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The Roles of T cells in Immune Checkpoint Inhibitor-Induced Arthritis
Maike Chen1, Huili Li2, Baicheng Qu1
1Department of Orthopaedics, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China.
Immune checkpoint inhibitor (ICI) therapy, a novel anti-tumor strategy, can specifically eliminate tumors by activating the immune system and inhibiting tumor immune escape. However, ICI therapy can lead to notable negative outcomes known as immune-related adverse events (irAEs). ICI-induced arthritis, also known as ICI arthritis, stands as the prevailing form of irAEs. The purpose of this review is to highlight the crucial functions of T cells in the progression of ICI arthritis. Under the influence of different signaling molecules, T cells could gather in large numbers within the synovial membrane of joints, releasing inflammatory substances and enzymes that harm healthy tissues, ultimately causing ICI arthritis. Moreover, considering the functions of T cells in triggering ICI arthritis, this review suggests several treatments to prevent ICI arthritis, including inhibiting the overstimulation of T cells at the synovial sac of joints, enhancing the precision of ICI medications, and directing ICI drugs specifically towards tumor tissues instead of joints. Collectively, T lymphocytes play a vital role in the onset of ICI arthritis, offering a hopeful perspective on treating ICI arthritis through the specific targeting of T cells within the affected joints.
Immune checkpoint inhibitor (ICI) therapy, a novel anti-tumor strategy, can specifically eliminate tumors by activating the immune system and inhibiting tumor immune escape. However, ICI therapy can lead to notable negative outcomes known as immune-related adverse events (irAEs). ICI-induced arthritis, also known as ICI arthritis, stands as the prevailing form of irAEs. The purpose of this review is to highlight the crucial functions of T cells in the progression of ICI arthritis. Under the influence of different signaling molecules, T cells could gather in large numbers within the synovial membrane of joints, releasing inflammatory substances and enzymes that harm healthy tissues, ultimately causing ICI arthritis. Moreover, considering the functions of T cells in triggering ICI arthritis, this review suggests several treatments to prevent ICI arthritis, including inhibiting the overstimulation of T cells at the synovial sac of joints, enhancing the precision of ICI medications, and directing ICI drugs specifically towards tumor tissues instead of joints. Collectively, T lymphocytes play a vital role in the onset of ICI arthritis, offering a hopeful perspective on treating ICI arthritis through the specific targeting of T cells within the affected joints.
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