Source: Interfolio F180


Dwight Kono

Professor Emeritus
Department of Immunology and Microbiology


 Email

Research Focus

Our laboratory seeks to define the etiopathogenesis of systemic lupus erythematosus (SLE) and to identify potential therapeutic targets using lupus susceptible mice strains as model systems. Areas of interest related to lupus include systemic autoimmunity, tolerance, normal immune function, and genetics. A major focus is the identification of susceptibility genes in spontaneous lupus-prone mouse strains and in an induced model. Defining the genetic basis for lupus is critical for understanding lupus pathogenesis, as genetic susceptibility appears to be a prerequisite for disease development. Classical genetics approaches are being used to identify loci, narrow intervals with congenic mice, and identify genes. A second area of research seeks to identify the essential effector genes in SLE using both forward and reverse genetics approaches. These, in contrast to susceptibility genes, are typically normal genes that have non-redundant functions in disease pathogenesis. As such, their identification should yield important insights into disease processes and is also likely to have therapeutic implications. A third general area of interest is the study of specific pathways in lupus pathogenesis. Recent studies have investigated interferons, nucleic acid-recognizing toll-like receptors, actin cytoskeleton regulation, and mechanisms of B cell tolerance as they relate to systemic autoimmunity.


Education

B.S. (Chemistry), University of Washington, 1973
M.D. (Medicine), University of Washington, 1977

Professional Experience

1977-1981 Medicine Res/Chief Res., University of Hawaii, Honolulu, HI
1981-1984 Postdoctoral Fellow, Rheumatology, University of California, Los Angeles, CA
1984-1985 Adjunct Instructor of Medicine, Co-Director, Arthritis Clinic, UCLA, Los Angeles, CA
1985-1986 Adjunct Assist. Prof. of Medicine, Co-Director, Arthritis Clinic, UCLA, Los Angeles, CA
1986-1988 Senior Res. Fellow, California Institute of Technology, Div Biology, Pasadena, CA
1988-1998 Assist. Prof., Dept. of Immunol., The Scripps Research Institute (TSRI), La Jolla, CA
1998-2007 Assoc. Prof., Dept. of Immunol., TSRI, La Jolla, CA
2008-pres Prof. of Immunology, Dept. of. Immunology and Microbial Science, TSRI, La Jolla, CA
2008-pres Faculty, Skaggs Graduate School of Chemical and Biological Sciences, TSRI, La Jolla, CA

Awards & Professional Activities

1973 B.S. with distinction, Cum laude, Phi Beta Kappa, University of Washington
1976 Medical Student Research Training Stipend, University of Washington
1978 Silver Hammer Award, University of Hawaii
1980 Third Year Resident of the Year, University of Hawaii
1984 New Investigator Award, Arthritis Foundation

Selected Publications

Pollard, K. M.; Hultman, P.; Kono, D. H. Using single-gene deletions to identify checkpoints in the progression of systemic autoimmunity. Annals of the New York Academy of Sciences 2003, 987, 236-239.

Mayeux, J. M.; Escalante, G. M.; Christy, J. M.; Pawar, R. D.; Kono, D. H.; Pollard, K. M. Silicosis and silica-induced autoimmunity in the diversity outbred mouse. Frontiers in Immunology 2018, 9.
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Haraldsson, M. K.; dela Paz, N. G.; Kuan, J. G.; Gilkeson, G. S.; Theofilopoulos, A. N.; Kono, D. H. Autoimmune alterations induced by the New Zealand Black Lbw2 locus in BWF1 mice. Journal of Immunology 2005, 174, 5065-5073.

Santiago-Raber, M. L.; Haraldsson, M. K.; Theofilopoulos, A. N.; Kono, D. H. Characterization of reciprocal MRL-Fas(lpr) and C57BL/6-Fas(lpr) congenic mice reveals significant effects from Lmb3. Journal of Immunology 2007, 178, 8195-8202.

Haraldsson, M. K.; Louis-Dit-Sully, C. A.; Lawson, B. R.; Sternik, G.; Santiago-Raber, M. L.; Gascoigne, N. R.; Theofilopoulos, A. N.; Kono, D. H. The lupus-related Lmb3 locus contains a disease-suppressing coronin-1A gene mutation. Immunity 2008, 28, 40-51.
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Kono, D. H.; Balomenos, D.; Pearson, D. L.; Park, M. S.; Hildebrandt, B.; Hultman, P.; Pollard, K. M. The prototypic Th2 autoimmunity induced by mercury is dependent on IFN-gamma and not Th1/Th2 imbalance. Journal of Immunology 1998, 161, 234-240.