Sclerosis, where it has shown considerable promise at preventing multiple sclerosis symptoms in Relapsing-Remitting patients. However, many patients treated with alemtuzumab went on to develop other autoimmune diseases, especially those involving the thymus, as well as a plethora of infections. In general, the data suggest that alemtuzumab is excellent at inducing immune suppression. However, as a SCITT agent, it appears to overstep the required immune modulation, placing patients at unnecessary risk. TCR αβ antibody treatment Antibodies directed against the αβ chains of the TCR have also been shown to be efficacious for the induction and restoration of immunological tolerance in animal models of autoimmunity and transplantation. Like anti-CD3 antibodies, the administration of anti-TCR αβ antibodies has generally been met with favorable effects in the treatment of autoimmune disease. Treatment of mice with anti-TCR αβ antibody at the time of Experimental autoimmune encephalomyelitis(EAE) disease induction completely prevented disease onset, while treatment during chronic EAE disease caused disease remission. Anti-TCR αβ antibody treatment induces tolerance through a number of mechanisms including the functional blockade of T cells at the site of inflammation, transient T-cell depletion, upregulation of Th2 cytokines, and an increase in the regulatory NKT cell population. In transplantation, the use of anti-TCR αβ antibody treatment may be more efficacious than anti-CD3 antibody treatment, and its potential for prolonging allograft survival has been demonstrated in multiple animal models of transplantation, such as renal allografts, heterotopic heart transplants, and corneal transplants. While this has yet to be defined completely, this is likely the combined result of preserving γδ T cells and the lack of mitogenic effects observed when peripheral blood monocytes are incubated with anti-αβ TCR antibodies. The ability for anti-αβ TCR antibodies to modulate T cells without inducing significant cytokine release is likely due in part because the αβ TCR lacks immunoreceptor tyrosine-based activation motifs (ITAM's). The ability for targeting the αβ TCR with monoclonal antibodies to prevent renal transplant rejection is currently the focus of the phase 2 clinical trial. Disadvantages of T-cell directed immune induction therapies Due to the activation, depletion, and immunosuppression following the administration of T-cell depleting therapies, there is a risk of infection to the patient. The most common infection is caused by the reactivation of latent Epstein–Barr virus infection. EBV reactivation in the context of T-cell depleting strategies can result in serious complications, such as post-transplant lymphoproliferative disorder, which can have fatal consequences. However, in