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December 8, 2025BloodOpen Access

Advanced myelofibrosis is marked by loss of NKG2D and DNAM-1 NK activating signaling and increased TIM-3 T CD8 exhaustion

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Authors

MMMariana MedeirosCGCamila GarcíaBABeatriz Adjafre

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Overview

Immunophenotyping reveals immune alterations in myelofibrosis patients, implying JAK2V617F mutation drives dysfunction in natural killer and T cells.

Key Points

  • NK cell dysfunction is marked by impaired maturation and loss of activating receptors in myelofibrosis patients.
  • Immunophenotyping showed distinct alterations in immune cell frequencies among untreated myelofibrosis patients.
  • Analysis using a chimeric murine model highlighted the role of JAK2V617F mutation in immune exhaustion.
  • Findings support the notion that both innate and adaptive immune dysfunction contribute to myelofibrosis progression.

Cite This Study

Medeiros et al. (2025) studied this question.

synapsesocial.com/papers/69362f604fa91c937236dd5chttps://doi.org/10.1182/blood-2025-1980
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