Tissue graft rejection in mice

The influence of H-2 subregions on graft survival in a liver slice-tokidney bed grafting system has been investigated. H-2K -region and H-2IA -region donor-recipient differences, either individually or in concert, cause acute graft rejection. H-2D -region donor-recipient differences cause chronic immunological reaction as evaluated by histological criteria. Grafts across this barrier may ultimately be rejected or may survive indefinitely. Several possible explanations for the variation in survival are proposed. The remaining known H-2 regions ( IB, IC, S , and G ) all appear to cause immunological reactivity in a recipient animal which differs from the liver tissue donor at any of these regions. However, only an IC -region difference may ultimately cause complete graft destruction following an extended chronic immunological course. Grafts across background histocompatibility barriers of several genetic types show rejection patterns equivalent to those seen across K and IA barriers. These patterns are unchanged, whether or not the donor and recipient are congenic for H-2 alleles. Different H-2 allelic donor-recipient differences do, however, show different times of survival, indicating variation in strength or number of donor antigens or differences in recipient immune response.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/46752/1/251_2005_Article_BF01575670.pd

Tissue graft rejection in mice

A tissue slice-to-kidney bed grafting system is used to study the mechanism of specific tissue rejection (in this case, rejection of liver tissue) over a series of histocompatibility barriers other than the H-2 barrier. Using the method described, it is possible to obtain a pattern or time-course picture of the immunological process, rather than a mean survival time. It is clear from histological observations of these patterns that, although there are considerable differences in numbers of liver grafts which survive for long period's across the several histocompatibility barriers studied, some grafts in almost every case survive the immunological challenge elicited by the genetic barriers. Grafts of liver tissue are therefore similar, but not identical, in survival patterns to grafts of tumor, ovary, and skin. These studies also indicate that immunological mechanisms controlling rejection of tissue over H barriers other than H-2 differ from those controlling rejection over the major histocompatibility barrier in the mouse.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/46754/1/251_2005_Article_BF01563948.pd

H-2 and Background influences on tissue grafts across the H-Y barrier

Male liver was grafted to kidney beds in syngeneic female mice. Relative influences of H-2 haplotype, genetic background or interaction of H-2 haplotype with genetic background on anti-H-Y response were evaluated using 27 inbred strains carrying eight H-2 haplotypes of independent origin and three naturally occurring recombinants. Females of H-2 b haplotype acutely rejected the male graft as is reported for other tissue graft systems. An H-2 haplotype influence was found for all haplotypes studied, with a greater variation of immunologic response revealed by histological analysis of liver grafts than is demonstrated by skin grafts. Strains carrying H-2 k , H-2 j and H-2 p haplotypes expressed the greatest range of immunological variability with responses ranging from graft proliferation to graft rejection. Strains carrying the H-2 d haplotype had the most consistent responses with little reaction to the graft. The strong immune response by SJL/J ( H-2 s ) female mice to the H-Y antigen is not typical of other H-2 s strains, but is compatible with the reported hyperresponsiveness of this strain to alloantigens.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/46755/1/251_2005_Article_BF01570432.pd

Actin polymerization in cellular oxidant injury

Microfilaments undergo an ATP-dependent disruption into shortened bundles following cellular exposure to oxidants. This phenomenon does not require a net change in the amount of polymerized actin. However, increased amounts of polymerized actin have been detected in oxidant-injured cells and it was the purpose of this study to determine the conditions under which the actin polymerization may occur. Utilizing the formation of oxidized glutathione (GSSG) as an indicator of cellular sulfhydryl oxidation, conditions were chosen to accentuate sulfhydryl oxidation within the target P388D1 cell line following exposure to the oxidants, H2O2 and diamide. Using the DNase I and flow cytometric assays of actin polymerization, significant polymerization of actin was detected only under conditions in which sulfhydryl oxidation occurred after exposure to the two oxidizing agents. Greater sulfhydryl oxidation early in the course of injury was associated with a greater rate and extent of actin polymerization in the injured cells. Experiments with cells depleted of glutathione (GSH) demonstrated that neither loss of GSH nor absolute levels of GSSG formed during oxidant exposure were responsible for the polymerization of actin. The data presented are consistent with the hypothesis that oxidizing conditions which induce significant sulfhydryl oxidation in target cells are correlated with assembly of polymerized actin and that this represents a process which is distinct and separate from the ATP-dependent gross disruption of microfilaments.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/29200/1/0000254.pd

Immunogenetic control of the response of female mice to male tissue grafts

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/46736/1/251_2005_Article_BF01561664.pd