Intragraft immune events causing vascularized organ graft rejection

T. B. Strom, C. B. Carpenter, N. L. Tilney, Manikkam Suthanthiran, G. R. Catto, A. P. Lundin, E. L. Milford

Research output: Contribution to journalArticle

4 Citations (Scopus)

Abstract

These studies indicate that CTLs are only one component of inexorable vascularized organ graft rejection. Although these cells are undeniably cytodestructive in vivo, abrogation of humoral injury by enhancing antibody allows graft recovery and longterm function. The remarkable absence of anti-Ia-like antibodies in the enhanced host suggests that anti-Ia responses contribute substantially to allograft rejection. Perhaps this response is abolished by suppressor cells in the enhanced recipient. It is likely that the entire repetoire of potentieal immunologic assault mechanisms are unleashed during unmodified rejection, including activation of both cellular and humoral effector arcs directed against both classical an nonclassical (Ia-like)MHC incompatibilities and other minor transplant antigens. We consider it unlikely that the rejection of vascularized organ grafts is the sole and specialized province of CTLs or even cell-mediated immunity. Graft death appears to result from a composite of cellular and humoral mechanisms.

Original languageEnglish
Pages (from-to)389-394
Number of pages6
JournalTransplantation Proceedings
Volume10
Issue number2
Publication statusPublished - 1 Dec 1978
Externally publishedYes

Fingerprint

Graft Rejection
Transplants
Blocking Antibodies
Recovery of Function
Cellular Immunity
Allografts
Antigens
Antibodies
Wounds and Injuries

ASJC Scopus subject areas

  • Surgery
  • Transplantation

Cite this

Strom, T. B., Carpenter, C. B., Tilney, N. L., Suthanthiran, M., Catto, G. R., Lundin, A. P., & Milford, E. L. (1978). Intragraft immune events causing vascularized organ graft rejection. Transplantation Proceedings, 10(2), 389-394.

Intragraft immune events causing vascularized organ graft rejection. / Strom, T. B.; Carpenter, C. B.; Tilney, N. L.; Suthanthiran, Manikkam; Catto, G. R.; Lundin, A. P.; Milford, E. L.

In: Transplantation Proceedings, Vol. 10, No. 2, 01.12.1978, p. 389-394.

Research output: Contribution to journalArticle

Strom, TB, Carpenter, CB, Tilney, NL, Suthanthiran, M, Catto, GR, Lundin, AP & Milford, EL 1978, 'Intragraft immune events causing vascularized organ graft rejection', Transplantation Proceedings, vol. 10, no. 2, pp. 389-394.
Strom TB, Carpenter CB, Tilney NL, Suthanthiran M, Catto GR, Lundin AP et al. Intragraft immune events causing vascularized organ graft rejection. Transplantation Proceedings. 1978 Dec 1;10(2):389-394.
Strom, T. B. ; Carpenter, C. B. ; Tilney, N. L. ; Suthanthiran, Manikkam ; Catto, G. R. ; Lundin, A. P. ; Milford, E. L. / Intragraft immune events causing vascularized organ graft rejection. In: Transplantation Proceedings. 1978 ; Vol. 10, No. 2. pp. 389-394.
@article{4af481d685a64fcfb27221c67669ae5e,
title = "Intragraft immune events causing vascularized organ graft rejection",
abstract = "These studies indicate that CTLs are only one component of inexorable vascularized organ graft rejection. Although these cells are undeniably cytodestructive in vivo, abrogation of humoral injury by enhancing antibody allows graft recovery and longterm function. The remarkable absence of anti-Ia-like antibodies in the enhanced host suggests that anti-Ia responses contribute substantially to allograft rejection. Perhaps this response is abolished by suppressor cells in the enhanced recipient. It is likely that the entire repetoire of potentieal immunologic assault mechanisms are unleashed during unmodified rejection, including activation of both cellular and humoral effector arcs directed against both classical an nonclassical (Ia-like)MHC incompatibilities and other minor transplant antigens. We consider it unlikely that the rejection of vascularized organ grafts is the sole and specialized province of CTLs or even cell-mediated immunity. Graft death appears to result from a composite of cellular and humoral mechanisms.",
author = "Strom, {T. B.} and Carpenter, {C. B.} and Tilney, {N. L.} and Manikkam Suthanthiran and Catto, {G. R.} and Lundin, {A. P.} and Milford, {E. L.}",
year = "1978",
month = "12",
day = "1",
language = "English",
volume = "10",
pages = "389--394",
journal = "Transplantation Proceedings",
issn = "0041-1345",
publisher = "Elsevier USA",
number = "2",

}

TY - JOUR

T1 - Intragraft immune events causing vascularized organ graft rejection

AU - Strom, T. B.

AU - Carpenter, C. B.

AU - Tilney, N. L.

AU - Suthanthiran, Manikkam

AU - Catto, G. R.

AU - Lundin, A. P.

AU - Milford, E. L.

PY - 1978/12/1

Y1 - 1978/12/1

N2 - These studies indicate that CTLs are only one component of inexorable vascularized organ graft rejection. Although these cells are undeniably cytodestructive in vivo, abrogation of humoral injury by enhancing antibody allows graft recovery and longterm function. The remarkable absence of anti-Ia-like antibodies in the enhanced host suggests that anti-Ia responses contribute substantially to allograft rejection. Perhaps this response is abolished by suppressor cells in the enhanced recipient. It is likely that the entire repetoire of potentieal immunologic assault mechanisms are unleashed during unmodified rejection, including activation of both cellular and humoral effector arcs directed against both classical an nonclassical (Ia-like)MHC incompatibilities and other minor transplant antigens. We consider it unlikely that the rejection of vascularized organ grafts is the sole and specialized province of CTLs or even cell-mediated immunity. Graft death appears to result from a composite of cellular and humoral mechanisms.

AB - These studies indicate that CTLs are only one component of inexorable vascularized organ graft rejection. Although these cells are undeniably cytodestructive in vivo, abrogation of humoral injury by enhancing antibody allows graft recovery and longterm function. The remarkable absence of anti-Ia-like antibodies in the enhanced host suggests that anti-Ia responses contribute substantially to allograft rejection. Perhaps this response is abolished by suppressor cells in the enhanced recipient. It is likely that the entire repetoire of potentieal immunologic assault mechanisms are unleashed during unmodified rejection, including activation of both cellular and humoral effector arcs directed against both classical an nonclassical (Ia-like)MHC incompatibilities and other minor transplant antigens. We consider it unlikely that the rejection of vascularized organ grafts is the sole and specialized province of CTLs or even cell-mediated immunity. Graft death appears to result from a composite of cellular and humoral mechanisms.

UR - http://www.scopus.com/inward/record.url?scp=0018139170&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0018139170&partnerID=8YFLogxK

M3 - Article

VL - 10

SP - 389

EP - 394

JO - Transplantation Proceedings

JF - Transplantation Proceedings

SN - 0041-1345

IS - 2

ER -