Human renal allograft rejection: Immune mechanisms, molecular correlates and treatment strategies

Manikkam Suthanthiran, Terry B. Strom

Research output: Contribution to journalReview article

1 Citation (Scopus)

Abstract

Renal allograft rejection is dependent upon the co-ordinated activation of alloreactive T cells and antigen-presenting cells (APC) such as monocyte-macrophages, dendritic cells and B cells. Whereas acute rejection is a T cell-dependent process, a broad array of effector mechanisms participate in the destruction of the allograft. Through the release of cytokines and cell-to-cell interactions, a diverse assembly of lymphocytes, including CD4+ cells, CD8+ cytotoxic T cells, antibody-forming B cells, and other pro-inflammatory leucocytes are recruited into the anti-allograft response. In this review, we discuss immune effector mechanisms, molecular correlates of rejection and therapeutic protocols. The recent expansion in our knowledge, coupled with the discovery and use of new immunosuppressants in the clinic, engenders optimism regarding management of allograft rejection, the most serious frequent complication in organ transplantation.

Original languageEnglish
Pages (from-to)1-12
Number of pages12
JournalNephrology
Volume2
Issue number1
Publication statusPublished - 1 Dec 1996
Externally publishedYes

Fingerprint

Allografts
Kidney
T-Lymphocytes
B-Lymphoid Precursor Cells
Viral Tumor Antigens
Organ Transplantation
Antigen-Presenting Cells
Immunosuppressive Agents
Cell Communication
Dendritic Cells
Monocytes
Leukocytes
B-Lymphocytes
Macrophages
Lymphocytes
Cytokines
Rejection (Psychology)
Antibodies
Therapeutics

Keywords

  • Anti-allograft response
  • Intragraft gene expression
  • Renal graft rejection

ASJC Scopus subject areas

  • Nephrology

Cite this

Human renal allograft rejection : Immune mechanisms, molecular correlates and treatment strategies. / Suthanthiran, Manikkam; Strom, Terry B.

In: Nephrology, Vol. 2, No. 1, 01.12.1996, p. 1-12.

Research output: Contribution to journalReview article

@article{faaf3a1cc1714267862ae3e96bb8a011,
title = "Human renal allograft rejection: Immune mechanisms, molecular correlates and treatment strategies",
abstract = "Renal allograft rejection is dependent upon the co-ordinated activation of alloreactive T cells and antigen-presenting cells (APC) such as monocyte-macrophages, dendritic cells and B cells. Whereas acute rejection is a T cell-dependent process, a broad array of effector mechanisms participate in the destruction of the allograft. Through the release of cytokines and cell-to-cell interactions, a diverse assembly of lymphocytes, including CD4+ cells, CD8+ cytotoxic T cells, antibody-forming B cells, and other pro-inflammatory leucocytes are recruited into the anti-allograft response. In this review, we discuss immune effector mechanisms, molecular correlates of rejection and therapeutic protocols. The recent expansion in our knowledge, coupled with the discovery and use of new immunosuppressants in the clinic, engenders optimism regarding management of allograft rejection, the most serious frequent complication in organ transplantation.",
keywords = "Anti-allograft response, Intragraft gene expression, Renal graft rejection",
author = "Manikkam Suthanthiran and Strom, {Terry B.}",
year = "1996",
month = "12",
day = "1",
language = "English",
volume = "2",
pages = "1--12",
journal = "Nephrology",
issn = "1320-5358",
publisher = "Wiley-Blackwell",
number = "1",

}

TY - JOUR

T1 - Human renal allograft rejection

T2 - Immune mechanisms, molecular correlates and treatment strategies

AU - Suthanthiran, Manikkam

AU - Strom, Terry B.

PY - 1996/12/1

Y1 - 1996/12/1

N2 - Renal allograft rejection is dependent upon the co-ordinated activation of alloreactive T cells and antigen-presenting cells (APC) such as monocyte-macrophages, dendritic cells and B cells. Whereas acute rejection is a T cell-dependent process, a broad array of effector mechanisms participate in the destruction of the allograft. Through the release of cytokines and cell-to-cell interactions, a diverse assembly of lymphocytes, including CD4+ cells, CD8+ cytotoxic T cells, antibody-forming B cells, and other pro-inflammatory leucocytes are recruited into the anti-allograft response. In this review, we discuss immune effector mechanisms, molecular correlates of rejection and therapeutic protocols. The recent expansion in our knowledge, coupled with the discovery and use of new immunosuppressants in the clinic, engenders optimism regarding management of allograft rejection, the most serious frequent complication in organ transplantation.

AB - Renal allograft rejection is dependent upon the co-ordinated activation of alloreactive T cells and antigen-presenting cells (APC) such as monocyte-macrophages, dendritic cells and B cells. Whereas acute rejection is a T cell-dependent process, a broad array of effector mechanisms participate in the destruction of the allograft. Through the release of cytokines and cell-to-cell interactions, a diverse assembly of lymphocytes, including CD4+ cells, CD8+ cytotoxic T cells, antibody-forming B cells, and other pro-inflammatory leucocytes are recruited into the anti-allograft response. In this review, we discuss immune effector mechanisms, molecular correlates of rejection and therapeutic protocols. The recent expansion in our knowledge, coupled with the discovery and use of new immunosuppressants in the clinic, engenders optimism regarding management of allograft rejection, the most serious frequent complication in organ transplantation.

KW - Anti-allograft response

KW - Intragraft gene expression

KW - Renal graft rejection

UR - http://www.scopus.com/inward/record.url?scp=1542739317&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=1542739317&partnerID=8YFLogxK

M3 - Review article

AN - SCOPUS:1542739317

VL - 2

SP - 1

EP - 12

JO - Nephrology

JF - Nephrology

SN - 1320-5358

IS - 1

ER -