Mitochondria determine response to anti-programmed cell death protein-1 (anti-PD-1) immunotherapy: An evidence-based
Hassan Akbari1, Farzad Taghizadeh-Hesary2, Moslem Bahadori3
1Department of Pathology, Shahid Beheshti University of Medical Sciences, Tehran, Iran; Traditional Medicine School, Tehran University of Medical Sciences, Tehran, Iran.
Abstract:
Immunotherapy based on programmed cell death protein-1 (PD-1) is a promising approach in oncology. However, a significant fraction of patients remain unresponsive. Therefore, it is imperative to clarify the relevant predictive factors. A decrease in cellular adenosine triphosphate (c-ATP) level can predispose to cellular dysfunction. ATP is a prerequisite for proper T cell migration and activation. Therefore, a decrease in the c-ATP level impairs T cell function and promotes cancer progression. This article gives an overview of the potential predictive factors of PD-1 blockade. Besides, it highlights the pivotal role of mitochondria in response to anti-PD-1 therapies.
Insights
Cellular adenosine triphosphate (ATP) levels predict response to cancer immunotherapy. Low ATP impairs T cell function, highlighting mitochondria
Area of Science:
- Oncology
- Immunology
- Cellular Biology
Background:
- Programmed cell death protein-1 (PD-1) immunotherapy shows promise in cancer treatment.
- A significant number of patients do not respond to PD-1 blockade therapy.
- Identifying predictive factors for PD-1 blockade response is crucial.
Purpose of the Study:
- To provide an overview of potential predictive factors for PD-1 blockade therapy.
- To emphasize the role of mitochondria in anti-PD-1 therapy response.
Main Methods:
- Literature review of predictive factors for PD-1 blockade.
- Analysis of the role of cellular adenosine triphosphate (c-ATP) in T cell function.
- Examination of mitochondrial involvement in immunotherapy response.
Main Results:
- Decreased cellular adenosine triphosphate (c-ATP) levels are linked to cellular dysfunction.
- ATP is essential for T cell migration and activation.
- Reduced c-ATP impairs T cell function and may promote cancer progression.
Conclusions:
- Cellular adenosine triphosphate (c-ATP) levels may serve as a predictive factor for PD-1 blockade efficacy.
- Mitochondrial function is critical for effective anti-PD-1 therapy.
- Further research into c-ATP and mitochondria could improve patient selection for immunotherapy.
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