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Biomedical subjects

W K Silvers

Publications and source records attributed to W K Silvers.

At least 73 records · Page 4Linked to original sources
PubMed1982

Evidence for major histocompatibility complex restriction in transplantation immunity.

Studies on the survival of histocompatibility-Y antigen (H-Y)-incompatible and skin-specific antigen (Skn)-incompatible skin grafts in mice, as well as those concerned with the survival of cultured parathyroid allografts in rats, indicate that grafts provoke a strong immune response only if they include donor macrophages (or Langerhans cells) or if major histocompatibility complex-compatible macrophages are available to react with cells bearing the foreign antigens.

Animals↗
PubMed1982

Synergistic interaction of H-Y and H-2K in elicitation of graft-versus-host response.

Lymph node cells from female bm-1 donors induced greater mortality among male than female (bm-1 X b)F1 hosts which had previously been sublethally irradiated. The same effect was not seen when wild type (b) parental donor cells were injected, nor in other combinations involving H-2K mutant C57BL/6 mice. The selective mortality encountered among male hosts in receipt of bm-1 female cells was shown to depend upon recognition of H-Y in the recipient, because this sex effect disappeared if the donors were first rendered tolerant of H-Y. However, absence of graft-versus-host (GVH) mortality with other combinations indicated that recognition of H-Y alone was not sufficient. When cells from donors tolerant of H-Y were mixed with cells from donors tolerant of H-2Kb, enhanced mortality among male F1 hosts was again observed. We interpret the results to indicate that there is a synergistic interaction of donor lymphocytes which recognize H-Y and H-2Kb during the GVH response.

Animals↗
PubMed1982

Transplantation of islets and bone marrow cells to animals with immune insulitis.

The results of islet transplantation in an animal model of spontaneous immune insulitis were studied to see whether this disease process might damage transplanted tissue. Since the insulitis occurs only in "BB" rats (which are not genetically uniform) syngeneic grafts could not be used, therefore allograft rejection was avoided by rendering "BB" rats tolerant of WF transplantation antigens by inoculating them neonatally with WF bone marrow cells. Despite the resultant tolerant state, which permitted successful engraftment of WF skin and islets transplanted to artificially diabetic "BB" rats, tolerant "BB" rats with spontaneous diabetes accepted transplanted WF islets only briefly before they were destroyed by immune insulitis. "BB" rats were found to have abnormalities in immune response (delayed skin graft rejection and decreased alloreactivity in mixed lymphocyte response). "BB" rats that were treated neonatally with WF bone marrow. Moreover, "BB" rats inoculated with WF bone marrow neonatally were found less likely to become diabetic than untreated "BB" controls. It is suggested that the chimeric state (persistence of WF bone marrow cells) may be responsible for the improved immune response and perhaps for the decreased susceptibility to diabetes.

Animals↗
PubMed1982

Studies on the behavior of H-Y incompatible skin grafts in rats.

Studies on the behavior of H-Y incompatible skin grafts in rats indicate that 1) there is considerable variation in the ability of females of different strains to reject male skin isografts; 2) small, male trunk skin isografts are more likely to be rejected than similarly sized ear or tail skin grafts; 3) other factors besides the MHC plan an important role in determining the ability of females to reject male skin isografts; 4) the ability of adult male skin grafts to induce unresponsiveness to H-Y depends upon their size (large grafts are more effective than small) and the genotype of the host; 5) even in those strains in which females usually accept small, male trunk skin isografts, such grafts are acutely rejected by sensitized females; and 6) the total amount of H-Y incompatible trunk skin the host is exposed to, rather than the size of each graft, determines their fate.

Animals↗
PubMed1981

Spontaneous diabetes in rats: destruction of islets is prevented by immunological tolerance.

Spontaneous diabetes occurring in "BB" rats (derived from a colony of outbred Wistar rats) is the result of destruction of pancreatic islets by infiltrating mononuclear cells (insulitis) and may be a disease very similar to human juvenile onset diabetes. Both diseases probably have an autoimmune etiology. Evidence is presented that islets transplanted to diabetic BB rats are destroyed by the original disease process. Inoculation of bone marrow from normal (nondiabetes-susceptible) rat donors into neonatal BB recipients usually prevented the development of hyperglycemia.

Animals↗
PubMed1981

An immunogenetic analysis Skn antigens in mice.

Studies on the fate of Skn-incompatible grafts indicate that both the immune response to and the potency of these antigens are influenced by the MHC. Evidence is also presented that strains CBA, C3H, and A possess different Skn antigens.

Aging↗
PubMed1981

Prevention of diabetes in rats by bone marrow transplantation.

Hyperglycemia, hypoinsulinemia and ketonemia often develop abruptly in previously normal young "BB" rats. The syndrome mimics human juvenile diabetes closely and is, thus, appropriate for assessing pancreatic transplantation. Transplantation of islet cells from closely histocompatible Wistar Furth (WF) donor resulted in permanent normoglycemia when immunosuppression with ALS was given. However, when islet cells from nondiabetic "BB" donors were transplanted to nonimmunosuppressed diabetic "BB" recipients, only transient normoglycemia followed. Transplantation of WF islets cells also failed in diabetic "BB" rats which were tolerant of WF antigens, again suggesting destruction of transplanted islet cells by the original disease process-possibly autoimmunity. Evidence for autoimmunity was strengthened by the finding that newly diabetic "BB" rats could be rendered normoglycemic by immunosuppression. Since genetic susceptibility to spontaneous autoimmune diabetes is unique to some members of the "BB" stock, an attempt was made to alter their vulnerability by modifying their cellular immune system. Accordingly, 50 million bone marrow cells from WF donors were inoculated into half the newborn members of "BB" litters, leaving the littermates as unmodified controls. Most bone marrow recipients were protected, only four of 37 (10.8%) ever becoming diabetic, while the incidence of diabetes in noninoculated littermates was 22 of 39 (56.4%). The ultimate goal in human diabetes, which also seems very likely to be an autoimmune disease, may not be replacement of destroyed islet cells but identification of potentially susceptible children and prevention of islet destruction by immunologic manipulation.

Animals↗
PubMed1980

An evaluation of nerve repair with nerve allografts in normal and immunologically tolerant rats.

Schwann cells survive longer in allografts of ganglia that contain minor, rather than major and minor, transplantation antigens. The authors have investigated whether a nerve allograft with minor antigens would be superior to one with major and minor incompatibilities in aiding in the repair of injured nerve. A segment of host peroneal nerve was removed from rats and replaced with a peroneal nerve allograft that contained either minor or major and minor antigens. The results showed that in normal rats, host nerve fibers could functionally regenerate through (that is, grow through and reinnervate muscle) nerve allografts 2 cm but not 4 cm in length, irrespective of the antigens the allografts contained. Host nerve fibers could, however, regenerate through 4-cm nerve allografts if the hosts were rendered immunologically tolerant of the transplantation antigens of the nerve donors. Furthermore, when sensitized lymphoid cells were injected into tolerant rats bearing functional nerve allografts, Schwann cell rejection and demyelination occurred in the graft but host nerve fibers remained. It is concluded that minor antigens alone are as potent as major and minor antigens together in evoking an immune response that prevents functional regeneration through long lengths of nerve allografts. Host nerve fibers can, however, regenerate through such nerve allografts if the hosts are immunosuppressed.

Animals↗