Journal of Clinical Immunology and Allergy is a world class open access journal intended to publish the cutting-edge research in the field of Immunology and Allergy.

Dying cells in the body can keep the immune system in check, thus preventing unwanted immune responses against the body's own tissues. Researchers have now identified a receptor on murine immune cells that activates this protective mechanism and can thus prevent dangerous autoimmune reactions in which the immune system attacks the patient's own body tissues.

Billions of cells die every day in the human body. This occurs as part of a highly regulated process called apoptosis or programmed cell death. The dying cells confront the immune system with large amounts of proteins, which ought to activate an immune response, but the apoptotic cells seem to actively suppress the immune system so that it does not attack the body's own tissues.

As soon as apoptosis is triggered, the dying cells transport proteins from the annexin family to the cell surface. The annexins act like a stop signal for the cells of the immune system and prevent an immune response from being triggered.

Dectin-1 protein as the annexin-binding receptor on the surface of dendritic cells: Dectin-1 recognizes the annexins and triggers a signaling pathway in dendritic cells that ultimately suppresses the immune response.

An important control mechanism for the immune system's 'self-tolerance'. "But we assume that the body has other protective functions to prevent autoimmune reactions too. That's why the loss of dectin-1 in the animals does not become apparent until later in life.

Dectin-1 has a dual role, Dectin-1 not only binds annexins; it also binds certain pathogens at a different binding site. This has the opposite effect and triggers an immune response. "We thus identified a crucial immune checkpoint which, depending on the binding partner, either triggers or suppresses the immune response,"  emphasizing the importance of the work.

A key link in the dectin-1 signaling pathway is the enzyme NADPH oxidase 2. People who lack this enzyme develop autoimmune diseases.

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