Eric L. Greidinger, M.D.
Associate Professor of Medicine
Description of Research
Dr. Greidinger's lab is i.investigating the forms of self and viral molecules that provoke self-aggressive immune responses, ii. the receptors that recognize these molecules, iii. the cells that signal in response to these recognition events,, iv. the determinants of tissue localization of the resulting responses, and v. the viruses implicated in these responses. A major focus has been on immune responses to U1-RNA, a component of the U1-snRNP that is targeted in autoimmunity and in response to UV damage. There is evidence that suggests that different forms of U1-RNA stimulate different innate immune receptors leading to different outcomes. The Trex1 endonuclease knockout system in mice and the human analog Aicardi-Goutierres syndrome are emerging models of excess self RNA recognition (including U1-RNA). We use mice knocked out for specific innate immune receptors and signaling molcules to further define clinically and immunologically relevant pathways (including TLR3, TLR7, TRIF, and STING). Another ongoing project is the dissection of the viral nucleic acid profiles of salivary gland tissue from patients with Primary Sjogren's Syndrome, an autoimmune condiiton associated with a substantial increase in B cell lymphoma risk. The data suggests that overexpression of latency phase genes from multiple viruses my be associated with primary but not secondary Sjogren's.
- Description of dendritic cell function in immune targeting to the lung and kidney
- Assessment of the ability to sustain anti-self responses in STING knockout mice (industry funded project, Co-PI with Dr. Glen Barber)
- Identification of U1-RNA and TLR3 as a key mediator of UV-induced inflammatory changes in the skin
Selected Cancer-Related Publications
Collaborating in the Multidisciplinary Research Program(s):