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Updated: Jul 7, 2026

Immunoglobulin Gene Sequence Analysis In Chronic Lymphocytic Leukemia: From Patient Material To Sequence Interpretation
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miR-155 impairs ICOSL and MHC-I expression in DLBCL lymphomas.

Esmerina Tili1,2, Teresa L Commisso2, Veronica Balatti2

  • 1Department of Anesthesiology, Wexner Medical Center, College of Medicine, The Ohio State University, Columbus, OH 43210.

Proceedings of the National Academy of Sciences of the United States of America
|April 18, 2025
PubMed
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High microRNA-155 (miR-155) levels in B cell cancers like DLBCL reduce ICOSL and MHC-I, hindering the immune system

Area of Science:

  • Immunology
  • Molecular Biology
  • Oncology

Background:

  • Elevated microRNA-155 (miR-155) is linked to aggressive B cell malignancies, including chronic lymphocytic leukemia (CLL) and diffuse large B cell lymphoma (DLBCL).
  • Previous studies in mouse models showed miR-155 down-regulates ICOSL, impairing T cell recognition of malignant cells.

Purpose of the Study:

  • To investigate the role of miR-155 in human DLBCL by examining its correlation with ICOSL and MHC-I levels.
  • To determine if miR-155 directly targets ICOSL and MHC-I transcripts in different DLBCL subtypes.

Main Methods:

  • Analysis of miR-155, ICOSL, and MHC-I levels in human DLBCL patient samples.
  • Investigation of miR-155's effect on ICOSL and MHC-I transcript levels in ABC and GCB DLBCL primary tumors and cell lines.
Keywords:
DLBCLICOSLMHC-IlymphomamicroRNA

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Main Results:

  • In human DLBCL samples, miR-155 levels negatively correlated with both ICOSL and MHC-I levels.
  • miR-155 reduced ICOSL transcript levels in ABC DLBCL but not GCB DLBCL.
  • No direct targeting of MHC-I transcripts by miR-155 was observed, suggesting indirect regulatory mechanisms.

Conclusions:

  • High miR-155 levels in DLBCL contribute to immune evasion by down-regulating ICOSL and potentially MHC-I.
  • The deficiency in ICOSL and MHC-I activity, driven by elevated miR-155, may explain the host immune system's failure to eliminate malignant B cells.