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Antonios O. Aliprantis, MD
Associate Physician, Brigham and Women's Hospital
Associate Professor of Medicine, Part-time, Harvard Medical School

Brigham and Women's Hospital
Department of Medicine
Rheumatology, Immunology
75 Francis Street
Boston, MA 02115

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Research Narrative:

As a rheumatologist and Assistant Professor in Medicine within the Division of Rheumatology, Allergy and Immunology at Brigham and Women’s Hospital (BWH), I have developed a keen interest in the aberrant tissue remodeling that underlies musculoskeletal diseases like rheumatoid arthritis, osteoporosis, osteoarthritis and scleroderma.  My group uses a combination of cell biology, mouse genetics and translational studies on human samples to unravel disease mechanisms.

A major focus of my laboratory is the osteoclast, a multinucleated bone-resorbing cell implicated in the pathogenesis of osteoporosis and rheumatoid arthritis.  My group has made two significant contributions to this field.  First, we provided the definitive demonstration that the transcription factor NFATc1 is the master regulator of osteoclast differentiation under physiologic and inflammatory situations and second, we identified an anion exchange channel, Slc4a2, which is absolutely required for osteoclasts to resorb bone. Current osteoclast projects include 1) identifying the universe of NFATc1 regulated genes in the osteoclast and deciphering the role of these genes in the bone resorption pathway by shRNA screening; 2) evaluating how Slc4a2 regulates intracellular pH and remodeling of the actin cytoskeleton; and 3) resolving the cellular identity of the osteoclast precursor in disease states.  We hope our findings will lead to novel therapeutics for disorders characterized by excessive bone destruction.


My group also has an interest in basic and translational aspects of osteoarthritis, also known as degenerative joint disease.  Osteoarthritis afflicts millions of Americans and though it costs the health care system tens of billions of dollars a year, there are currently no available therapies.  As Director of the Osteoarthritis Center at BWH, my group is currently tackling the problem on two fronts.  First, we use a mouse model of osteoarthritis to test for genes involved in pathogenesis.  Currently we are looking at the role of the protease HtrA1 as well as the inflammasome in our model.  Second, we have a biomarkers program, which uses clinical repositories of serum and synovial fluid at BWH and the NIH to identify markers of disease progression by mass spectrometry.

Lastly, my group is also interested in the pathogenesis of scleroderma, an autoimmune disease characterized by skin and internal organ fibrosis.  Few treatments are available for this devastating rheumatic disease.  In the past 4 years, we have generated exciting data suggesting that a mouse model of graft versus host disease mimics the early stages of scleroderma.  We have also found that the cytokine Interleukin 13, and the chemokine CCL2, are critical mediators of this model and are currently exploring whether biotherapeutics targeting these molecules might ameliorate this disease.

New York University School of Medicine, 2001, MD

Publications (Pulled from Harvard Catalyst Profiles):

1. Ravi A, Chang M, van de Pol M, Yang S, Aliprantis A, Thornton B, Carayannopoulos LN, Bautmans A, Robberechts M, De Lepeleire I, Singh D, Hohlfeld JM, Sterk PJ, Krug N, Lutter R. Rhinovirus-16 induced temporal interferon responses in nasal epithelium links with viral clearance and symptoms. Clin Exp Allergy. 2019 Aug 10.

2. Joshi N, Yan J, Levy S, Bhagchandani S, Slaughter KV, Sherman NE, Amirault J, Wang Y, Riegel L, He X, Rui TS, Valic M, Vemula PK, Miranda OR, Levy O, Gravallese EM, Aliprantis AO, Ermann J, Karp JM. Author Correction: Towards an arthritis flare-responsive drug delivery system. Nat Commun. 2018 05 11; 9(1):1954.

3. Joshi N, Yan J, Levy S, Bhagchandani S, Slaughter KV, Sherman NE, Amirault J, Wang Y, Riegel L, He X, Rui TS, Valic M, Vemula PK, Miranda OR, Levy O, Gravallese EM, Aliprantis AO, Ermann J, Karp JM. Towards an arthritis flare-responsive drug delivery system. Nat Commun. 2018 04 03; 9(1):1275.

4. Xiong Y, Berrueta L, Urso K, Olenich S, Muskaj I, Badger GJ, Aliprantis A, Lafyatis R, Langevin HM. Stretching Reduces Skin Thickness and Improves Subcutaneous Tissue Mobility in a Murine Model of Systemic Sclerosis. Front Immunol. 2017; 8:124.

5. O'Brien W, Fissel BM, Maeda Y, Yan J, Ge X, Gravallese EM, Aliprantis AO, Charles JF. RANK-Independent Osteoclast Formation and Bone Erosion in Inflammatory Arthritis. Arthritis Rheumatol. 2016 12; 68(12):2889-2900.

6. Yan J, Herzog JW, Tsang K, Brennan CA, Bower MA, Garrett WS, Sartor BR, Aliprantis AO, Charles JF. Gut microbiota induce IGF-1 and promote bone formation and growth. Proc Natl Acad Sci U S A. 2016 11 22; 113(47):E7554-E7563.

7. Urso K, Alvarez D, Cremasco V, Tsang K, Grauel A, Lafyatis R, von Andrian UH, Ermann J, Aliprantis AO. IL4RA on lymphatic endothelial cells promotes T cell egress during sclerodermatous graft versus host disease. JCI Insight. 2016 Aug 04; 1(12).

8. Sargent JL, Li Z, Aliprantis AO, Greenblatt M, Lemaire R, Wu MH, Wei J, Taroni J, Harris A, Long KB, Burgwin C, Artlett CM, Blankenhorn EP, Lafyatis R, Varga J, Clark SH, Whitfield ML. Identification of Optimal Mouse Models of Systemic Sclerosis by Interspecies Comparative Genomics. Arthritis Rheumatol. 2016 08; 68(8):2003-15.

9. Ge X, Ritter SY, Tsang K, Shi R, Takei K, Aliprantis AO. Sex-Specific Protection of Osteoarthritis by Deleting Cartilage Acid Protein 1. PLoS One. 2016; 11(7):e0159157.

10. Urso K, Charles JF, Shull GE, Aliprantis AO, Balestrieri B. Anion Exchanger 2 Regulates Dectin-1-Dependent Phagocytosis and Killing of Candida albicans. PLoS One. 2016; 11(7):e0158893.