Reimagining Psoriasis: Spotlight on New Elements of Pathophysiology and Disease Burden

Date: Friday 24 September 2021
Time: 13.15-13.45 CET

Speakers:

Prof. April Armstrong, MD, MPH

Associate Dean

Department of Dermatology

Keck School of Medicine

University of Southern California

United States

 

Dr. Andrew Blauvelt, MD, MBA

President

Oregon Medical Research Center

United States

 

Prof. Seemal R. Desai, MD, FAAD

Founder and Medical Director

Innovative Dermatology

Clinical Assistant Professor

Department of Dermatology

University of Texas Southwestern Medical Center

United States

 

Program Description:

 

Bristol Myers Squibb is delighted to invite you to a virtual symposium where 3 renowned dermatologists will explore the disease burden and unmet need in the psoriasis treatment landscape and spotlight the role of TYK2 in the pathology of psoriasis and other autoimmune diseases. Many patients with psoriasis are not treated or are undertreated, despite an abundance of available treatments.1,2 Understanding patients’ preferences and needs may improve patient satisfaction and psoriasis treatment success.1,3 The TYK2/JAK-STAT pathways play a significant role in intracellular signaling of cytokines in numerous cellular processes important both in normal and in pathological states, such as immune-mediated inflammatory diseases.4-6  In psoriasis, TYK2/JAK mediation is involved in signaling of many proinflammatory cytokines, including IL-23, which stimulates the differentiation of T cells to Th17 cells,  which in turn causes recruitment of various cytokines to psoriatic lesion sites and therefore the perpetuation of lesions.4,7,8 Beyond psoriasis, these pathways play an important role in the pathology of psoriatic arthritis, inflammatory bowel diseases, and lupus, among other disorders.9-12 This demonstrates how a key pathogenic signaling axis may be shared across a range of different immune-mediated inflammatory diseases.7-12

13:15- 13:25

Talk 1 – Understanding the Unmet Need in the Treatment of Psoriasis

Prof. April Armstrong (USA)

A detailed review of the attributes of available therapies for psoriasis and differences in patients’ and physicians’ perspectives on the treatment burdens and successes.

 

13:25- 13:35

Talk 2 – Exploring the Differences of TYK2 versus Janus Kinases

Dr. Andrew Blauvelt (USA)

 

A review of the cellular actions of the TYK/JAK family in cytokine signal transduction, highlighting each member’s unique roles in vivo, including the consequences of deficiency.

13:35-13:45

Talk 3 – TYK2: Mediating a Key Axis of Inflammation

Prof. Seemal R. Desai (USA)

 

A dive into the role of TYK2 in the pathologic signaling of a range of inflammatory and autoimmune disorders, with a special focus on psoriasis initiation and perpetuation.

Abbreviations:

 

JAK = Janus Kinase; STAT = Signal Transducer and Activator of Transcription; TYK2 = Tyrosine Kinase 2.

 

 

References:

1. Lebwohl MG, Kavanaugh A, Armstrong AW, Van Voorhees AS. US perspectives in the management of psoriasis and psoriatic arthritis: patient and physician results from the population-based Multinational Assessment of Psoriasis and Psoriatic Arthritis (MAPP) survey. Am J Clin Dermatol. 2016;17(1):87-97. doi:10.1007/s40257-015-0169-x

2. Armstrong AW, Koning JW, Rowse S, Tan H, Mamolo C, Kaur M. Under-treatment of patients with moderate to severe psoriasis in the United States: analysis of medication usage with health plan data. Dermatol Ther (Heidelb). 2017;7(1):97-109. doi:10.1007/s13555-016-0153-2

3. Alcusky M, Lee S, Lau G, et al. Dermatologist and patient preferences in choosing treatments for moderate to severe psoriasis. Dermatol Ther (Heidelb). 2017;7(4):463-483. doi:10.1007/s13555-017-0205-2

4. Bannerjee S, Biehl A, Gadina M, Hasni S, Schwartz DM. JAK-STAT signaling as a target for inflammatory and autoimmune diseases: current and future prospects. Drugs.
2017;77(5):521-546. doi:10.1007/s40265-017-0701-9

5. Babon JJ, Lucet IS, Murphy JM, Nicola NA, Varghese LN. The molecular regulation of Janus kinase (JAK) activation. Biochem J. 2014 ;462(1) :1-13. doi:10.1042/BJ20140712

6. Kreins AY, Ciancanelli MJ, Okada S, et al. Human TYK2 deficiency: mycobacterial and viral infections without hyper-IgE syndrome. J Exp Med. 2015;212(10):1641-1662. doi:10.1084/jem.
20140280

7. Hawkes JE, Chan TC, Krueger JG. Psoriasis pathogenesis and the development of novel targeted immune therapies. J Allergy Clin Immunol. 2017;140(3):645-653. doi:10.1016/j.jaci.2017.07.004

8. Rendon A, Schäkel K. Psoriasis pathogenesis and treatment. Int J Mol Sci. 2019;20(6):1475. doi:10.3390/ijms20061475

9. Suzuki E, Mellins ED, Gershwin ME, Nestle FO, Adamopoulos IE. The IL-23/IL-17 axis in psoriatic arthritis. Autoimmun Rev. 2014;13(4-5):496-502. doi:10.1016/j.autrev.2014.01.050

10. Salas A, Hernandez-Rocha C, Duijvestein M, et al. JAK-STAT pathway targeting for the treatment of inflammatory bowel disease. Nat Rev Gastroenterol Hepatol. 2020;17(6):323-337. doi:10.1038/s41575-020-0273-0

11. Larosa M, Zen M, Gatto M, et al. IL-12 and IL-23/Th17 axis in systemic lupus erythematosus. Exp Biol Med (Maywood). 2019;244(1):42-51. doi:10.1177/1535370218824547

12. Gaffen SL, Jain R, Garg AV, Cua DJ. The IL-23–IL-17 immune axis: from mechanisms to therapeutic testing. Nat Rev Immunol. 2014;14(9):585-600. doi:10.1038/nri3707