Janus Kinase Inhibitors Differentially Inhibit Specific Cytokine Signals in the Mesenteric Lymph Node Cells of Inflammatory Bowel Disease Patients

J Crohns Colitis. 2024 Apr 23;18(4):628-637. doi: 10.1093/ecco-jcc/jjad173.

Abstract

Background: Janus kinase [JAK] inhibitors [JAKinibs] are effective small molecule therapies for treating Crohn's disease [CD] and ulcerative colitis [UC], collectively known as inflammatory bowel disease [IBD]. By preventing JAKs from phosphorylating signal transducer and activator of transcription proteins, JAKinibs disrupt cytokine signalling pathways that promote inflammation. Despite considerable overlap in the JAKs they target, first- and second-generation JAKinibs display different clinical efficacies in CD and UC.

Methods: We conducted a comparative phosflow study of four JAKinibs [filgotinib, upadacitinib, tofacitinib, and deucravacitinib] to observe subtle mechanistic differences that may dictate their clinical behaviour. Resected mesenteric lymph node [MLN] cells from 19 patients [9 CD, 10 UC] were analysed by flow cytometry in the presence or absence of different cytokine stimuli and titrated JAKinibs.

Results: We found a higher potency of the JAK 1/3-preferential inhibitor, tofacitinib, for JAK 3-dependent cytokine signalling pathways in comparison to filgotinib, but a higher potency of the JAK 1-preferential inhibitors, filgotinib and upadacitinib, for JAK 3-independent cytokine signalling pathways. Deucravacitinib, a TYK2-preferential inhibitor, demonstrated a much narrower selectivity by inhibiting only IL-10 and IFN-β pathways, albeit more potently than the other JAKinibs. Additionally, we found some differences in the sensitivity of immune cells from CD versus UC, and patients with versus without a CD-associated NOD2 polymorphism, to phosphorylate signal transducer and activator of transcriptions in response to specific cytokine stimulation.

Conclusions: Despite their similarities, differences exist in the relative potencies of different JAKinibs against distinct cytokine families, to explain their clinical efficacy.

Keywords: Janus kinase; deucravacitinib; filgotinib; tofacitinib; upadacitinib.

Publication types

  • Comparative Study

MeSH terms

  • Adult
  • Benzamides / pharmacology
  • Benzamides / therapeutic use
  • Colitis, Ulcerative / drug therapy
  • Colitis, Ulcerative / immunology
  • Colitis, Ulcerative / pathology
  • Crohn Disease / drug therapy
  • Crohn Disease / pathology
  • Cytokines* / metabolism
  • Female
  • Heterocyclic Compounds, 3-Ring / pharmacology
  • Heterocyclic Compounds, 3-Ring / therapeutic use
  • Humans
  • Inflammatory Bowel Diseases / drug therapy
  • Inflammatory Bowel Diseases / pathology
  • Janus Kinase 1 / antagonists & inhibitors
  • Janus Kinase 1 / metabolism
  • Janus Kinase 3 / antagonists & inhibitors
  • Janus Kinase 3 / metabolism
  • Janus Kinase Inhibitors* / pharmacology
  • Janus Kinase Inhibitors* / therapeutic use
  • Lymph Nodes* / drug effects
  • Lymph Nodes* / pathology
  • Male
  • Mesentery
  • Middle Aged
  • Piperidines* / pharmacology
  • Piperidines* / therapeutic use
  • Pyridines*
  • Pyrimidines* / pharmacology
  • Pyrimidines* / therapeutic use
  • Pyrroles* / pharmacology
  • Pyrroles* / therapeutic use
  • Pyrrolidines / pharmacology
  • Pyrrolidines / therapeutic use
  • Quinazolinones / pharmacology
  • Quinazolinones / therapeutic use
  • Signal Transduction / drug effects
  • Triazoles*

Substances

  • tofacitinib
  • Janus Kinase Inhibitors
  • Piperidines
  • Pyrimidines
  • Cytokines
  • upadacitinib
  • GLPG0634
  • Pyrroles
  • Pyrrolidines
  • Janus Kinase 3
  • Heterocyclic Compounds, 3-Ring
  • Quinazolinones
  • Janus Kinase 1
  • Benzamides
  • Pyridines
  • Triazoles

Grants and funding