The complement pathway plays key roles in host defence, but its excessive activation or dysregulation can lead to a variety of disorders.
Human T cells engineered to express chimeric antigen receptors (CARs) are 'living drugs' designed to eliminate cancer cells.
Much of biomedical research and the development of therapeutics is focused on a small fraction of the human genome, ignoring many disease-relevant proteins and the associated scientific and commercial opportunities.
Anticancer immunotherapy has shown spectacular results in the clinic, indicating that it has the potential to transform the treatment of cancer. At present, the majority of immunotherapeutic anticancer approaches target or use cytotoxic T cells.
The discovery of T helper 17 cells and interleukin-17 (IL-17) — a pro-inflammatory cytokine that plays a key part in inflammation, autoimmunity and host defence — are recent milestones in the field of immunology and inflammation research.
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Cancer cells exhibit metabolic changes when compared to their normal counterparts, owing to both genetic and epigenetic causes. During the last decade, the metabolic circuitries of cancer cells have been characterised in detail, and the potential of strategies to target these pathways for cancer therapy has been intensively investigated.
Although the underlying causes of type 1 and type 2 diabetes differ, reduced insulin-producing pancreatic β-cell mass is a central feature of both forms of the disease.
Overnutrition and obesity are associated with the activation of the immune system and the induction of an inflammatory response, which contribute to the development of insulin resistance and, ultimately, type 2 diabetes.
Efforts to harness the immune system to treat cancer date back more than a century, but progress was slow for decades. However, the recent clinical success of several anticancer immunotherapies has provided a boost to the field.
Anticoagulants are used for the prevention and treatment of thrombosis, the leading cause of morbidity and mortality in the Western world. Warfarin — the prototype oral anticoagulant — is a vitamin K antagonist that has been in clinical use since the 1950s. Although they are effective, vitamin K antagonists have several drawbacks, the most notable of which is the propensity to cause bleeding.
Defects in the expression or function of proteins with either pro-apoptotic (indicated in red) or anti-apoptotic (green) consequences have a causative or contributing role in the pathogenesis or progression of several diseases.