Division of Rheumatology

The Role of the TWEAK Molecule in Lupus: Part II

BRONX, NY - April 26, 2015 - Dr. Chaim Putterman, Professor of Medicine and of Microbiology & Immunology and Chief of the Division of Rheumatology, is currently studying whether a molecule known as TWEAK (TNF-related weak inducer of apoptosis) or other potential mediators of inflammation can act on brain cells to promote some of the neurologic signs and symptoms that lupus patients suffer from, and whether in experimental systems they can be treated or prevented. These particular studies, for which Dr. Putterman was recently awarded a large grant by the National Institute of Arthritis and Musculoskeletal and Skin Diseases, draw from his extensive history of research into lupus-related abnormalities of the immune system and how they present in tissues and organs throughout the body.   

This article is the second in a series exploring Dr. Chaim Putterman’s investigatory efforts to bring about significant improvements in diagnosing and treating lupus, and improving the quality of life and short- and long-term prognosis of patients affected by this disease. 

Part II: A “Rash” of Questions

Lupus is an autoimmune, inflammatory disease that can simultaneously affect different systems of the body, including the blood, kidneys, skin, and brain. Amidst his research into the effects of lupus on the kidneys, Dr. Chaim Putterman received a call from the Einstein’s Institute for Animal Studies, the facility responsible for the health and well-being of laboratory animals throughout campus. He was told that some of his mice had developed a pronounced rash and would need to be removed from the study. 

As he considered the problem, an important question came to mind: Were these the standard, unmanipulated (so called “wild-type”) lupus mice that were affected by the severe rash, or the Fn14 knockout lupus strain? If they were the regular lupus mice, the conclusion would appear to be that the TWEAK receptor played an important role not only in the kidneys but also in skin disease.


Dr. Chaim Putterman Rheumatology Albert Einstein College of Medicine Montefiore Medical Center Bronx NY
Chaim Putterman, MD

As it turned out, all of the mice with the rash were the mice that had a working TWEAK receptor, signifying that TWEAK signaling affected not only the kidney disease but also the rashes, scarring, and other symptoms of cutaneous lupus erythematosus (skin disease) that commonly occur in these lupus mice (and, potentially, also in lupus patients). Dr. Putterman began collaborating with Dr. Adam Friedman, Assistant Professor of Medicine and of Physiology & Biophysics,  and Director of Dermatologic Research for the Division of Dermatology, to explore the role of the TWEAK molecule in skin diseases.

Following a similar path to that charted  in his exploration of kidney disease, Dr. Putterman’s laboratory used both skin cells in culture as well as various mouse strains that develop induced or spontaneous lupus-like skin lesions to investigate how the TWEAK pathway contributes to skin disease. Furthermore, since sunlight is known to be a potent trigger of skin rash in lupus patients and ultraviolet rays have similar effects on skin cells as exposure to TWEAK, Jessica Doerner, a Sue Golding graduate student in Dr. Putterman’s lab, is investigating whether ultraviolet rays and TWEAK may act together to trigger or worsen lupus skin disease. 

Related 

Part I: Chance Favors the Prepared Mind>> 

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Division of Rheumatology
Albert Einstein College of Medicine
Jack and Pearl Resnick Campus
1300 Morris Park Avenue
Forchheimer Bldg., Rm 701N
Bronx, NY 10461

(718) 430-2078
Fax: (718) 430-8789

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