Brian S. Kim
Brian S. Kim | |
|---|---|
| Born | New York, NY |
| Education | Haverford College, University of Washington School of Medicine, University of Pennsylvania School of Medicine |
| Occupation(s) | Sol and Clara Kest Professor, Vice Chair of Research, Site Chair, Director of Mark Lebwohl Center |
| Medical career | |
| Field | Dermatology, Allergy, Immunology, Neuroimmunology, Sensory Biology |
| Institutions | Mount Sinai Health System |
| Website | Kim Lab |
Brian S. Kim is the Sol and Clara Kest Professor, Vice Chair of Research, and Site Chair of Mount Sinai West and Morningside in the Kimberly and Eric J. Waldman Department of Dermatology at Icahn School of Medicine at Mount Sinai.[1][2][3] He is also Director of the Mark Lebwohl Center for Neuroinflammation and Sensation.[4]
Education
[edit]Kim received his B.S. in chemistry with honors from Haverford College in 2001 and his M.D. from the University of Washington in 2007. He was a Howard Hughes Medical Institute-National Institutes of Health Research Scholar under Stephen I. Katz, and completed his residency in dermatology at the Perelman School of Medicine at the University of Pennsylvania.[5][6] He completed a postdoctoral fellowship under David Artis,[7] leading to a Master of Translational Research.
Research
[edit]He was the first to identify IL-4 receptor signaling on sensory neurons,[8] which critically informed new therapies like dupilumab.[9] Kim's group also was the first lab to identify JAK1 signaling in sensory neurons,[10] building on previous research which showed a significant reduction of itch symptoms in response to treatment with JAK inhibitors.[11][12] While these previous works investigated JAK inhibition as an anti-inflammatory treatment, Kim and colleagues found that disruption of neuronal JAK1 signaling limits both inflammatory and non-inflammatory itch, suggesting that JAK inhibitors may represent a novel neuromodulatory approach to target itch in atopic dermatitis[13] Kim also designed the pivotal phase 2 clinical trial that ultimately led to the approval of topical ruxolitinib for atopic dermatitis.[14]
References
[edit]- ^ "Brian S. Kim - Dermatology | Mount Sinai - New York". Mount Sinai Health System. Retrieved August 29, 2022.
- ^ "Brian S. Kim". Brian Kim Lab. Retrieved August 29, 2022.
- ^ "Brian S. Kim | Icahn School of Medicine". Icahn School of Medicine at Mount Sinai. Retrieved August 29, 2022.
- ^ "Top Researcher of Itch and Inflammatory Skin Conditions to Join Mount Sinai's Department of Dermatology | Mount Sinai - New York". Mount Sinai Health System. Retrieved August 29, 2022.
- ^ "Dr. Brian Kim, MD – New York, NY | Dermatology on Doximity". Doximity. Retrieved August 29, 2022.
- ^ "ORCID". orcid.org. Retrieved August 29, 2022.
- ^ "T32 Past Trainees". Penn Dermatology Training. Retrieved August 29, 2022.
- ^ Oetjen, LK; Mack, MR; Feng, J; Whelan, TM; Niu, H; Guo, CJ; Chen, S; Trier, AM; Xu, AZ; Tripathi, SV; Luo, J; Gao, X; Yang, L; Hamilton, SL; Wang, PL; Brestoff, JR; Council, ML; Brasington, R; Schaffer, A; Brombacher, F; Hsieh, CS; Gereau RW, 4th; Miller, MJ; Chen, ZF; Hu, H; Davidson, S; Liu, Q; Kim, BS (September 21, 2017). "Sensory Neurons Co-opt Classical Immune Signaling Pathways to Mediate Chronic Itch". Cell. 171 (1): 217–228.e13. doi:10.1016/j.cell.2017.08.006. PMC 5658016. PMID 28890086.
{{cite journal}}: CS1 maint: numeric names: authors list (link) - ^ Guttman-Yassky, E; Bissonnette, R; Ungar, B; Suárez-Fariñas, M; Ardeleanu, M; Esaki, H; Suprun, M; Estrada, Y; Xu, H; Peng, X; Silverberg, JI; Menter, A; Krueger, JG; Zhang, R; Chaudhry, U; Swanson, B; Graham, NMH; Pirozzi, G; Yancopoulos, GD; D Hamilton, JD (January 2019). "Dupilumab progressively improves systemic and cutaneous abnormalities in patients with atopic dermatitis". The Journal of Allergy and Clinical Immunology. 143 (1): 155–172. doi:10.1016/j.jaci.2018.08.022. PMID 30194992. S2CID 52177141.
- ^ Oetjen, LK; Mack, MR; Feng, J; Whelan, TM; Niu, H; Guo, CJ; Chen, S; Trier, AM; Xu, AZ; Tripathi, SV; Luo, J; Gao, X; Yang, L; Hamilton, SL; Wang, PL; Brestoff, JR; Council, ML; Brasington, R; Schaffer, A; Brombacher, F; Hsieh, CS; Gereau RW, 4th; Miller, MJ; Chen, ZF; Hu, H; Davidson, S; Liu, Q; Kim, BS (September 21, 2017). "Sensory Neurons Co-opt Classical Immune Signaling Pathways to Mediate Chronic Itch". Cell. 171 (1): 217–228.e13. doi:10.1016/j.cell.2017.08.006. PMC 5658016. PMID 28890086.
{{cite journal}}: CS1 maint: numeric names: authors list (link) - ^ Levy, LL; Urban, J; King, BA (September 2015). "Treatment of recalcitrant atopic dermatitis with the oral Janus kinase inhibitor tofacitinib citrate". Journal of the American Academy of Dermatology. 73 (3): 395–9. doi:10.1016/j.jaad.2015.06.045. PMID 26194706.
- ^ Bissonnette, R; Papp, KA; Poulin, Y; Gooderham, M; Raman, M; Mallbris, L; Wang, C; Purohit, V; Mamolo, C; Papacharalambous, J; Ports, WC (November 2016). "Topical tofacitinib for atopic dermatitis: a phase IIa randomized trial". The British Journal of Dermatology. 175 (5): 902–911. doi:10.1111/bjd.14871. PMID 27423107. S2CID 3581619.
- ^ Oetjen, LK; Mack, MR; Feng, J; Whelan, TM; Niu, H; Guo, CJ; Chen, S; Trier, AM; Xu, AZ; Tripathi, SV; Luo, J; Gao, X; Yang, L; Hamilton, SL; Wang, PL; Brestoff, JR; Council, ML; Brasington, R; Schaffer, A; Brombacher, F; Hsieh, CS; Gereau RW, 4th; Miller, MJ; Chen, ZF; Hu, H; Davidson, S; Liu, Q; Kim, BS (September 21, 2017). "Sensory Neurons Co-opt Classical Immune Signaling Pathways to Mediate Chronic Itch". Cell. 171 (1): 217–228.e13. doi:10.1016/j.cell.2017.08.006. PMC 5658016. PMID 28890086.
{{cite journal}}: CS1 maint: numeric names: authors list (link) - ^ Kim, BS; Howell, MD; Kang, S; Nasir, A; Kuligowski, ME (February 2020). "Treatment of atopic dermatitis with ruxolitinib cream (JAK1/2 inhibitor) or triamcinolone cream". Journal of Allergy and Clinical Immunology. 145 (2): 572–582. doi:10.1016/j.jaci.2019.08.042. PMID 31629805. S2CID 204812790.
This article incorporates text by Brian S. Kim available under the CC BY-SA 3.0 license. The text and its release have been received by the Wikimedia Volunteer Response Team.
