Antibodies in action: the role of humoral immunity in the fight against atherosclerosis
Abstract The sequestering of oxidation-modified low-density lipoprotein by macrophages results in the accumulation of fatty deposits within the walls of arteries. Necrosis of these cells causes a release of intercellular epitopes and the activation of the adaptive immune system, which we predict lea...
| Main Authors: | , , , |
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| Format: | Article |
| Language: | English |
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BMC
2022-12-01
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| Series: | Immunity & Ageing |
| Subjects: | |
| Online Access: | https://doi.org/10.1186/s12979-022-00316-6 |
| _version_ | 1811207844871012352 |
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| author | Joshua A. Taylor Mark A. Hutchinson Patricia J. Gearhart Robert W. Maul |
| author_facet | Joshua A. Taylor Mark A. Hutchinson Patricia J. Gearhart Robert W. Maul |
| author_sort | Joshua A. Taylor |
| collection | DOAJ |
| description | Abstract The sequestering of oxidation-modified low-density lipoprotein by macrophages results in the accumulation of fatty deposits within the walls of arteries. Necrosis of these cells causes a release of intercellular epitopes and the activation of the adaptive immune system, which we predict leads to robust autoantibody production. T cells produce cytokines that act in the plaque environment and further stimulate B cell antibody production. B cells in atherosclerosis meanwhile have a mixed role based on subclass. The current model is that B-1 cells produce protective IgM antibodies in response to oxidation-specific epitopes that work to control plaque formation, while follicular B-2 cells produce class-switched antibodies (IgG, IgA, and IgE) which exacerbate the disease. Over the course of this review, we discuss further the validation of these protective antibodies while evaluating the current dogma regarding class-switched antibodies in atherosclerosis. There are several contradictory findings regarding the involvement of class-switched antibodies in the disease. We hypothesize that this is due to antigen-specificity, and not simply isotype, being important, and that a closer evaluation of these antibodies’ targets should be conducted. We propose that specific antibodies may have therapeutical potential in preventing and controlling plaque development within a clinical setting. |
| first_indexed | 2024-04-12T04:11:43Z |
| format | Article |
| id | doaj.art-2817a44b255949d38e988ab5d19ab25a |
| institution | Directory Open Access Journal |
| issn | 1742-4933 |
| language | English |
| last_indexed | 2024-04-12T04:11:43Z |
| publishDate | 2022-12-01 |
| publisher | BMC |
| record_format | Article |
| series | Immunity & Ageing |
| spelling | doaj.art-2817a44b255949d38e988ab5d19ab25a2022-12-22T03:48:29ZengBMCImmunity & Ageing1742-49332022-12-0119111610.1186/s12979-022-00316-6Antibodies in action: the role of humoral immunity in the fight against atherosclerosisJoshua A. Taylor0Mark A. Hutchinson1Patricia J. Gearhart2Robert W. Maul3Laboratory of Molecular Biology and Immunology, National Institute on Aging, NIHLaboratory of Molecular Biology and Immunology, National Institute on Aging, NIHLaboratory of Molecular Biology and Immunology, National Institute on Aging, NIHLaboratory of Molecular Biology and Immunology, National Institute on Aging, NIHAbstract The sequestering of oxidation-modified low-density lipoprotein by macrophages results in the accumulation of fatty deposits within the walls of arteries. Necrosis of these cells causes a release of intercellular epitopes and the activation of the adaptive immune system, which we predict leads to robust autoantibody production. T cells produce cytokines that act in the plaque environment and further stimulate B cell antibody production. B cells in atherosclerosis meanwhile have a mixed role based on subclass. The current model is that B-1 cells produce protective IgM antibodies in response to oxidation-specific epitopes that work to control plaque formation, while follicular B-2 cells produce class-switched antibodies (IgG, IgA, and IgE) which exacerbate the disease. Over the course of this review, we discuss further the validation of these protective antibodies while evaluating the current dogma regarding class-switched antibodies in atherosclerosis. There are several contradictory findings regarding the involvement of class-switched antibodies in the disease. We hypothesize that this is due to antigen-specificity, and not simply isotype, being important, and that a closer evaluation of these antibodies’ targets should be conducted. We propose that specific antibodies may have therapeutical potential in preventing and controlling plaque development within a clinical setting.https://doi.org/10.1186/s12979-022-00316-6AIDAtherosclerosisB cellsAntibodies |
| spellingShingle | Joshua A. Taylor Mark A. Hutchinson Patricia J. Gearhart Robert W. Maul Antibodies in action: the role of humoral immunity in the fight against atherosclerosis Immunity & Ageing AID Atherosclerosis B cells Antibodies |
| title | Antibodies in action: the role of humoral immunity in the fight against atherosclerosis |
| title_full | Antibodies in action: the role of humoral immunity in the fight against atherosclerosis |
| title_fullStr | Antibodies in action: the role of humoral immunity in the fight against atherosclerosis |
| title_full_unstemmed | Antibodies in action: the role of humoral immunity in the fight against atherosclerosis |
| title_short | Antibodies in action: the role of humoral immunity in the fight against atherosclerosis |
| title_sort | antibodies in action the role of humoral immunity in the fight against atherosclerosis |
| topic | AID Atherosclerosis B cells Antibodies |
| url | https://doi.org/10.1186/s12979-022-00316-6 |
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