Brian S. Kim

Last updated

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]

Contents

Education

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

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]

Related Research Articles

Janus kinase (JAK) is a family of intracellular, non-receptor tyrosine kinases that transduce cytokine-mediated signals via the JAK-STAT pathway. They were initially named "just another kinase" 1 and 2, but were ultimately published as "Janus kinase". The name is taken from the two-faced Roman god of beginnings, endings and duality, Janus, because the JAKs possess two near-identical phosphate-transferring domains. One domain exhibits the kinase activity, while the other negatively regulates the kinase activity of the first.

<span class="mw-page-title-main">Dermatitis</span> Inflammatory disease of the skin

Dermatitis is inflammation of the skin, typically characterized by itchiness, redness and a rash. In cases of short duration, there may be small blisters, while in long-term cases the skin may become thickened. The area of skin involved can vary from small to covering the entire body. Dermatitis is often called eczema, and the difference between those terms is not standardized.

<span class="mw-page-title-main">Psoriasis</span> Skin disease

Psoriasis is a long-lasting, noncontagious autoimmune disease characterized by patches of abnormal skin. These areas are red, pink, or purple, dry, itchy, and scaly. Psoriasis varies in severity from small localized patches to complete body coverage. Injury to the skin can trigger psoriatic skin changes at that spot, which is known as the Koebner phenomenon.

<span class="mw-page-title-main">Itch</span> Uncomfortable skin sensation

An itch is a sensation that causes a strong desire or reflex to scratch. Itches have resisted many attempts to be classified as any one type of sensory experience. Itches have many similarities to pain, and while both are unpleasant sensory experiences, their behavioral response patterns are different. Pain creates a withdrawal reflex, whereas itches leads to a scratch reflex.

<span class="mw-page-title-main">Pimecrolimus</span> Immunosuppressive drug

Pimecrolimus is an immunosuppressant drug of the calcineurin inhibitor class used in the treatment of atopic dermatitis (eczema).

<span class="mw-page-title-main">Atopic dermatitis</span> Long-term form of skin inflammation

Atopic dermatitis (AD), also known as atopic eczema, is a long-term type of inflammation of the skin (dermatitis). It results in itchy, red, swollen, and cracked skin. Clear fluid may come from the affected areas, which can thicken over time. AD may also simply be called eczema, a term that generally refers to a larger group of skin conditions.

<span class="mw-page-title-main">Interleukin 33</span> IL-33 induces helper T cells, mast cells, eosinophils and basophils to produce type 2 cytokines.

Interleukin 33 (IL-33) is a protein that in humans is encoded by the IL33 gene.

<span class="mw-page-title-main">Interleukin 31</span>

Interleukin-31 (IL-31) is a protein that in humans is encoded by the IL31 gene that resides on chromosome 12. IL-31 is an inflammatory cytokine that helps trigger cell-mediated immunity against pathogens. It has also been identified as a major player in a number of chronic inflammatory diseases, including atopic dermatitis.

<span class="mw-page-title-main">Sodium voltage-gated channel alpha subunit 9</span> Protein-coding gene in the species Homo sapiens

Sodium voltage-gated channel alpha subunit 9 is a sodium ion channel that in humans is encoded by the SCN9A gene. It is usually expressed at high levels in two types of neurons: the nociceptive (pain) neurons at the dorsal root ganglion (DRG) and trigeminal ganglion; and sympathetic ganglion neurons, which are part of the autonomic (involuntary) nervous system.

<span class="mw-page-title-main">CCL17</span> Mammalian protein found in Homo sapiens

CCL17 is a powerful chemokine produced in the thymus and by antigen-presenting cells like dendritic cells, macrophages, and monocytes. CCL17 plays a complex role in cancer. It attracts T-regulatory cells allowing for some cancers to evade an immune response. However, in other cancers, such as melanoma, an increase in CCL17 is linked to an improved outcome. CCL17 has also been linked to autoimmune and allergic diseases.

<span class="mw-page-title-main">Neuropeptide S receptor</span> Protein-coding gene in the species Homo sapiens

The neuropeptide S receptor (NPSR) is a member of the G-protein coupled receptor superfamily of integral membrane proteins which binds neuropeptide S (NPS). It was formerly an orphan receptor, GPR154, until the discovery of neuropeptide S as the endogenous ligand. Increased expression of this gene in ciliated cells of the respiratory epithelium and in bronchial smooth muscle cells is associated with asthma. This gene is a member of the G protein-coupled receptor 1 family and encodes a plasma membrane protein. Mutations in this gene have also been associated with this disease.

