II molecules on murine T cells explains why these cells cannot inactivate the host response against donor class II alloantigens. Finally, donor CD4 cells and CD8 cells were equivalently effective for preventing rejection of F1 marrow in parental recipients, suggesting that veto activity is not restricted solely to the CD8 subset of murine T cells. A veto mechanism could enable donor T cells to prevent allogeneic marrow graft rejection without causing GVHD.

scholarly journals Rapamycin, a potent inhibitor of T-cell function, prevents graft rejection in murine recipients of allogeneic T-cell-depleted donor marrow [published erratum appears in Blood 1994 Jun 1;83(11):3424-5]

Blood ◽  
1994 ◽  
Vol 83 (2) ◽  
pp. 600-609
Author(s):  
BR Blazar ◽  
PA Taylor ◽  
SN Sehgal ◽  
DA Vallera
Keyword(s):  
T Cell ◽  
Mhc Class I ◽  
Graft Rejection ◽  
Cell Function ◽  
Class Ii ◽  
Class I ◽  
Therapeutic Modality ◽  
Hematopoietic Recovery ◽  
Cell Subpopulations ◽  
T Cell Subpopulations

We investigated the ability of the macrolide antifungal agent rapamycin (RAPA) to inhibit the rejection of T-cell-depleted (TCD) donor bone marrow (BM) transplanted into major histocompatibility complex (MHC)- disparate irradiated recipients. RAPA (1.5 mg/kg) was administered for 14 days beginning on the day of transplant. In the present study, we have tested RAPA administration in two types of fully allogeneic BM transplantation (BMT) systems in which host T cells mediate the rejection of TCD BM grafts (DBA/1 transplanted into C57BL/6 and BALB/c transplanted into C57BL/6). In both instances, RAPA administration prevented the rejection of the donor graft, accelerated post-BMT hematopoietic recovery, and did not compromise recipient survival. Sequential post-BMT fluorescence-activated cell sorter analysis of the spleen showed that RAPA administration inhibited host CD4+ and CD8+ T- cell expansion that leads to graft rejection. To further investigate the effect of RAPA on T-cell subpopulations, we used two congenic donor mouse stains with isolated MHC class I (bm1) or class II (bm12) mutations. In these studies, we showed that RAPA administration can inhibit MHC class I-restricted CD8+ or class II-restricted CD4+ T-cell- mediated graft rejection without compromising recipient survival. The RAPA-facilitated alloengraftment is multilineage and durable. We have also shown that RAPA speeds hematopoietic recovery post-BMT. We conclude that RAPA represents a new therapeutic modality for promoting alloengraftment and accelerating hematopoietic recovery.

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