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Related Experiment Video

Updated: Jul 26, 2025

Analysis of Human T Cell Activity in an Allogeneic Co-Culture Setting of Pre-Treated Tumor Cells

Analysis of Human T Cell Activity in an Allogeneic Co-Culture Setting of Pre-Treated Tumor Cells

Published on: March 7, 2025

B-cell-specific checkpoint molecules that regulate anti-tumour immunity.

Lloyd Bod^1,2,3,4, Yoon-Chul Kye^1,2,3, Jingwen Shi^1,2,5

¹Evergrande Center for Immunologic Diseases, Harvard Medical School and Brigham and Women's Hospital, Boston, MA, USA.

|June 21, 2023

Summary

Researchers discovered a specific B cell subset that expands during melanoma growth. Targeting this TIM-1 expressing B cell subset significantly inhibited tumor growth and boosted anti-tumor immunity.

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Area of Science:

Immunology
Oncology
Cell Biology

Background:

The role of B cells in anti-tumor immunity is not fully understood.
Current immunotherapies primarily target T cells and natural killer cells.

Purpose of the Study:

To investigate the role of B cells in anti-tumor immunity during melanoma progression.
To identify specific B cell subsets involved in tumor growth and immune response.

Main Methods:

High-throughput flow cytometry
Bulk and single-cell RNA-sequencing
B-cell-receptor-sequencing
Analysis of B cells during B16F10 melanoma growth in mice

Main Results:

Identified an expanding subset of B cells in the draining lymph node expressing T cell immunoglobulin and mucin domain 1 (TIM-1).
This subset also expressed co-inhibitory molecules like PD-1, TIM-3, TIGIT, and LAG-3.
Selective deletion of TIM-1 (Havcr1) in B cells inhibited tumor growth and enhanced effector T cell responses.
Loss of TIM-1 boosted type 1 interferon response, increasing B cell activation, antigen presentation, and co-stimulation, leading to greater tumor-specific effector T cell expansion.

Conclusions:

TIM-1 expressing B cells play a crucial role in regulating anti-tumor immunity.
Targeting TIM-1 on B cells can enhance adaptive immunity and inhibit tumor growth.
This highlights a novel strategy for cancer immunotherapy by engaging B cells.