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T Cell Activation and Clonal Selection

T Cell Activation and Clonal Selection

T cells are integral to our adaptive immune system, recognizing and effectively responding to foreign antigens. T cell activation and clonal selection are pivotal in orchestrating this immune response. This article elucidates these mechanisms, detailing the roles of cluster of differentiation (CD) markers, major histocompatibility complex (MHC) molecules, costimulatory signals, and the process of clonal selection.
Naive T cells that have not yet encountered an antigen express two primary CD...

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Tailoring In Vivo Cytotoxicity Assays to Study Immunodominance in Tumor-specific CD8+ T Cell Responses

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Systemic Cysteine Elevation Sustains T-Cell Activation to Potentiate PD-1 Blockade.

Xiaoshuang Wang, Zi Wang, Yuqi Guo

Biorxiv : the Preprint Server for Biology

|March 27, 2026

Summary

Probiotics restore sensitivity to anti-PD-1 therapy in pancreatic cancer by increasing systemic cysteine levels, which enhances T cell function and tumor control. This suggests targeting cysteine metabolism can improve cancer immunotherapy outcomes.

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Area of Science:

Immunology
Microbiome research
Cancer biology

Background:

Immune checkpoint inhibitors (ICIs) like anti-PD-1 therapy show limited efficacy in pancreatic cancer.
Resistance to anti-PD-1 therapy is a significant challenge in treating pancreatic ductal adenocarcinoma.

Purpose of the Study:

To investigate the potential of probiotics to overcome resistance to anti-PD-1 therapy in pancreatic cancer.
To elucidate the underlying mechanisms, particularly metabolic pathways, involved in restoring immunotherapy sensitivity.

Main Methods:

Utilized pancreatic cancer mouse models treated with anti-PD-1 therapy alone or in combination with probiotics.
Analyzed tumor control, microbial pathways, serum and intratumoral metabolite levels (cysteine), and T cell function.
Assessed the impact of oral cysteine supplementation on anti-PD-1 therapy efficacy.

Main Results:

Concurrent administration of probiotics with anti-PD-1 therapy led to robust tumor control in mice.
This combination therapy was associated with enriched microbial cysteine biosynthesis pathways and elevated serum cysteine levels.
Serum cysteine levels inversely correlated with tumor burden and were found to directly promote T cell survival, activation, and cytotoxicity.
Oral cysteine supplementation mimicked the immune-restorative effects of probiotics, synergizing with anti-PD-1 therapy.

Conclusions:

Probiotics can restore sensitivity to anti-PD-1 therapy in pancreatic cancer by modulating systemic cysteine availability.
Systemic cysteine is a critical factor for T cell function and a potential metabolic target to enhance cancer immunotherapy.
Targeting cysteine metabolism presents a promising strategy to improve treatment outcomes for pancreatic cancer patients resistant to ICIs.