Identification of MPN-specific Antigens and Anti-MPN TCRs in Myeloproliferative Neoplasm
Key claim: This observational study aims to identify MPN-specific antigens and T cell receptors (TCRs) in bone marrow and blood of MPN patients, with the goal of enabling future TCR-based immunotherapies.
Abstract
The goal of this observational study is to learn how the immune system responds to myeloproliferative neoplasms (MPN) in adults with known or suspected MPN. Researchers also want to identify immune cells that could help develop future immune-based treatments for MPN.
The main questions it aims to answer are:
- Are there T cells in the bone marrow that can recognize MPN cells?
- Which targets (antigens) on MPN cells are recognized by these immune cells?
- Can researchers identify T cell receptors (TCRs) that may be used in future TCR-based therapies?
Researchers will study samples from adults with polycythemia vera (PV), essential thrombocythemia (ET), primary myelofibrosis (PMF), post-PMF, or unclassifiable MPN. Samples from healthy donors without blood disorders will also be included for comparison.
By providing blood and bone marrow samples, participants will:
- Allow researchers to study immune cells and genetic material from these samples
- Allow researchers to perform laboratory tests to study how immune cells recognize MPN cells
Researchers will use laboratory methods such as genetic sequencing, cell analysis, and cell culture experiments to better understand immune responses in MPN.
Participants will not receive direct medical benefit from this study. The results may help researchers better understand MPN and support the future development of immune-based therapies.
Why this matters
This is the first systematic effort to identify MPN-specific antigens and cognate TCRs across PV, ET, PMF, and MPN-U, opening adoptive TCR-based immunotherapy as a new therapeutic axis distinct from JAK inhibition, interferon, and CALR-directed agents. Because the study spans multiple subtypes, it could reveal whether immunogenic antigen landscapes differ by driver mutation (JAK2 vs CALR vs MPL) or by subtype natural history, with particular relevance for PMF where curative options remain restricted to allogeneic HSCT and for MPN-U where targeted molecular options are scarce.