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CD84 regulates PD-1/PD-L1 expression and function in chronic lymphocytic leukemia.
Hadas Lewinsky1, Avital F Barak1, Victoria Huber1
1Department of Immunology and.
CD84 interaction upregulates PD-L1/PD-1, suppressing T cell antitumor responses in chronic lymphocytic leukemia (CLL). Blocking CD84 may reverse this immune suppression, offering a new therapeutic strategy for CLL patients.
Area of Science:
- Immunology
- Oncology
- Cell Biology
Background:
- Chronic lymphocytic leukemia (CLL) involves abnormal B lymphocyte accumulation and immune defects, leading to infections.
- T cells in CLL are dysfunctional, impairing antitumor immunity and contributing to T cell exhaustion.
- Immune checkpoints, like PD-L1/PD-1, are implicated in CLL-mediated T cell exhaustion.
Purpose of the Study:
- To investigate the role of CD84 in regulating T cell function and immune checkpoints in CLL.
- To determine if CD84 mediates the upregulation of PD-L1 on CLL cells and PD-1 on T cells.
- To assess the therapeutic potential of targeting CD84 to overcome immune suppression in CLL.
Main Methods:
- Studied CD84-mediated cell-cell interactions in human and mouse CLL models.
- Assessed the expression of PD-L1 on CLL cells and PD-1 on T cells following CD84 engagement.
- Evaluated the impact of CD84 on T cell responses and activity in vitro and in vivo.
Main Results:
- CD84-mediated cell-cell interactions significantly upregulate PD-L1 on CLL cells and their microenvironment.
- CD84 engagement leads to increased PD-1 expression on T cells.
- This upregulation of immune checkpoints results in suppressed T cell activity and antitumor responses.
Conclusions:
- CD84 plays a critical role in regulating immune checkpoints in CLL by modulating PD-L1/PD-1 expression.
- CD84 blockade emerges as a promising therapeutic strategy to reverse tumor-induced immune suppression in CLL.
- Targeting CD84 could restore T cell function and enhance antitumor immunity in CLL patients.
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