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Increased TIGIT expression correlates with impaired NK cell function in diffuse large B-cell lymphoma.

Hui Lu1, Xiaoyan Zhao2, Liqiong Liu3

  • 1Department of Hematology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.

Frontiers in Oncology
|April 15, 2025
PubMed
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Natural killer (NK) cell numbers and function are reduced in diffuse large B-cell lymphoma (DLBCL). Blocking T-cell immunoreceptor with Ig and ITIM domains (TIGIT) restores NK cell antitumor activity, suggesting TIGIT as a therapeutic target for DLBCL.

Area of Science:

  • Immunology
  • Oncology
  • Cell Biology

Background:

  • Diffuse large B-cell lymphoma (DLBCL) is an aggressive non-Hodgkin lymphoma.
  • Natural killer (NK) cells play a crucial role in antitumor immunity.
  • NK cell dysfunction is implicated in DLBCL pathogenesis and immune evasion.

Purpose of the Study:

  • To investigate NK cell status in DLBCL patients.
  • To elucidate the role of T-cell immunoreceptor with Ig and ITIM domains (TIGIT) in regulating NK cells within the DLBCL microenvironment.
  • To evaluate TIGIT blockade as a potential therapeutic strategy.

Main Methods:

  • Analysis of NK cell populations and TIGIT family molecule expression (TIGIT, CD226, CD96) in DLBCL patients versus healthy controls using multiparametric flow cytometry.
Keywords:
CD226CD56 dim NK cellsDLBCLNK cellsTIGIT

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  • Assessment of NK cell function, including cytotoxicity and cytokine secretion.
  • Evaluation of TIGIT blockade effects on NK cell activity in vitro and in vivo models.

    • Main Results:

    • DLBCL patients showed reduced NK cell numbers and impaired function compared to controls.
    • Upregulated TIGIT and downregulated CD226 expression were observed on NK cells in DLBCL.
    • TIGIT blockade significantly restored NK cell cytotoxicity against DLBCL cells.

    Conclusions:

    • Aberrant TIGIT pathway signaling contributes to NK cell dysfunction in DLBCL.
    • Targeting TIGIT represents a promising approach to enhance NK cell-mediated antitumor immunity in DLBCL.
    • Restoring NK cell function via TIGIT blockade could overcome tumor immune escape in DLBCL.