The relationship between immunodominance, DM editing, and the kinetic stability of MHC class II:peptide complexes
Immunodominance refers to the restricted antigen specificity of T cells detected in the immune response after immunization with complex antigens. Despite the presence of many potential peptide epitopes within these immunogens, the elicited T‐cell response apparently focuses on a very limited number...
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| Published in | Immunological reviews Vol. 207; no. 1; pp. 261 - 278 |
|---|---|
| Main Authors | , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Oxford, UK; Malden, USA
Munksgaard International Publishers
01.10.2005
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| Subjects | |
| Online Access | Get full text |
| ISSN | 0105-2896 1600-065X |
| DOI | 10.1111/j.0105-2896.2005.00307.x |
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| Abstract | Immunodominance refers to the restricted antigen specificity of T cells detected in the immune response after immunization with complex antigens. Despite the presence of many potential peptide epitopes within these immunogens, the elicited T‐cell response apparently focuses on a very limited number of peptides. Over the last two decades, a number of distinct explanations have been put forth to explain this very restricted specificity of T cells, many of which suggest that endosomal antigen processing restricts the array of peptides available to recruit CD4 T cells. In this review, we present evidence from our laboratory that suggest that immunodominance in CD4 T‐cell responses is primarily due to an intrinsic property of the peptide:class II complexes. The intrinsic kinetic stability of peptide:class II complexes controls DM editing within the antigen‐presenting cells and thus the initial epitope density on priming dendritic cells. Additionally, we hypothesize that peptides that possess high kinetic stability interactions with class II molecules display persistence at the cell surface over time and will more efficiently promote T‐cell signaling and differentiation than competing, lower‐stability peptides contained within the antigen. We discuss this model in the context of the existing data in the field of immunodominance. |
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| AbstractList | Immunodominance refers to the restricted antigen specificity of T cells detected in the immune response after immunization with complex antigens. Despite the presence of many potential peptide epitopes within these immunogens, the elicited T‐cell response apparently focuses on a very limited number of peptides. Over the last two decades, a number of distinct explanations have been put forth to explain this very restricted specificity of T cells, many of which suggest that endosomal antigen processing restricts the array of peptides available to recruit CD4 T cells. In this review, we present evidence from our laboratory that suggest that immunodominance in CD4 T‐cell responses is primarily due to an intrinsic property of the peptide:class II complexes. The intrinsic kinetic stability of peptide:class II complexes controls DM editing within the antigen‐presenting cells and thus the initial epitope density on priming dendritic cells. Additionally, we hypothesize that peptides that possess high kinetic stability interactions with class II molecules display persistence at the cell surface over time and will more efficiently promote T‐cell signaling and differentiation than competing, lower‐stability peptides contained within the antigen. We discuss this model in the context of the existing data in the field of immunodominance. Immunodominance refers to the restricted antigen specificity of T cells detected in the immune response after immunization with complex antigens. Despite the presence of many potential peptide epitopes within these immunogens, the elicited T-cell response apparently focuses on a very limited number of peptides. Over the last two decades, a number of distinct explanations have been put forth to explain this very restricted specificity of T cells, many of which suggest that endosomal antigen processing restricts the array of peptides available to recruit CD4 T cells. In this review, we present evidence from our laboratory that suggest that immunodominance in CD4 T-cell responses is primarily due to an intrinsic property of the peptide:class II complexes. The intrinsic kinetic stability of peptide:class II complexes controls DM editing within the antigen-presenting cells and thus the initial epitope density on priming dendritic cells. Additionally, we hypothesize that peptides that possess high kinetic stability interactions with class II molecules display persistence at the cell surface over time and will more efficiently promote T-cell signaling and differentiation than competing, lower-stability peptides contained within the antigen. We discuss this model in the context of the existing data in the field of immunodominance.Immunodominance refers to the restricted antigen specificity of T cells detected in the immune response after immunization with complex antigens. Despite the presence of many potential peptide epitopes within these immunogens, the elicited T-cell response apparently focuses on a very limited number of peptides. Over the last two decades, a number of distinct explanations have been put forth to explain this very restricted specificity of T cells, many of which suggest that endosomal antigen processing restricts the array of peptides available to recruit CD4 T cells. In this review, we present evidence from our laboratory that suggest that immunodominance in CD4 T-cell responses is primarily due to an intrinsic property of the peptide:class II complexes. The intrinsic kinetic stability of peptide:class II complexes controls DM editing within the antigen-presenting cells and thus the initial epitope density on priming dendritic cells. Additionally, we hypothesize that peptides that possess high kinetic stability interactions with class II molecules display persistence at the cell surface over time and will more efficiently promote T-cell signaling and differentiation than competing, lower-stability peptides contained within the antigen. We discuss this model in the context of the existing data in the field of immunodominance. |
| Author | Richards, Katherine A. Weaver, J. M. Chaves, Francisco A. Lazarski, Christopher A. Jenks, Scott A. Sant, Andrea J. Menges, Paula |
| Author_xml | – sequence: 1 givenname: Andrea J. surname: Sant fullname: Sant, Andrea J. email: andrea_sant@urmc.rochester.edu organization: David H. Smith Center for Vaccine Biology and Immunology, Aab Institute and Department of Microbiology and Immunology, University of Rochester, Rochester, NY, USA – sequence: 2 givenname: Francisco A. surname: Chaves fullname: Chaves, Francisco A. organization: David H. Smith Center for Vaccine Biology and Immunology, Aab Institute and Department of Microbiology and Immunology, University of Rochester, Rochester, NY, USA – sequence: 3 givenname: Scott A. surname: Jenks fullname: Jenks, Scott A. organization: David H. Smith Center for Vaccine Biology and Immunology, Aab Institute and Department of Microbiology and Immunology, University of Rochester, Rochester, NY, USA – sequence: 4 givenname: Katherine A. surname: Richards fullname: Richards, Katherine A. organization: David H. Smith Center for Vaccine Biology and Immunology, Aab Institute and Department of Microbiology and Immunology, University of Rochester, Rochester, NY, USA – sequence: 5 givenname: Paula surname: Menges fullname: Menges, Paula organization: David H. Smith Center for Vaccine Biology and Immunology, Aab Institute and Department of Microbiology and Immunology, University of Rochester, Rochester, NY, USA – sequence: 6 givenname: J. M. surname: Weaver fullname: Weaver, J. M. organization: David H. Smith Center for Vaccine Biology and Immunology, Aab Institute and Department of Microbiology and Immunology, University of Rochester, Rochester, NY, USA – sequence: 7 givenname: Christopher A. surname: Lazarski fullname: Lazarski, Christopher A. organization: David H. Smith Center for Vaccine Biology and Immunology, Aab Institute and Department of Microbiology and Immunology, University of Rochester, Rochester, NY, USA |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/16181342$$D View this record in MEDLINE/PubMed |
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| SubjectTerms | Animals Antigen Presentation - immunology Antigen-Presenting Cells - immunology CD4-Positive T-Lymphocytes HLA-D Antigens - immunology Humans Immunodominant Epitopes Models, Immunological Peptides - immunology Peptides - metabolism |
| Title | The relationship between immunodominance, DM editing, and the kinetic stability of MHC class II:peptide complexes |
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