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Updated: Feb 10, 2026
Evaluation of the Spindle Assembly Checkpoint Integrity in Mouse Oocytes
Published on: September 13, 2022
The expanding constellation of immune checkpoints: a DNAMic control by CD155
Abstract:
The clinical benefits that have been achieved for a group of cancer patients with metastatic disease on checkpoint inhibitor therapy have kindled intense interest in understanding tumor-induced escape from T lymphocyte control. Other lymphoid cells also participate in tumor control; in particular, NK cells can limit hematogenous cancer metastasis spread and are also subject to negative regulation by developing cancers. In this issue of the JCI, Li and colleagues define an unanticipated role for the stress-induced protein CD155 in cancer metastasis. The presence of CD155 on the surface of cancer cells was shown to promote tumor invasiveness, while its upregulation in tumor environment-infiltrating myeloid cells restrained antitumor immunity by impairing antitumor T lymphocytes and NK cell function. Together, these results support further exploration of strategies for targeting CD155.
Insights
The stress-induced protein CD155 promotes cancer metastasis by increasing tumor invasiveness and suppressing anti-tumor immunity from T lymphocytes and NK cells. Targeting CD155 may offer new cancer treatment strategies.
Area of Science:
- Immunology
- Oncology
- Molecular Biology
Background:
- Checkpoint inhibitor therapy shows clinical benefits for metastatic cancer.
- Tumor-induced immune escape, particularly from T lymphocyte control, is a key challenge.
- Natural Killer (NK) cells also play a role in controlling cancer metastasis and are negatively regulated by tumors.
Purpose of the Study:
- To define the role of the stress-induced protein CD155 in cancer metastasis.
- To investigate how CD155 influences tumor invasiveness and anti-tumor immunity.
Main Methods:
- Analysis of CD155 expression in cancer cells and tumor-infiltrating myeloid cells.
- Assessment of CD155's impact on tumor cell invasiveness.
- Evaluation of CD155's effect on T lymphocyte and NK cell function in the tumor microenvironment.
Main Results:
- CD155 expression on cancer cells promotes tumor invasiveness.
- Upregulation of CD155 in myeloid cells within the tumor environment impairs anti-tumor T lymphocyte and NK cell functions.
- CD155 acts as a negative regulator of anti-tumor immunity.
Conclusions:
- CD155 plays an unanticipated role in promoting cancer metastasis.
- Targeting CD155 presents a potential therapeutic strategy for overcoming immune escape in cancer.
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