Might there be a new way to combat potentially deadly blood clots in lupus?
Natalia Beglova, Ph.D. (Beth Israel Deaconess Medical Center, Harvard Medical School, Boston) will test whether a molecule she created effectively blocks the activity of a protein (beta2-glycoprotein I) that’s more commonly present in people with lupus who also suffer from multiple blood clots inside blood vessels called “thromboses.” By countering the protein, the destructive clots might be less likely to occur.
Is restoring damaged blood vessels in lupus back to health a possibility?
Robert Clancy, Ph.D. (New York University School of Medicine, New York) aims to refute the notion that the “bad” things that happen to blood vessels are irrevocable by testing whether infusing mice with the “active protein C” might actually restore healthy blood vessels—preventing worsening of lupus kidney disease in particular.
Why do lupus relapses happen in some people and not in others?
Stephen H. Clarke, Ph.D. (University of North Carolina at Chapel Hill, NC) will explore the novel concept that during lupus relapse, a group of B cells unique to people with the disease turns on the production of antibodies targeted at otherwise healthy organs—causing a rise in disease activity. The insight could help in identifying which patients truly need (and which can be spared) powerful immune system suppressive “maintenance” drugs such as prednisone.
Is it all about estrogen?
Tyler Curiel, M.D., M.P.H. (Division of Hematology and Oncology, University of Texas Health Science Center, San Antonio, TX) will explore possible scientific causes for the prevalence of lupus in females. A cancer specialist, he’ll study how specific cell pathways that regulate the immune system make women more susceptible than men to lupus and other autoimmune illnesses.
What is it about the sun and lupus?
Theresa Lu, M.D., Ph.D. (Hospital for Special Surgery, New York) asks why some people with lupus suffer from inflammatory skin lesions after sun exposure. Could it be a heightening of the initial blood vessel activation in lupus that permits inflammatory cells from the bloodstream to enter the skin? Findings could lead to exciting new ways to prevent or treat the photosensitivity and skin manifestations that afflict so many people with lupus.
Could there be a glitch in the function of “master regulators” of the immune system in lupus?
Carla Rothlin, Ph.D. (Yale University, New Haven, CT) has discovered a novel mechanism in “dendritic cells”—master regulators of the immune system—that restrains their hyper-activation and misguided attack against “self-proteins.” New therapeutic approaches for treating lupus might be uncovered by exploring how this mechanism is set in motion in vivo.
Might cutting-edge technologies reveal new lupus markers to explore?
Amr Sawalha, M.D. (University of Oklahoma Health Sciences Center, Oklahoma City, OK) will draw on his diverse expertise in lupus genetics and new technologies to identify molecules in human tissue that might serve as new “early markers” of disease development and treatment effectiveness.
Could a specially engineered mouse hold the answers on how T calls cause lupus damage?
Mark Shlomchik, M.D., Ph.D. (Yale University, New Haven, CT)
In lupus, the immune system responds to the body, targeting “nucleic acids” essential to cell function. While scientists have shown how B cells are activated in this process, T cells also are implicated. Dr. Shlomchik will now aim to engineer a new line of research mouse that illustrates how T cells that act against the body’s own tissues and organs are “turned on” in lupus.
Would selectively inactivating damaging lupus antibodies with a certain kind of “suppressor cell” make a difference?
Chenthamarakshan Vasu, Ph.D. (University of Illinois, Chicago)
Since current therapies for lupus are largely ineffective and pose an increased risk for serious complications such as infections, Dr. Vasu will test the viability of using “nuclear antigen specific suppressor cells” for very selectively inactivating certain cells involved in disease while sparing cells that fight bacteria, viruses, and other infection-causing agents.
Which interferons are to blame for causing lupus damage—and might be good drug targets?
Mark Walter, Ph.D. (University of Alabama, Birmingham) will identify which type 1 interferon (IFNαs) molecules in human tissue lead to the overactive immune response that causes such damage in lupus. The goal: new lupus treatments with fewer side effects through the use of more precise anti-IFN—targeted agents.
Might restoring good behavior to cells that cause destabilization of the immune system in lupus make a difference?
Yisong Wan, Ph.D. (University of North Carolina at Chapel Hill, NC) will investigate ways to manipulate and return normal function to faulty “immune-suppressive regulatory T cells” (Tregs) so crucial to guiding the body in distinguishing its own tissue from outside invaders.
Why is there such a risk for preeclampsia in lupus?
Robert Winchester, M.D. (Columbia University College of Physicians and Surgeons, New York) will examine why a lifethreatening condition called preeclampsia is more common in lupus. With preeclampsia, pregnant women experience very high blood pressure that can lead to serious complications for the mother and child. He plans to find new ways to identify and prevent or stop this response.