![Clinical and biological response of the TIM-3–deficient patient to various immunosuppressive treatments. (A) PET-CT scan analysis showing hyperactive lesions in patient’s subcutaneous tissues (arrows) before (December 2017; left) and their absence 7 months after (July 2019; right) initiation of ruxolitinib therapy. (B) Plots showing the patient’s high serum levels of inflammatory markers (sCD25, CXCL10 chemokine, and IL-18 cytokine) over time under various treatments (under ruxolitinib therapy [Ruxolitinib +] or not [Ruxolitinib −]), as compared with control (Ctrl). Data are means plus or minus standard deviation (SD) from 6 different controls. sCD25, CXCL10, and IL-18 were quantified by enzyme-linked immunosorbent assay. (C) Patient’s increased serum levels of IFN-γ and IL-6 during flare (Ruxolitinib −; December 2018) and their normalization under ruxolitinib therapy (Ruxolitinib +; July 2019) as compared with control. Data are means plus or minus SD from 6 different controls. (D) Increased proportion of highly activated (CD38+HLA-DR+) CD8 T cells from patient during flare (Ruxolitinib −; December 2018), as compared with control (Ctrl CD8 T cells), which normalized under ruxolitinib therapy (Ruxolitinib +; July 2019). (E) High increased proportion of effector memory CD8 T lymphocytes (CD45RA−CCR7−) at the expense of naive CD8 T lymphocytes (CD45RA+CCR7+) in the patient during flare (blue bars; December 2018) that normalized under ruxolitinib therapy (green bars; July 2019). The shaded area indicates our in-house normative values. EMRA, effector memory reexpressing CD45RA.](https://ash.silverchair-cdn.com/ash/content_public/journal/bloodadvances/4/7/10.1182_bloodadvances.2020001497/1/advancesadv2020001497f2.png?Expires=1735813972&Signature=xcmC05yqS4X~DK5-Eq-eC~zmFW3NyOmH2cyrL-ZiuLv37q7N5widR-yCDWlND-qGhFJbKNYK59VJMqWCG5Tlg2-Ryr6NOBOLadMbicWZaQtouPmOyEIlQuFA5R2KPKbeomZJOrZNNAQcjPrxUyzvrkogSYkpNmG74s1715~nU1mizzzU0v5O7sAMcSuP3C8GXv1rbx5F1BnWI1ZxkZl0-VpL8zvWufpGvscmKn3XkyqN4R56bO6Bnfl5dtwVIB432QOjR3q8MteZKfvRvv3WdeQ43HJhfVy619vPa7tfEjfJwsCLwWitSZ5eyj9GW1kOSEwTPPSV35hZ0K4YU-KgNA__&Key-Pair-Id=APKAIE5G5CRDK6RD3PGA)
Clinical and biological response of the TIM-3–deficient patient to various immunosuppressive treatments. (A) PET-CT scan analysis showing hyperactive lesions in patient’s subcutaneous tissues (arrows) before (December 2017; left) and their absence 7 months after (July 2019; right) initiation of ruxolitinib therapy. (B) Plots showing the patient’s high serum levels of inflammatory markers (sCD25, CXCL10 chemokine, and IL-18 cytokine) over time under various treatments (under ruxolitinib therapy [Ruxolitinib +] or not [Ruxolitinib −]), as compared with control (Ctrl). Data are means plus or minus standard deviation (SD) from 6 different controls. sCD25, CXCL10, and IL-18 were quantified by enzyme-linked immunosorbent assay. (C) Patient’s increased serum levels of IFN-γ and IL-6 during flare (Ruxolitinib −; December 2018) and their normalization under ruxolitinib therapy (Ruxolitinib +; July 2019) as compared with control. Data are means plus or minus SD from 6 different controls. (D) Increased proportion of highly activated (CD38+HLA-DR+) CD8 T cells from patient during flare (Ruxolitinib −; December 2018), as compared with control (Ctrl CD8 T cells), which normalized under ruxolitinib therapy (Ruxolitinib +; July 2019). (E) High increased proportion of effector memory CD8 T lymphocytes (CD45RA−CCR7−) at the expense of naive CD8 T lymphocytes (CD45RA+CCR7+) in the patient during flare (blue bars; December 2018) that normalized under ruxolitinib therapy (green bars; July 2019). The shaded area indicates our in-house normative values. EMRA, effector memory reexpressing CD45RA.