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Bleeding and clotting: new therapies and old issues revisited 1

It has been demonstrated that prior treatment with CD4 monoclonal antibody can induce tolerance to foreign protein in mice [1]. Tolerogenic therapies include Campath 1, which depletes T cells [2]; Rituximab, an antibody to CD20 which depletes B cells; and tolerogenic dendritic cells [3]. It is possible to induce tolerance in skin grafts in mice by the combination of CD4 and CD8 antibodies. The mechanisms of T-cell tolerance include Thymic (central) control involving clonal depletion and Peripheral one, which is organ-specific. Regulatory T cells control the peripheral tolerance and are in turn under the control of transforming growth factor beta (TGF-b). In the mouse anti-CD4 turns on the FOXP3 gene, which is important for regulatory T cells. This is dependent on TGF-b and it is possible to expose dendritic cells to TGF-b to make them induce tolerance in the mouse [4]. The immune privilege of the foetus has been found to be dependent on indoleamine 2,3-dioxygenase (IDO), the first enzyme in the tryptophan pathway. IDO-expressing macrophages catabolize tryptophan and there is no T-cell rejection response. However, 1-methyltryptophan inhibits IDO and this causes foetal rejection [5]. Other anatomical sites that are naturally protected from immune responses include the anterior chamber of the eye, the testis and the brain. It is possible to induce immune privilege: regulatory T cells can interact with cells presenting antigen, e.g. dendritic cells and induce gene products, such as FoxP3, which confers a state of immune privilege, which can be sustained by generating further regulatory T cells.