<span class="mw-page-title-main">SMPD2</span> Protein-coding gene in the species Homo sapiens

Sphingomyelin phosphodiesterase 2 is an enzyme that in humans is encoded by the SMPD2 gene.

A Janus kinase inhibitor, also known as JAK inhibitor or jakinib, is a type of immune modulating medication, which inhibits the activity of one or more of the Janus kinase family of enzymes, thereby interfering with the JAK-STAT signaling pathway in lymphocytes.

Senile pruritus is one of the most common conditions in the elderly or people over 65 years of age with an emerging itch that may be accompanied with changes in temperature and textural characteristics. In the elderly, xerosis, is the most common cause for an itch due to the degradation of the skin barrier over time. However, the cause of senile pruritus is not clearly known. Diagnosis is based on an elimination criteria during a full body examination that can be done by either a dermatologist or non-dermatologist physician.

Perianal cellulitis, also known as perianitis or perianal streptococcal dermatitis, is a bacterial infection affecting the lower layers of the skin (cellulitis) around the anus. It presents as bright redness in the skin and can be accompanied by pain, difficulty defecating, itching, and bleeding. This disease is considered a complicated skin and soft tissue infection (cSSTI) because of the involvement of the deeper soft tissues.

Mark G. Lebwohl is an American dermatologist and author who is Professor and Chairman Emeritus of the Kimberly and Eric J. Waldman Department of Dermatology and the Dean for Clinical Therapeutics at the Icahn School of Medicine at Mount Sinai in New York City.

<span class="mw-page-title-main">Interleukin 23</span> Heterodimeric cytokine acting as mediator of inflammation

Interleukin 23 (IL-23) is a heterodimeric cytokine composed of an IL-12B (IL-12p40) subunit and an IL-23A (IL-23p19) subunit. IL-23 is part of the IL-12 family of cytokines. The functional receptor for IL-23 consists of a heterodimer between IL-12Rβ1 and IL-23R.

<span class="mw-page-title-main">Oclacitinib</span> Medication

Oclacitinib, sold under the brand name Apoquel among others, is a veterinary medication used in the control of atopic dermatitis and pruritus from allergic dermatitis in dogs at least 12 months of age. Chemically, it is a synthetic cyclohexylamino pyrrolopyrimidine janus kinase inhibitor that is relatively selective for JAK1. It inhibits signal transduction when the JAK is activated and thus helps downregulate expression of inflammatory cytokines.

<span class="mw-page-title-main">Abrocitinib</span> Chemical compound

Abrocitinib, sold under the brand name Cibinqo, is a medication used for the treatment of atopic dermatitis (eczema). It is a Janus kinase inhibitor and it was developed by Pfizer. It is taken by mouth.

<span class="mw-page-title-main">Kanaka Rajan</span> Indian-American computational neuroscientist

Kanaka Rajan is a computational neuroscientist in the Department of Neurobiology at Harvard Medical School and founding faculty in the Kempner Institute for the Study of Natural and Artificial Intelligence at Harvard University. Rajan trained in engineering, biophysics, and neuroscience, and has pioneered novel methods and models to understand how the brain processes sensory information. Her research seeks to understand how important cognitive functions — such as learning, remembering, and deciding — emerge from the cooperative activity of multi-scale neural processes, and how those processes are affected by various neuropsychiatric disease states. The resulting integrative theories about the brain bridge neurobiology and artificial intelligence.

References

  1. ↑ "Brian S. Kim - Dermatology | Mount Sinai - New York". Mount Sinai Health System. Retrieved August 29, 2022.
  2. ↑ "Brian S. Kim". Brian Kim Lab. Retrieved August 29, 2022.
  3. ↑ "Brian S. Kim | Icahn School of Medicine". Icahn School of Medicine at Mount Sinai. Retrieved August 29, 2022.
  4. ↑ "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.
  5. ↑ "Dr. Brian Kim, MD – New York, NY | Dermatology on Doximity". Doximity. Retrieved August 29, 2022.
  6. ↑ "ORCID". orcid.org. Retrieved August 29, 2022.
  7. ↑ "T32 Past Trainees". Penn Dermatology Training. Retrieved August 29, 2022.
  8. ↑ 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)
  9. ↑ 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.
  10. ↑ 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)
  11. ↑ 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.
  12. ↑ 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.
  13. ↑ 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)
  14. ↑ 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.

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