The human immune response has both a rapid innate component and a slower but more specific adaptive component. The adaptive immune response involves cells and immune mediators such as T cells, B cells, and antibodies. The innate immune response involves the action of phagocytic and cytotoxic cells, which migrate to the site of infection and produce antimicrobial compounds. Innate immunity regulates the inflammatory response as well as playing a key role in the activation of adaptive immunity. Thus, a robust innate immune response is critical for fighting infection.
Of course, too much of a good thing is not necessarily good. If the innate immune response becomes activated chronically, then this can contribute to the pathogenesis of many different diseases with an inflammatory component. Thus it is critical not only that innate immunity is activated when needed (upon infection) but that this response is also self-limiting and ultimately inactivated when not needed to prevent disease.
Dr. Alper's laboratory is focused on understanding the regulation of the innate immune response, particularly as it relates to the basis for these inflammatory diseases. The signaling pathways involved in the activation of innate immunity have been studied by numerous labs over the last 15 years. In contrast, the pathways that terminate this response are much less understood. We are studying two signaling pathways that terminate one class of innate immune signaling pathway, Toll-like receptor (TLR) signaling. Understanding how the maintenance of TLR signaling is regulated offers the potential to devise ways to ensure that inflammation is limited, activated to fight infection but terminated to prevent diseases with an inflammatory component such as COPD, atherosclerosis, and cancer.
The Alper lab is supported by grants from the National Institute of Environmental Health Sciences and the Wendy Siegel Fund for Leukemia and Cancer Research.
Learn about open positions in this lab.
- Innate Immunity Gene Discovery
- Regulation of alternative pre-mRNA splicing in the TLR pathway to limit inflammation
- Spatiotemporal regulation of TLR signaling by a novel RAB-GAP