Abstract
Many autoimmune diseases and cancers have an underlying immune basis, and these include Systemic Lupus Erythematosus (SLE), rheumatoid arthritis, systemic sclerosis, ankylosing spondylitis, as well as breast cancer. Biological therapies are monoclonal antibodies and fusion proteins which contain specific recognition components that have antibody function. This principle takes advantage of antigen specificity to produce monoclonal antibodies to the desired antigen. Problems of biological therapies include ethical, regulatory, and licensing issues, documentation of trials, funding, adverse effects, media attention and publicity, selection issues, time considerations and risk-benefit analysis. Therefore, proper and strict regulation of research on humans as well as use of these biological agents should be carefully enforced and monitored by the authorities, to ensure maintenance of transparency and good standards.
Highlights
Many diseases have been observed to have an underlying immune basis and include auto-immune diseases like systemic lupus erythematosus (SLE), rheumatoid arthritis and systemic sclerosis [1]
Auto-reactive T cells are kept under control by the regulatory T cells (Treg cells) and absence of co-stimulatory signalling leads to loss of Treg cells [2]
CD28 super-agonists have been observed to cause selective expansion and activation of the regulatory T cells over conventional T cells (Tconv cells) and so it was thought that this anti-CD28 antibody represented a promising new treatment option for the large number of human auto-immune diseases [3]
Summary
Many diseases have been observed to have an underlying immune basis and include auto-immune diseases like systemic lupus erythematosus (SLE), rheumatoid arthritis and systemic sclerosis [1]. CD28 super-agonists have been observed to cause selective expansion and activation of the regulatory T cells over conventional T cells (Tconv cells) and so it was thought that this anti-CD28 antibody represented a promising new treatment option for the large number of human auto-immune diseases [3]. This monoclonal antibody rapidly stopped the disease progression and produced disease remission even after the onset of symptoms [2] This evidence was supported by adoptive transfer experiments which revealed that transfer of CD28 super-agonist-activated Treg cells protected recipient animals from the clinical signs of EAE, and CD4+ CD25- T cells (Tconv) cells were observed to lack any protective effect in spite of ten times greater dose of administration [8]. This is because TNF-α is required for the formation of localised tuberculous granuloma, which helps to localise the infection in one place and so may remain dormant for a long time
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