Untitled Document

Seunghee Cha

Oral Surgery, Assistant Professor

Oral Biology, Joint Assistant Professor

scha@dental.ufl.edu
phone: (352) 273-6687
fax: (352) 392-250

PO Box 100416

Ph.D., University of Florida, Immunology/Microbiology, 2001
DDS, 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 whose target tissues are the exocrine lacrimal and salivary glands, resulting in dry eyes and dry mouth. We have characterized and established the non-obese diabetic (NOD) mouse as an animal model for SjS in our laboratory for the close resemblance to the phenotype of human SjS. Additionally, various congenic strains with the NOD mouse and knockout models have been studied to narrow down susceptibility loci and examine the roles of various cytokines in the disease process.

Current and future studies include:

investigation of effects of IFN-gamma on abnormal salivary gland organogenesis in the NOD mouse at birth and, a subsequent disease onset and progression
epitope mapping and the screening of human sera as well as mouse sera for the presence of anti-muscarinic 3 receptor (M 3 R) autoantibodies using transfected cell lines
investigation of biological effects of anti-M3R autoantibodies in the generation of dryness via regulating calcium signaling pathways
identification of susceptibility genes by the application of functional genomics and proteomics
development of preventive and therapeutic strategies to restore secretory function in human patients with SjS.

Selected Publications:

Nguyen C., Cha, S., and Peck AB. (2006). The role of B lymphocytes in Sjögren’s syndrome-like disease of the NOD mouse model. Frontiers in Bioscience (in press).

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 Sjogren'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 Sjogren'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 Sjogren's syndrome-like autoimmunity. Adv Exp Med Biol, 506(Pt B), 1035-9.

Humphreys-Beher, M.G., Brayer, J., Cha, S., Nagashima, H., Diggs, S., & Peck, A.B. (2002). Immunogenetics of autoimmune exocrinopathy in the nod mouse: more than meets the eye. Adv Exp Med Biol, 506(Pt B), 999-1007.

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 (Sjogren'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.

Cha, S., van Blockland, S.C., Versnel, M.A., Homo-Delarche, F., Nagashima, H., Brayer, J., Peck, A.B., & Humphreys-Beher, M.G. (2001). Abnormal organogenesis in salivary gland development may initiate adult onset of autoimmune exocrinopathy. Exp Clin Immunogenet, 18(3), 143-60.

Brayer, J.B, Cha, S., Nagashima, H., Yasunari, U., Lindberg, A., Diggs, S., Martinez , J., Goa , J., Humphreys-Beher, M.G., & Peck, A.B. (2001). IL-4-dependent effector phase in autoimmune exocrinopathy as defined by the NOD.IL-4-gene knockout mouse model of Sjogren's syndrome. Scand J Immunol, 54(1-2), 133-40.

Clarke, M.Y., Brayer, J., Heintz, K., Nagashima, H., Cha, S., Oxford , G.E., Nanni, J.M., Peck, A.B., Zelles, T., & Humphreys-Beher, M.G. (2001). Differential absorption and distribution of epidermal growth factor and insulin-like growth factor in diabetic NOD mice. J Diabetes Complications, 15(2), 103-11.

Brayer, J., Lowry, J., Cha, S., Robinson, C.P., Yamachika, S., Peck, A.B., & Humphreys-Beher, M.G. (2000). Alleles from chromosomes 1 and 3 of NOD mice combine to influence Sjogren's syndrome-like autoimmune exocrinopathy. J Rheumatol, 27(8), 1896-904.