The Major Histocompatibility Complex of the Rat

Tj, Gill; Hw, Kunz; Dn, Misra; Al, Hassett

doi:10.1016/b978-0-12-233750-5.50090-7

Cited by 77 publications

(43 citation statements)

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“…Interestingly, upon cessation of CsA treatment following autologous or syngeneic BMT in man and rodents, a syndrome similar to GVHD has been shown to develop (7)(8)(9)(10)(11)(12)(13)(14)(15). Syngeneic GVHD (SGVHD) could be adoptively transferred with T cells from diseased animals into irradiated but not normal secondary recipients, suggesting that normal an· imals may maintain regulatory mechanism(s) to control autoreactivity (7,8).…”

Section: Discussionmentioning

confidence: 99%

Variable Chimerism, Graft-Versus-Host Disease, and Tolerance After Different Kinds of Cell and Whole Organ Transplantation From Lewis to Brown Norway Rats

et al. 1995

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Section: Discussionmentioning

confidence: 99%

Variable Chimerism, Graft-Versus-Host Disease, and Tolerance After Different Kinds of Cell and Whole Organ Transplantation From Lewis to Brown Norway Rats

et al. 1995

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“…This distinction was made with affinity-purified biotinylated mAb 163 and mAb 42, which are specific for the RT1.A 1 antigen (LEW MHC class I) and the RT1.A n antigen (BN MHC class I), respectively. 17 Cy-chrome-conjugated streptavidin (PharMingen, San Diego, CA) was used as a secondary antibody. In addition, donor MHC class II ϩ cells were identified by mAb L21-6, which is Macrophages.…”

Section: Flow Cytometrymentioning

confidence: 99%

Donor and recipient leukocytes in organ allografts of recipients with variable donor-specific tolerance: With particular reference to chronic rejection

et al. 2000

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We have attributed organ engraftment to clonal exhaustion-deletion of host-versus-graft and graft-versus-host reactions that are reciprocally induced and governed by migratory donor and recipient leukocytes. The so-called donor passenger leukocytes that migrate from the allograft into the recipients have been thoroughly studied (chimerism), but not the donor leukocytes that remain in, or return to, the transplanted organ. Therefore, using flow cytometry we determined the percentage and lineages of donor leukocytes in cell suspensions prepared from Lewis (LEW) cardiac allografts to 100 days posttransplantation. The LEW hearts were transplanted to naïve untreated Brown Norway (BN) recipients (group 2), to naïve BN recipients treated with a 28-day or continuous course of tacrolimus (TAC) (groups 3 and 4), and to drug-free BN recipients pretolerized by earlier bone marrow cell (BMC) or orthotopic LEW liver transplantation (groups 5 and 6). The findings in the heart cell suspensions were correlated with the results from parallel histopathologic-immunocytochemical studies and other studies of the grafts and of host tissues. Although the LEW heart allografts were rejected in 9.6 days by the unmodified recipients of group 2, all beat for 100 days in the recipients of groups 3 through 6. Nevertheless, all of the long-surviving cardiac allografts (but not the isografts in group 1) were the targets of an immune reaction at 5 days, reflected by dramatic increases in the ratio of leukocytes to nonleukocyte nucleated cells from normal values of 1:5-1:6 to 1:1-5:1 and by manifold other evidence of a major inflammatory event. The acute changes returned to baseline by 100 days in the chronic rejection (CR) free hearts of groups 4 and 6, but not in the CR-afflicted hearts of short-course TAC group 3 or the less-severely damaged hearts of the BMC-prime group 5.The freedom from CR in groups 4 and 6 was associated with a large donor contribution to the intracardiac leukocyte population at 5 days (28.6% and 22% in the respective groups) and at 100 days (30.5% in group 4 and 8.4% in group 6) compared with 2% and 1.2% at 100 days in the CR-blighted allografts of the partially tolerant animals of groups 3 and 5. Whether large or small, the donor leukocyte fraction always included a subset of class II leukocytes that had histopathologic features of dendritic cells. These class II ؉ cells were of mixed myeloid (CD11-b/c ؉ ) and lymphoid lineages; their migration was markedly inhibited by TAC and accelerated by donor-specific priming and TAC discontinuance. Although a large donor leukocyte population and a normal leukocyte/nonleukocyte cell ratio were associated with freedom from CR, these findings and the lineage profile of the intracardiac leukocytes were not associated with tolerance in the animals of groups 3 and 4 under active TAC treatment. The findings in this study, singly and in their entirety, are compatible with our previously proposed leukocyte migration-localization paradigm of organ allograft acceptance and tolerance. (Liver ...

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“…Assuming similar radioiodination of all of the heavy chains, the intensity of the p2m component precipitated by the anti-p2m antiserum represents 30 (= 12 x 2.5) different class I antigens. Serological, im munochemical and molecular biological studies, however, have shown that the rat expresses only a small number (4-5) of class I antigens [34,35]. The most probable explanation for the results is, there fore, that there are many free p2m molecules on the surface of rat lymphocytes.…”

Section: Discussionmentioning

confidence: 88%

Beta-2-Microglobulin of Rat Major Histocompatibility Complex Class I Antigens

Misra

Kunz²,

Gill³

1989

Int Arch Allergy Immunol

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Detection of the β₂-microglobulin (β₂m) component of the rat MHC class I antigens has been difficult. In the present report, we have addressed this issue by a systematic study of rat class I antigens from red blood cells or from lymphocytes that were freshly isolated or cultured in the presence of autologous or heterologous sera and surface-labeled with ¹²⁵I or intrinsically labeled with radioactive amino acids. First, specific radioiodination of rat β₂m in association with the antigen heavy chain on red blood cells or lymphocytes is minimal, resulting in its poor identification by SDS-PAGE. Second, labeling with radioactive methionine or lysine gives a more intense β₂m band with respect to the heavy chain than labeling with arginine or tyrosine. Third, the β₂m component shows a large increase in intensity compared to the heavy chain when the antigens are isolated from lymphocytes that are cultured in the presence of fetal bovine serum prior to ¹²⁵I-labeling. This increase is due to exchange of endogenous rat β₂m with bovine β₂m and to a much higher level of radioiodination of the latter. Fourth, rat red blood cells and lymphocytes contain free surface β₂m molecules in addition to those associated with the antigen heavy chains. The free molecules show a much higher level of radioiodination than those associated with the heavy chains, and there is little exchange between the antigen-bound and the free β₂m after radioiodination. Thus, intrinsic labeling with suitable radioactive amino acids rather than surface labeling with ¹²⁵I is the method of choice for unambiguous detection of the endogenous β₂m component of the rat MHC class I antigens.

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The Major Histocompatibility Complex of the Rat

Cited by 77 publications

References 0 publications

Variable Chimerism, Graft-Versus-Host Disease, and Tolerance After Different Kinds of Cell and Whole Organ Transplantation From Lewis to Brown Norway Rats

Variable Chimerism, Graft-Versus-Host Disease, and Tolerance After Different Kinds of Cell and Whole Organ Transplantation From Lewis to Brown Norway Rats

Donor and recipient leukocytes in organ allografts of recipients with variable donor-specific tolerance: With particular reference to chronic rejection

Beta-2-Microglobulin of Rat Major Histocompatibility Complex Class I Antigens

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