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2016 TIL Grants

Lupus Research Alliance Commits over $4 Million for Studies to Improve Lupus Treatment

The Lupus Research Alliance announces the 2016 recipients of its Target Identification in Lupus (TIL) grants. The goal is to speed the creation of new lupus treatments by funding research to uncover new molecular or cellular mechanisms to target in drug development. Recipients of this year’s awards, which run for up to three years, are conducting promising studies that range from blocking harmful B cells to discovering the role of DNA-releasing immune cells in causing lupus skin rashes. All seven projects share a reliance on state-of-the-art scientific techniques and a commitment to identifying new targets to improve lupus treatment.

Anne Davidson, MBBS

Feinberg Institute for Medical Research, Manhasset, NY << view more >>
THE ROLE OF TLR8 IN LUPUS NEPHRITIS

Dr. Davidson and her team have discovered that one immune system protein, TLR8, may help foster lupus nephritis, the kidney inflammation that is a leading cause of illness and death in lupus patients. By using lupus-prone animals in which we have introduced the human TLR8 protein, we will investigate whether higher amounts of TLR8 induce inflammation and worsen kidney deterioration. We will also determine how the extra amounts of TLR8 regulate the function of kidney resident immune cells that accelerate lupus nephritis. Drugs to block proteins that are related to TLR8 are already under development, and the study could indicate whether creating drugs to block TLR8 is worthwhile.

What this means for people with lupus: The new Lupus Research Alliance-funded project promises to help illuminate how lupus leads to kidney damage and why the disease is more common in women than in men. The results of Dr. Davidson’s work may help the pharmaceutical and biotech industries decide which proteins to target with potential treatments.

Rong Fan, PhD

Yale School of Medicine, New Haven, CT<< view more >>
DISSECTING THE EFFECTOR FUNCTION OF PATHOGENIC TFH CELLS IN HUMAN LUPUS

Immune system cells communicate with each other by releasing chemicals known as cytokines. We have created a microchip that allows us to eavesdrop on immune cells by measuring what cytokines they are producing. We will use our microchip to analyze blood cells from lupus patients. We plan to profile a type of T cell that promotes the tissue destruction of lupus, determining which cytokines these cells release and how they respond to treatment.

What this means for people with lupus: Dr. Fan developed a microchip that can monitor the biomolecules released by immune cells. He and his team hope the chip can reveal how one type of T cell triggers tissue damage in lupus and provide clues about how to prevent it.

Roger Greenberg, MD, PhD

Perelman School of Medicine, Univ. of Pennsylvania, Philadelphia, PA << view more >>
BRISC DUB ACTIVITY AS A NOVEL TARGET FOR LUPUS


Dr. Greenberg and his team have discovered that mice that lack a certain cluster of interacting proteins, known as BRISC, don’t develop lupus. Their previous research identified several molecules that block BRISC and might be able to quell lupus symptoms. With their TIL grant, they now plan to test whether these molecules are beneficial in mice that develop the disease. His team also intends to fine-tune the molecules to make them more effective, with the hope that they will lead to new therapies for the disease.

What this means for people with lupus: Dr. Greenberg and his team have identified a new culprit in lupus, a group of interacting proteins. They are developing molecules that will block these proteins, which could lead to new treatments for lupus.

Ming-Lin Liu, MD, PhD

Perelman School of Medicine, Univ. of Pennsylvania, Philadelphia, PA << view more >>
A NOVEL TARGET FOR NEUTROPHIL NETOSIS IN LUPUS SKIN INFLAMMATION


Lupus patients develop skin rashes in response to sunlight and other triggers. Immune cells called neutrophils promote these lesions by spewing out their DNA. Dr. Liu’s team has discovered that a protein known as ROCK is crucial to this process. They will now test whether blocking ROCK stops neutrophils from releasing their DNA, thereby reducing skin inflammation in mice that are prone to lupus. The results of their study could suggest new ways to reduce skin rashes in lupus patients.

What this means for people with lupus: Skin rashes are common in lupus patients. Dr. Lieu’s research will ask whether preventing certain immune cells from releasing their DNA curbs skin inflammation.

Mark J. Mamula, PhD

Yale School of Medicine, New Haven, CT<< view more >>
Targeting the miR-182-96-183 Cluster to Ameliorate Lupus

B cells are doubly destructive in lupus. They can directly stimulate T cells to attack patients’ own tissues. Dr. Mamula’s team has found that B cells also indirectly trigger T cell attacks by interacting with other immune cells. Although current lupus drugs can prevent B cells from directly stimulating T cells, they do not stop B cells from interacting with other immune cells. The goal of Dr. Mamula’s TIL-funded research is to discover molecules that thwart B cells’ indirect effects on the immune system and identify approaches to potential new treatments for the disease.

What this means for people with lupus: Dr. Mamula and his team are working to identify molecules that block one harmful impact of B cells and reduce the tissue damage triggered by these cells.

Laurence Morel, PhD

University of Florida, Gainesville, FL<< view more >>
TARGETING FOLLICULAR HELPER CD4 T CELLS IN SLE


A specific type of T cell drives the tissue damage that occurs in lupus. These cells need more energy than normal cells, and that might be their Achilles heel. We have found that we can cut the numbers of these T cells in mice with common diabetes treatments such as metformin that deprive the cells of the sugar they need to survive. Now, Dr. Morel’s team plans to test whether we can use these drugs as a lupus therapy that will eliminate the problematic T cells.

What this means for people with lupus: Dr. Morel and her team want to determine whether it is possible to treat lupus by shutting off the food supply to immune cells that promote the disease.

Kerstin Nündel, PhD

University of Massachusetts Medical School, Worcester, MA<< view more >>
TLR9 REGULATES AXL DEPENDENT MIGRATION OF AUTOREACTIVE B CELLS


In lupus, proteins in the immune system known as toll-like receptors help trigger the damaging effects of the disease. But one of the proteins, known as TLR9, is the black sheep of the toll-like receptor family—it reduces the severity of lupus symptoms. Our research suggests that TLR9 is helpful because it prevents immune cells known as B cells from moving into tissues where they can cause injury. Dr. Nündel and her team now want to uncover how TLR9 controls B cells’ movements and identify an approach for treatment that can stop their migration.

What this means for people with lupus: The immune system is the villain in lupus, but one immune system protein appears to protect patients’ cells. Dr. Nündel seeks to find out how, and whether this insight can lead to a potential treatment.

Learn more about the many grants funded by the Lupus Research Alliance to advance scientific discovery in lupus.


1.5 million

people in the U.S. have Lupus.

172 million

dollars committed to lupus research by the Lupus Research Alliance.


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