1981
DOI: 10.1084/jem.154.5.1332
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The vascular bed as the primary target in the destruction of skin grafts by antiserum. II. Loss of sensitivity to antiserum in long-term xenografts of skin.

Abstract: Rat skin that survives for long periods of time on immunosuppressed mice becomes resistant to anti-graft serum and remains so for as long as it survives. When long-standing grafts are removed and placed on new immunosuppressed mice, they remain resistant to antiserum for as long as they survive. The acquired resistance to antiserum seems, therefore, to be due to changes in the grafts rather than to changes in their hosts. Furthermore, it was found that the acquisition of resistance is correlated with replaceme… Show more

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Cited by 39 publications
(15 citation statements)
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“…During rejection of Mig-deficient skin allografts, the chemokine protein was clearly present in the vascular endothelium of the lower dermis and was associated with cells around the vessels. These results are consistent with the neovascularization of the skin allograft by recipient endothelium [23][24][25] and the importance of this source of Mig in directing T-cell infiltration into the allograft. In contrast, Mig protein was not detected in vascular structures in the upper dermal vascular plexus of Mig Ϫ/Ϫ allografts and there was little to no detectable T-cell infiltration into this area of the allograft until late in the delayed rejection of the grafts.…”
Section: Discussionsupporting
confidence: 79%
“…During rejection of Mig-deficient skin allografts, the chemokine protein was clearly present in the vascular endothelium of the lower dermis and was associated with cells around the vessels. These results are consistent with the neovascularization of the skin allograft by recipient endothelium [23][24][25] and the importance of this source of Mig in directing T-cell infiltration into the allograft. In contrast, Mig protein was not detected in vascular structures in the upper dermal vascular plexus of Mig Ϫ/Ϫ allografts and there was little to no detectable T-cell infiltration into this area of the allograft until late in the delayed rejection of the grafts.…”
Section: Discussionsupporting
confidence: 79%
“…Free grafts of skin, unlike primarily vascularized grafts, do not have vascular connections with their hosts until about the 4th d after transplantation, a point that is affirmed by our studies with fluorescein-labeled antibodies. It would not be possible, therefore, to induce immediate vascular injury in recently placed grafts, and the induction of vascular injury seems to be a sine qua non of antiserum-mediated destruction of organized tissue grafts (4). This explains the resistance of grafts for the 1st 4 d after transplantation, but even after grafts are vascularized they remain resistant to antiserum for an additional 2 or 3 d and peak sensitivity is not acquired until about the 12th or 14th d after grafting.…”
Section: Discussionmentioning
confidence: 99%
“…34). It may also be relevant that long-term surviving skin grafts can undergo gradual replacement of endothelial cells in small vessels by recipient-derived cells (35), whereas replacement of endothelial cells in transplanted organs is usually limited (36), although some reports suggest it to be present in varying degrees (37,38). On the other hand, considerable evidence now supports the view that the derivation of the majority of neointimal cells, bearing ␣-actin markers characteristic of smooth muscle cells, is from the recipient, although their origin, in different situations, may be either from bone marrow (39,40) or from adjacent vessel walls (41).…”
Section: Discussionmentioning
confidence: 99%