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Seunghee Cha, D.D.S., Ph.D.

Seunghee Cha

Department of Oral & Maxillofacial Diagnostic Sciences

Section of Oral Medicine, Associate Professor
Oral Biology, Joint Associate Professor

Phone: 352-273-6687
Fax: 352-846-0588
P.O. Box 100414
Gainesville, FL 32610-0416


  • Ph.D., University of Florida, Immunology/Microbiology, 2001
  • D.D.S., Yonsei University, Seoul, Korea, 1993

Main Interests

Our main research interests are to understand the pathogenesis of Sjögren’s syndrome (SjS) using the various tools of molecular biology, immunology, and genetics. SjS is an autoimmune disorder that attacks exocrine lacrimal and salivary glands, resulting in dry eyes and dry mouth. Our current work focuses on the identification of molecular regulation of pro-inflammatory caspase-1 and -11, which appear to be activated through the inflammasome, in infiltrating macrophages. These molecules are believed to be critical in the generation of pro-inflammatory microenvironment and subsequent apoptosis in the salivary glands prior to disease onset. In addition, pathological roles of autoantibodies targeting muscarinic type-3 receptor (M3R), which is the major receptor subtype for fluid secretion in the salivary glands, are being investigated to understand secretory dysfunction in SjS. Identifying molecular mechanisms of hyposalivation in SjS will allow us to develop strategies that can improve secretory function as well as the quality of life in SjS patients. In vitro cell culture system, mouse models, and human specimen are available in the laboratory for the investigation of disease pathogenesis for SjS.

Current and future studies include:

  • Investigation of pro-inflammatory microenvironment in the salivary glands to understand target tissue specificity in SjS: Molecular pathways involving inflammatory caspases and the inflammasome
  • Investigation of molecular mechanisms of hyposalivation in SjS: Identification of altered trafficking of aquaporin-5 and calcium signaling pathways by anti-M3R autoantibodies
  • Investigation of pathological roles of anti-M3R autoantibodies: Roles of different subclasses of anti-M3R antibodies, generation of monoclonal anti-M3R antibody, epitope mapping and autoantibody screening
  • Identification of susceptibility genes by applying functional genomics and proteomics
  • Application of receptor mediated siRNA delivery in SjS
  • Development of preventive and therapeutic strategies to restore secretory function in patients with SjS.

Selected Publications

  • Bulosan M., Pauley K., Yo K, Chan E, Katz J, Peck A, and Cha S. 2008 Inflammatory caspases are critical for enhanced cell death in the target tissue of Sjögren’s syndrome prior to disease onset. Immunology and Cell Biology, Submitted.
  • Stewart, C, Cha S., Bhattacharyya, I., Bulosan, M., Berg, K., Peck, AB., and Katz J. 2008 “Relationship between apoptosis and IL-4 receptor in Sjögren’s syndrome salivary glands: findings from a preliminary study.” Scandinavian journal of Rheumatology, Submitted
  • Stewart C., Cha S., Bhattacharyya I., Berg K., and Reeves W. 2008. “Salivary gland dysfunction and quality of life in Sjögren’s syndrome : A critical oral-systemic connection”, Journal of American Dental Association, 139(3):291-9.
  • Stewart C., Cha S., Caudle R., Berg K., and Katz J. 2008 “Decreased levels of soluble receptor for advanced glycation end products (sRAGE) in patients with primary Sjögren’s syndrome”, Rheumatology International, 2008 Jun;28(8):771-6.
  • Stewart C., Bhattacharyya I., Nair M., Pettigrew J., Cha S., and Katz J. “Salivary gland disorders”, Book Chapter In Oral Medicine, Radiology and Pathology, Elselvier Publisher, In Press.
  • Nguyen C, Cha S, and Peck AB. 2007. “Sjögren’s syndrome (SjS)-like disease of mice: the importance of B lymphocytes and autoantibodies.” Frontiers in Bioscience. 1(12):1767-89.
  • Nguyen C., Singson E., Kim J-Y., Cornelius J.G., Attia R., Doyle M.E., Bulosan M., Cha S. & Peck A.B. 2006. “Sjögren’s syndrome-like disease of C57BL/6.NOD-Aec1Aec2 mice: Gender differences in keratoconjunctivitis sicca defined by a cross-over in the chromosome 3 Aec1 locus.” Scand. J. Immunology. 64(3):295-307.
  • Cha S., Singson E., Cornellius J., Jarajapu Y., Knot H., and Peck AB. (2006). Muscarinic acetylcholine type-3 receptor desensitization due to chronic exposure to Sjögren’s Syndrome-associated autoantibodies. Journal of Rheumatology. 33(2):296-306.
  • Gao J., Killedar S., Cornelius J., Nguyen C., Cha, S., and Peck AB. (2006). Impact of the cytokine IL-4 on the clinical course of Sjögren’s syndrome- like disease in the NOD mouse model. Journal of Autoimmunity. 26(2):90-103.
  • Nguyen C., Singson E., Cornelius J., Killedar S., Cha. S., and Peck AB. (2006). Role of complement and B cells in Sjögren’s syndrome- like autoimmune exocrinopathy in the NOD.B10.H2 b mouse model. Molecular Immunology. 43(9):1332-9.
  • Cha, S., Brayer, J., Gao, J., Brown, V., Killedar, S., Yasunari, U., & Peck, A.B. (2004). A dual role for interferon-gamma in the pathogenesis of Sjögren’s syndrome-like autoimmune exocrinopathy in the nonobese diabetic mouse. Scand J Immunol, 60(6), 552-65.
  • Gao, J., Cha, S., Jonsson, R., Opalko, J., & Peck, A.B. (2004). Detection of anti-type 3 muscarinic acetylcholine receptor autoantibodies in the sera of Sjögren’s syndrome patients by use of a transfected cell line assay. Arthritis Rheum, 50(8), 2615-21.
  • Cha, S., Nagashima, H., Peck, A.B., & Humphreys-Beher, M.G. (2002). IDD3 and IDD5 alleles from nod mice mediate Sjögren’s syndrome-like autoimmunity. Adv Exp Med Biol, 506(Pt B), 1035-9.
  • Cha, S., Nagashima, H., Brown, V.B., Peck, A.B., & Humphreys-Beher, M.G. (2002). Two NOD Idd-associated intervals contribute synergistically to the development of autoimmune exocrinopathy (Sjögren’s syndrome) on a healthy murine background. Arthritis Rheum, 46(5), 1390-8.
  • Cha, S., Peck, A.B., & Humphreys-Beher, M.G. (2002). Progress in understanding autoimmune exocrinopathy using the non-obese diabetic mouse: an update. Crit Rev Oral Biol Med, 13(1), 5-16.