Dr. Lin specializes in the diagnosis and treatment of all rheumatologic conditions such as rheumatoid arthritis, lupus, myositis, gout, and seronegative spondyloarthropathies. She has received additional training in autoimmune skin diseases and has a special clinical and research interest for psoriasis/psoriatic arthritis, dermatomyositis, cutaneous lupus/systemic lupus, and scleroderma. Dr. Lin is a graduate of USSONAR (Ultrasound School of North American Rheumatologists) program and performs diagnostic musculoskeletal ultrasound evaluation and ultrasound-guided injections.

Clinical Focus

  • Rheumatology
  • Rheumatology-Dermatology

Academic Appointments

Professional Education

  • Board Certification: Rheumatology, American Board of Internal Medicine (2013)
  • Residency:Icahn School of Medicine at Mount Sinai Hospital Internal Medicine Residency (2011) NY
  • Medical Education:Tufts University School of Medicine Office of the Registrar (2008) MA
  • Subspecialty Fellowship, Brigham and Women's Hospital, Harvard Medical School. Dermatology-Rheumatology Fellowship, MA (2014)
  • Fellowship:New York University Division of Rheumatology (2013) NY
  • Board Certification: Internal Medicine, American Board of Internal Medicine (2011)


All Publications

  • Tofacitinib Citrate for Refractory Cutaneous Dermatomyositis: An Alternative Treatment. JAMA dermatology Kurtzman, D. J., Wright, N. A., Lin, J., Femia, A. N., Merola, J. F., Patel, M., Vleugels, R. A. 2016

    View details for DOI 10.1001/jamadermatol.2016.0866

    View details for PubMedID 27120749

  • Comment on "the effects of bariatric surgery weight loss on knee pain in patients with osteoarthritis of the knee". Arthritis Lin, J., Parikh, M., Samuels, J. 2013; 2013: 517803-?

    View details for DOI 10.1155/2013/517803

    View details for PubMedID 23710356

  • The TNF alpha locus is altered in monocytes from patients with systemic lupus erythematosus CLINICAL IMMUNOLOGY Sullivan, K. E., Suriano, A., Dietzmann, K., Lin, J., Goldman, D., Petri, M. A. 2007; 123 (1): 74-81


    In systemic lupus erythematosus, TNFalpha is elevated in the serum and correlates with disease activity and triglyceride levels. The stimuli that drive TNFalpha in this setting are incompletely understood. This study was designed to evaluate monocyte chromatin at the TNFalpha locus to identify semi-permanent changes that might play a role in altered expression of TNFalpha. SLE patients with relatively quiescent disease (mean Physician Global Assessment=0.6) and healthy controls were recruited for this study. TNFalpha expression was measured by intracellular cytokine staining of different monocyte subsets in patients (n=24) and controls (n=12). Histone acetylation at the TNFalpha locus was measured by chromatin immunoprecipitation using a normalized quantitative PCR in patients (n=46) and controls (n=24). There were no differences in the overall fractions of cells expressing CD14 in SLE patients compared to controls; however, the fraction of DR+/CD16+ cells expressing CD14 was slightly higher as was true in the monocyte subset defined by DR+/CD11b+. Within the monocyte population defined by physical characteristics and DR+/CD14+, TNFalpha expressing cells were more frequent in SLE patients compared to controls. Both the fraction of positive cells and the mean fluorescence intensity were higher in patients than controls. Consistent with this was the finding that monocytes from patients had increased TNFalpha transcripts and more highly acetylated histones at the TNFalpha locus compared to controls. Furthermore, patients with the highest levels of TNFalpha histone acetylation were more likely to have had consistently elevated erythrocyte sedimentation rates, and to have required cytotoxic use. Histone acetylation, associated with increased transcriptional competence of TNFalpha, may play a role in certain inflammatory aspects of the disease.

    View details for DOI 10.1016/j.clim.2006.12.008

    View details for Web of Science ID 000245252600010

    View details for PubMedID 17276734

  • Renal biopsy in lupus patients with low levels of proteinuria JOURNAL OF RHEUMATOLOGY Christopher-Stine, L., Siedner, M., Lin, J., Haas, M., Parekh, H., Petri, M., Fine, D. M. 2007; 34 (2): 332-335


    Early and accurate detection of kidney involvement in systemic lupus erythematosus (SLE) improves outcomes. Renal biopsy is required for definitive diagnosis of lupus nephritis (LN). In the absence of acute renal failure (ARF), moderate levels of proteinuria (> 1000 mg/24 h) have been recommended by some to justify biopsy. We investigated whether patients with lower levels of proteinuria without ARF have significant renal disease and should be routinely biopsied.We retrospectively evaluated 21 SLE patients with 24-h urine protein < 1000 mg who underwent kidney biopsies. Indications for biopsy included new-onset proteinuria, increasing proteinuria, or hematuria (> 5 red blood cells per high power field). No patient had ARF.Sixteen of 21 (77%) biopsies were diagnostic of LN: 3 class II, 10 class III (5 superimposed class V), 2 class IV (one superimposed class V), and one with class V. One patient had thrombotic microangiopathy. The remaining 4 (23%) patients had non-lupus renal disease. Thirteen patients with class III or greater LN required alterations in therapeutic regimen because of biopsy findings. Of 7 patients without hematuria at the time of biopsy, 4 (57%) had class III, IV, or V LN. One patient without hematuria and < 500 mg/24 h proteinuria had class III LN.We found significant renal involvement (Class III, IV, or V LN) in SLE patients with < 1000 mg proteinuria with or without hematuria. Our findings suggest that biopsy be strongly considered in this patient population.

    View details for Web of Science ID 000244112900017

    View details for PubMedID 17183619

  • Risk factors for renal failure among 72 consecutive patients with rhabdomyolysis related to illicit drug use AMERICAN JOURNAL OF MEDICINE Fine, D. M., Gelber, A. C., Melamed, M. L., Lin, J. C., Lin, Z., Eustace, J. A. 2004; 117 (8): 607-610

    View details for DOI 10.1016/j.amjmed.2004.02.051

    View details for Web of Science ID 000224439300010

    View details for PubMedID 15465510