Congratulations to Diego Prado De Maio from the Covey Lab for receiving a fellowship with the American Association of Immunologists!
In the Covey lab, they are investigating the mechanisms that regulate normal and aberrant immune responses. When an individual encounters a foreign substance or pathogen it triggers the immune system to become activated so that it can 1) identify the substance as foreign, 2) prevent its spread, and 3) eliminate it completely from the body. A key aspect of our immune system is the capability to mount a response that is both highly specific to the pathogen and is able to create a ‘memory bank’ to protect against subsequent reinfection. Two prominent players in this adaptive response are T cells and B cells. Their lab focuses on a major subset of T cells, the CD4 helper T cells, which, as their name implies, provide ‘help’ to other immune cells to boost their functional properties. One of the most critical signals provided to B cells activates the CD40 pathway and this occurs through binding of T cell-expressed CD40L with CD40 expressed on B cells. Their lab had previously identified a novel pathway which regulates levels of CD40L on T cells. By removing this pathway in mice, they are attempting to understand the importance of this pathway and how varying CD40L levels can impact typical and atypical immune responses.
Diego's project, which the American Association of Immunologists granted us the Careers in Immunology Fellowship for, is to investigate how this particular pathway of CD40L expression can affect the autoimmune disease lupus erythematosus or lupus. In lupus, T cells and B cells identify some of the body’s own molecules and cells as foreign (similar to a pathogen) and begin mounting a defense against them. This generates an ongoing immune response which can damage tissues and cause chronic disease. They are confident that their current research will shine new light on the fine details that lead an immune response to attack their own body. Their overall goal with this research is that it will provide new avenues for targeted therapies that can decrease autoimmune responses without leaving individuals vulnerable to attack by other pathogens.
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