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Biomedical subjects

W K Silvers

Publications and source records attributed to W K Silvers.

At least 127 records · Page 7Linked to original sources
PubMed1972

The role of passenger leukocytes in the anomalous survival of neonatal skin grafts in mice.

The anomalous survival of neonatal C3H skin grafts on CBA mice is correlated with the emigration of passenger leukocytes from the graft vasculature. Thus, newborn homografts whose leukocyte populations are eliminated by X-irradiation or by transient sojourn on an intermediate adult C3H host, do not display prolonged survival. Moreover, the continued presence of the newborn grafts is not requisite to the maintenance of the unresponsive state, an observation consonant with the demonstration that CBA mice bearing long-term neonatal C3H skin grafts are leukocyte chimeras. In contrast, neonatal male C57 skin grafts may persist on C57 females after heavy irradiation of the donor, or after passage on an intermediate adult male host. In addition, tolerance is broken by removal of long-persistant newborn grafts from hitherto unresponsive females, and chimerism is not detectable in female C57 mice tolerant of infant male isografts. Finally, leukocytes of neonatal C3H origin, inoculated subcutaneously into CBA males, may occasionally render these animals unresponsive to subsequent adult C3H skin homografts, whereas those taken from infant C57 males usually sensitize their adult female hosts. Thus, passenger leukocytes are implicated in the extended survival of C3H neonatal homografts on CBA recipients, but not in the persistence of H-Y-incompatible neonatal skin isografts on C57 females.

Age Factors↗
PubMed1971

Skin homografts: tolerogenic versus immunogenic influences in mice.

In strain combinations involving multiple non-H-2 disparities, neonatal skin grafts may survive significantly longer than adult grafts of similar genotype on normal adult hosts, and repeatedly outlive grafts of adult origin on immunosuppressed recipients. Moreover, newborn grafts of long-standing may render their hosts unresponsive to adult skin grafts from the same donor strain. With some H-2-compatible strain combinations in which homozygous neonatal grafts are rejected, F(1) hybrid (heterozygous) grafts of similar age not only may survive indefinitely, but also may induce tolerance of subsequent adult parental strain homografts. These tolerogenic and gene dosage effects, although much weaker, can likewise be revealed with H-2-incompatible neonatal skin grafts.

Alleles↗
PubMed1970

Mixed lymphocyte reactions and tissue transplantation tolerance.

The induction of tolerance of Lewis histocompatibility antigens in BN rats inoculated at birth with BNI Lewis F(1) hybrid bone marrow cells, as revealed by the prolonged survival of Lewis skin grafts, is accompanied by markedly decreased reactivity in the mixed lymphocyte interaction. Blood lymphocytes from animals inoculated with lymph node cell suspensions also display diminished proliferative reactivity to hybrid BN/Lewis cells in the interaction. However, these recipients are not tolerant of Lewis skin grafts. Blood lymphocytes from BN rats inoculated neonatally with Lewis thymocytes fail to display any level of unresponsiveness in vitro, and such animals are not tolerant of Lewis skin grafts. The results suggest that in rats skin and marrow cells have histocompatibility antigens that are absent or poorly expressed on lymph node cells and thymocytes.

Animals↗
PubMed1970

Studies on the migratory behavior of melanocytes in guinea pig skin.

Pigment spread is the natural or experimentally procured (through grafting) progressive encroachment of pigmentation from black or red skin areas into juxtaposed white skin areas, or from black skin areas into red skin areas in spotted guinea pigs and other mammals. So far as spread from black into white skin is concerned, it had previously been shown that migration of epidermal melanocytes into skin lacking homologues of these cells was responsible. However, since red skin already has its own complement of phenotypically "red" melanocytes, the intriguing possibility remained that when black pigment encroaches upon red, rather than melanocyte migration being responsible, phaeomelanin (red)-producing melanocytes are transformed into eumelanin (black)-producing cells by some kind of serially transmissible factor derived from contiguous eumelanotic melanocytes. By utilizing two isogenic strains (Nos. 2 and 13) of spotted guinea pigs and their F(1) hybrids, the mechanism underlying the spread of pigment from black into red skin has been analyzed, employing cellular transplantation antigens as melanocyte "markers." The findings demonstrate unequivocally that a physical migration of pigment cells is responsible. By comparing the extents of pigment spread from black ear skin grafts, or from epidermal cell suspensions prepared therefrom, from parental strain or from F(1) hybrid donors in white host skin areas of F(1) hybrid guinea pigs, it has been possible to evaluate the influence of the intimate contact of melanocytes with alien transplantation antigens on their survival and migratory behavior. No evidence was forthcoming that pigment spread takes place less readily when the cells responsible are confronted by epidermal cells bearing foreign antigens than when they are confronted by cells of their own antigenic constitution. These findings are contrary to expectation if the phenomena of allogeneic inhibition or contact-induced cytotoxicity apply to normal cells in in vivo situations.

Animals↗