01509nas a2200241 4500000000100000008004100001260002400042653002400066653002700090653001700117100001400134700001600148700001600164700001500180700001400195700001600209700001300225245016400238856008000402490000700482520075300489022002501242 2021 d bFapUNIFESP (SciELO)10aInfectious Diseases10aMicrobiology (medical)10aParasitology1 aKurizky P1 aMotta JDOCD1 aBezerra NVF1 aSousa MCDS1 aCorazza D1 aBorges TKDS1 aGomes CM00aDramatic secukinumab-mediated improvements in refractory leprosy-related neuritis via the modulation of T helper 1 (Th1) and T helper 17 (Th17) immune pathways uhttps://www.scielo.br/j/rsbmt/a/PwmPvgV7YY6m7FBrpmBrrZj/?format=pdf&lang=en0 v543 a

A 39-year-old woman was diagnosed with relapsed multibacillary leprosy and refractory neuritis. Here, we describe an evident loss of therapeutic effectiveness after the third pulse of corticosteroids, which may be attributed to tachyphylaxis and the posterior modulation of interferon- γ (IFN-γ), tumor necrosis factor- α (TNF-α,) interleukin-17A (IL-17A), and IL-12/23p40 after the induction phase of secukinumab. In this case, plasma cytokine analysis showed that secukinumab induced a reduction in IL-17 concomitant with impressive clinical improvements in the patient's neural function. Interestingly, secukinumab induced reductions in cytokines related to Th1 responses and earlier stages of the Th17 response, including IL-23/12.

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