Brian S. Kim, M.D.

Assistant Professor
Internal Medicine

Immunology Program

  • (314) 362-8187

  • (314) 362-7015

  • (314) 362-8159

  • 8123

  • Clinical Sciences Research Building 6649

  • BKim33@WUSTL.EDU


  •, @itchdoctor

  • Atopic dermatitis, basophils, innate lymphoid cell, itch, JAK, microbiota, pruritus, type 2 cytokine

  • Understanding the intersection of immunity and sensory perception

Research Abstract:

The ultimate goal of the Kim Lab is to understand how the immune system interacts with the nervous system to shape sensory perception. By studying the sensation of itch, we seek to understand three fundamental aspects of inflammation and sensory dysfunction. First, our lab is focused on understanding the regulatory mechanisms that arise from the skin barrier to influence immune cells that orchestrate immunity and inflammation. Second, we are interested in solving how factors released from the epidermis directly trigger sensory neurons to evoke the sensation of itch. Third, and finally, we aim to unravel the precise mechanisms by which tissue-resident immune cells directly stimulate with the sensory nervous system in the setting of chronic itch. Collectively, these scientific programs have therapeutic implications for numerous inflammatory skin disorders and chronic itch disorders including atopic dermatitis or eczema and chronic idiopathic dermatitis. More broadly, the fundamental mechanisms unveiled by our studies may extend to a number of other inflammatory and neurophysiological disorders beyond the skin including asthma, food allergy, migraines, and irritable bowel syndrome.

Selected Publications:

1. Piezo2 channel-Merkel cell signaling modulates the conversion of touch to itch. Feng J, Luo J, Yang P, Du J, Kim BS, Hu H. Science (New York, N.Y.). 2018; 360(6388):530-533.PMID: 29724954

2.Interactions of the immune and sensory nervous systems in atopy. Oetjen LK, Kim BS. The FEBS journal. 2018. PMID: 29637705

3.Transient receptor potential vanilloid 4-expressing macrophages and keratinocytes contribute differentially to allergic and nonallergic chronic itch.Luo J, Feng J, Yu G, Yang P, Mack MR, Du J, Yu W, Qian A, Zhang Y, Liu S, Yin S, Xu A, Cheng J, Liu Q, O`Neil RG, Xia Y, Ma L, Carlton SM, Kim BS, Renner K, Liu Q, Hu H. The Journal of allergy and clinical immunology. 2018; 141(2):608-619.e7.PMID: 28807414

4.Commensal microbiota modulate gene expression in the skin. Meisel JS, Sfyroera G, Bartow-McKenney C, Gimblet C, Bugayev J, Horwinski J, Kim B, Brestoff JR, Tyldsley AS, Zheng Q, Hodkinson BP, Artis D, Grice EA.
Microbiome. 2018; 6(1):20. PMID: 29378633

5. Sensory TRP channels contribute differentially to skin inflammation and persistent itch. Feng J, Yang P, Mack MR, Dryn D, Luo J, Gong X, Liu S, Oetjen LK, Zholos AV, Mei Z, Yin S, Kim BS, Hu H. Nature communications. 2017; 8(1):980. PMID: 29081531

6. Sensory Neurons Co-opt Classical Immune Signaling Pathways to Mediate Chronic Itch. 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.
Cell. 2017; 171(1):217-228.e13.PMID: 28890086

7. The antimicrobial peptide human beta-defensin 2 promotes itch through Toll-like receptor 4 signaling in mice. Feng J, Luo J, Mack MR, Yang P, Zhang F, Wang G, Gong X, Cai T, Mei Z, Kim BS, Yin S, Hu H. The Journal of allergy and clinical immunology. 2017; 140(3):885-888.e6.PMID: 28442325

8. Immune dysregulation underlies a subset of patients with chronic idiopathic pruritus. Xu AZ, Tripathi SV, Kau AL, Schaffer A, Kim BS. Journal of the American Academy of Dermatology. 2016; 74(5):1017-20. PMID: 27085236

9. Basophils promote innate lymphoid cell responses in inflamed skin. Kim BS, Wang K, Siracusa MC, Saenz SA, Brestoff JR, Monticelli LA, Noti M, Tait Wojno ED, Fung TC, Kubo M, Artis D. Journal of immunology (Baltimore, Md. : 1950). 2014; 193(7):3717-25. PMID: 25156365

10. TSLP elicits IL-33-independent innate lymphoid cell responses to promote skin inflammation. Kim BS, Siracusa MC, Saenz SA, Noti M, Monticelli LA, Sonnenberg GF, Hepworth MR, Van Voorhees AS, Comeau MR, Artis D. Science translational medicine. 2013; 5(170):170ra16. PMID: 23363980

Last Updated: 6/20/2018 9:49:32 AM

The original identification of ILC2s in inflamed skin
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