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Related Concept Videos

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Immunotherapy is a treatment that boosts or manipulates the immune system to fight diseases, including cancer. For instance, by stimulating an immune response through vaccinations against viruses that cause cancers, like hepatitis B virus and human papillomavirus, these diseases can be prevented. Nonetheless, some cancer cells can avoid the immune system due to their rapid mutation and division. The immune response to many cancers involves three phases: elimination, equilibrium, and escape.
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An antigen is any substance the immune system identifies as foreign and potentially harmful to the body, prompting an immune response. Antigens have two functional properties: immunogenicity and reactivity. Immunogenicity is the ability of an antigen to stimulate a specific immune response. At the same time, reactivity describes the antigen's ability to react with the cells and antibodies produced in response to it.
Complete Antigens
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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.
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The Tumor Microenvironment02:17

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Every normal cell or tissue is embedded in a complex local environment called stroma, consisting of different cell types, a basal membrane, and blood vessels. As normal cells mutate and develop into cancer cells, their local environment also changes to allow cancer progression. The tumor microenvironment (TME) consists of a complex cellular matrix of stromal cells and the developing tumor. The cross-talk between cancer cells and surrounding stromal cells is critical to disrupt normal tissue...
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Antigen receptors are essential components of the immune system crucial in defending the body against foreign invaders. These receptors are present on the surface of B and T cells, enabling them to recognize antigens and mount an appropriate immune response.
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Cytotoxic T cells are a vital component of the immune system. They have the remarkable ability to identify and target antigens on infected or abnormal cells. These antigens often originate from intracellular pathogens such as viruses or abnormal proteins cancer cells produce.
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Using X-ray Crystallography, Biophysics, and Functional Assays to Determine the Mechanisms Governing T-cell Receptor Recognition of Cancer Antigens
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Structural changes from wild-type define tumor-rejecting neoantigens.

Anngela C Adams1,2, Anne M Macy1,2, Elizabeth S Borden1,2

  • 1Department of Dermatology, The University of Arizona College of Medicine Phoenix, Phoenix, Arizona, USA.

Journal for Immunotherapy of Cancer
|October 22, 2025
PubMed
Summary
This summary is machine-generated.

Predicting neoantigens for cancer vaccines is challenging. This study identified structural changes in neoantigens that improve T cell recognition, aiding the development of personalized neoantigen vaccines for cutaneous squamous cell carcinoma.

Keywords:
Major histocompatibility complex - MHCSkin CancerT cell

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Area of Science:

  • Oncology
  • Immunology
  • Cancer Genomics

Background:

  • Predicting neoantigens that trigger tumor rejection is crucial for effective cancer vaccines, particularly in high-mutation cancers like cutaneous squamous cell carcinoma (cSCC).
  • Current neoantigen prioritization methods often fail to elicit robust T cell responses, highlighting the need for improved predictive criteria.

Purpose of the Study:

  • To develop improved criteria for predicting tumor-rejecting neoantigens.
  • To establish a clinically relevant mouse model for studying neoantigen vaccines in cSCC.
  • To identify specific structural features of neoantigens that enhance T cell recognition and mediate tumor rejection.

Main Methods:

  • A mouse model of ultraviolet light-induced cSCC was generated and compared to human cSCC mutational data.
  • Neoantigens were prioritized in the mouse model, and tumor-rejecting neoantigens were identified using ELISpot and in vivo vaccination assays.
  • Major histocompatibility complex (MHC) class I binding and structural characteristics of neoantigens were analyzed using computational modeling.

Main Results:

  • A mouse model recapitulating human cSCC mutational signatures and driver mutations was established.
  • Two MHC class I neoantigens were identified that mediated cSCC growth constraint.
  • Tumor-rejecting neoantigens exhibited altered MHC binding or increased solvent accessibility of mutated residues, distinguishing them from non-immunogenic neoantigens.

Conclusions:

  • The limited sharing of mutations in cSCC supports the need for personalized neoantigen vaccines.
  • A validated mouse model and two defined tumor-rejecting neoantigens are provided for future research.
  • Structural features influencing T cell receptor accessibility are key determinants of neoantigen immunogenicity and can improve neoantigen selection for personalized vaccines.