Research Interest

Autoimmune diseases (Rheumatoid arthritis, Ankylosing spondylitis, Systemic sclerosis), Inflammation, DAMPs, NETosis, Citrullination

Research Summary

Inflammation is our body's immune response to infection or tissue injury. It is a protective response to clear pathogen or damaged cells from our body, ultimately to restore health. However, if the inflammation is not tightly regulated or not resolved well, the reaction causes excessive tissue damage and inflammatory disease such as rheumatoid arthritis, atherosclerosis, sepsis, and even cancer. The endogenous products from tissue injury are called Damaged Associated Molecular Patterns (DAMPs) or alarmins, which can initiate and perpetuate a noninfectious inflammatory response through the interaction with pattern recognition receptors such as toll-like receptor or Nod-like receptor. Recent studies show that the elevated levels of DAMPs in chronic inflammatory diseases, suggesting that DAMPs and their receptors could provide novel targets for therapy and biomarkers. Our research goal is to identify key regulators of inflammation, and to investigate the underlying mechanisms of rheumatoid arthritis and other inflammatory diseases. These studies will contribute to the development of novel therapeutic strategies and biomarkers.

Selected publication

1. Lee HN, Kim A, Kim Y, Kim GT, Sohn DH, Lee SG. Higher serum uric acid levels are associated with reduced risk of hip osteoporosis in postmenopausal women with rheumatoid arthritis. Medicine (Baltimore). 2020 Jun 12;99(24):e20633.

2. Lee B, Song YS, Rhodes C, Goh TS, Roh JS, Jeong H, Park J, Lee HN, Lee SG, Kim S, Kim M, Lee SI, Sohn DH*, Robinson WH*. Protein phosphatase magnesium-dependent 1A induces inflammation in rheumatoid arthritis. Biochem Biophys Res Commun. 2020 Feb 12;522(3):731-735. (*Equal contribution)

3. Kragstrup TW, Sohn DH, Lepus CM, Onuma K, Wang Q, Robinson WH, Sokolove J. Fibroblast-like synovial cell production of extra domain A fibronectin associates with inflammation in osteoarthritis. BMC Rheumatol. 2019 Dec 2;3:46.

4. Ha M, Jeong H, Roh JS, Lee B, Han ME, Oh SO, Sohn DH*, Kim YH*. DYSF expression in clear cell renal cell carcinoma: A retrospective study of 2 independent cohorts. Urol Oncol. 2019 Oct;37(10):735-741. (*Equal contribution)

5. Wang Q, Onuma K, Liu C, Wong H, Bloom MS, Elliott EE, Cao RR, Hu N, Lingampalli N, Sharpe O, Zhao X, Sohn DH, Lepus CM, Sokolove J, Mao R, Cisar CT, Raghu H, Chu CR, Giori NJ, Willingham SB, Prohaska SS, Cheng Z, Weissman IL, Robinson WH. Dysregulated integrin αVβ3 and CD47 signaling promotes joint inflammation, cartilage breakdown, and progression of osteoarthritis. JCI Insight. 2019 Sep 19;4(18). e128616.

6. Sohn DH*, Nguyen TT*, Kim S, Shim S, Lee S, Lee Y, Jhun H, Azam T, Kim J, Kim S. Structural characteristics of seven IL-32 variants. Immune Netw. 2019 Apr;19(2):e8. (*Equal contribution)

7. Park YJ, Park B, Lee M, Jeong YS, Lee HY, Sohn DH, Song JJ, Lee JH, Hwang JS, Bae YS. A novel antimicrobial peptide acting via formyl peptide receptor 2 shows therapeutic effects against rheumatoid arthritis. Sci Rep. 2018 Oct 2;8(1):14664

8. Roh JS, Sohn DH. Damage-associated molecular patterns in inflammatory diseases. Immune Netw. 2018 Aug 13;18(4):e27

9. Sohn DH, Jeong H, Roh JS, Lee HN, Kim E, Koh JH, Lee SG. Serum CCL11 level is associated with radiographic spinal damage in patients with ankylosing spondylitis. Rheumatol Int. 2018 Aug;38(8):1455-1464

10. Sohn DH. NETosis in autoimmune diseases. J Rheum Dis. 2016 Apr;23(2):82-87.

11. Sohn DH, Rhodes C, Onuma K, Zhao X, Sharpe O, Gazitt T, Shiao R, Fert-Bober J, Cheng D, Lahey LJ, Wong HH, Van Eyk J, Robinson WH, Sokolove J. Local joint inflammation and histone citrullination in a murine model of the transition from preclinical autoimmunity to inflammatory arthritis. Arthritis Rheumatol. 2015 Nov;67(11):2877-87