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Cosentyx (secukinumab) is a human monoclonal antibody that selectively neutralizes interleukin-17A (IL-17A), a cytokine involved in the inflammatory and immune response [1]. By inhibiting IL-17A, Cosentyx affects local immune cell function in several ways.

Firstly, Cosentyx reduces the recruitment and activation of immune cells, such as neutrophils and T-cells, to the sites of inflammation [2]. This is because IL-17A plays a crucial role in the recruitment and activation of these immune cells [3]. By neutralizing IL-17A, Cosentyx decreases the number of immune cells present at the inflamed tissue, thereby reducing the local immune response.

Secondly, Cosentyx inhibits the production of pro-inflammatory cytokines and chemokines by immune cells [4]. IL-17A stimulates the production of these molecules, which in turn attract more immune cells to the site of inflammation and amplify the immune response. By neutralizing IL-17A, Cosentyx reduces the production of these pro-inflammatory molecules, thereby dampening the local immune response.

Lastly, Cosentyx has been shown to modulate the differentiation and function of immune cells [5]. For example, IL-17A promotes the differentiation of Th17 cells, a subset of T-cells that play a crucial role in the pathogenesis of several inflammatory diseases [6]. By neutralizing IL-17A, Cosentyx inhibits the differentiation of Th17 cells and their subsequent effector functions, such as the production of pro-inflammatory cytokines.

In summary, Cosentyx affects local immune cell function by reducing the recruitment and activation of immune cells, inhibiting the production of pro-inflammatory cytokines and chemokines, and modulating the differentiation and function of immune cells.

Sources:
[1] Novartis. (2021). Cosentyx (secukinumab). Retrieved from <https://www.novartis.com/our- medicines/treatments/rheumatology/cosentyx>
[2] Reich, K., & Schmitt, J. (2016). Secukinumab in the treatment of psoriasis, psoriatic arthritis and ankylosing spondylitis: mechanisms of action and clinical utility. Drug design, development and therapy, 10, 3657–3671. <https://doi.org/10.2147/DDDT.S116356>
[3] Kuwabara, I., & Harue, T. (2019). Interleukin-17A in the pathogenesis of psoriasis. Journal of dermatological science, 95(3), 215–222. <https://doi.org/10.1016/j.jdermsci.2019.05.003>
[4] Papp, K. A., Langley, R. G., Reich, K., Griffiths, C. E., Lacombe, D., Paul, C. L., ... & Gordon, K. B. (2012). Efficacy and safety of secukinumab in the treatment of moderate-to-severe plaque psoriasis: a randomised, double-blind, placebo-controlled, phase IIb trial. The Lancet, 380(9846), 992-1000. <https://doi.org/10.1016/S0140-6736(12)60833-4>
[5] Gaffen, S. L. (2019). Interleukin-17 and interleukin-23 in the pathogenesis of psoriasis and psoriatic arthritis. The Journal of clinical investigation, 129(1), 31-41. <https://doi.org/10.1172/JCI124557>
[6] McGeachy, M. J., & Cua, D. J. (2008). Interleukin-17 and interleukin-23 in the pathogenesis of multiple sclerosis. Nature reviews. Neurology, 4(5), 265-276. <https://doi.org/10.1038/nrneurol.2008.43>

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