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Review
. 2001 Oct;108(7):943-8.
doi: 10.1172/JCI14142.

Challenges to achieving clinical transplantation tolerance

A D Salama  1 , G Remuzzi, W E Harmon, M H Sayegh
Affiliations
Review

Challenges to achieving clinical transplantation tolerance

A D Salama et al. J Clin Invest. 2001 Oct.
No abstract available

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Figures

Figure 1
Figure 1
The fate of alloreactive T cells. Upon antigen engagement and in the presence of adequate costimulatory signals, the alloreactive T cell becomes activated, proliferates, and is subject to a number of different fates. The first is differentiation to an effector cell, orchestrating the immune response directed toward the target antigen. Some of the T cells will differentiate into memory cells, able to provide rapid recall responses upon antigenic restimulation. Other cells will have their effector functions terminated either by anergy or by apoptotic death (which may be passive or may involve activation-induced cell death [AICD]), or as a consequence of regulation by other cells or soluble factors. CTL, cytotoxic T lymphocyte; DTH, delayed-type hypersensitivity.
Figure 2
Figure 2
The balance of the immune system. This cartoon represents the balance between the effector and regulatory functions of the immune system and emphasizes the role of effector clone size in dictating the outcome of an immune response. In the presence of large numbers of effector cells (red circles), the regulatory mechanisms, consisting of regulatory cells (green circles) and suppressive soluble factors such as cytokines, are unable to attenuate the effector’s response, which therefore predominates. In the context of transplantation this results in rejection. However, in the presence of low effector cell numbers these mechanisms can regulate the effectors and keep them in check. If these responses are sufficiently robust, transplant tolerance may result. Adapted from ref. .
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