Article ; Online: SARS-CoV-2 Vaccine-Elicited Immunity after B Cell Depletion in Multiple Sclerosis.
ImmunoHorizons
2024 Volume 8, Issue 3, Page(s) 254–268
Abstract: The impact of B cell deficiency on the humoral and cellular responses to SARS-CoV2 mRNA vaccination remains a challenging and significant clinical management question. We evaluated vaccine-elicited serological and cellular responses in 1) healthy ... ...
| Abstract | The impact of B cell deficiency on the humoral and cellular responses to SARS-CoV2 mRNA vaccination remains a challenging and significant clinical management question. We evaluated vaccine-elicited serological and cellular responses in 1) healthy individuals who were pre-exposed to SARS-CoV-2 (n = 21), 2) healthy individuals who received a homologous booster (mRNA, n = 19; or Novavax, n = 19), and 3) persons with multiple sclerosis on B cell depletion therapy (MS-αCD20) receiving mRNA homologous boosting (n = 36). Pre-exposure increased humoral and CD4 T cellular responses in immunocompetent individuals. Novavax homologous boosting induced a significantly more robust serological response than mRNA boosting. MS-α CD20 had an intact IgA mucosal response and an enhanced CD8 T cell response to mRNA boosting compared with immunocompetent individuals. This enhanced cellular response was characterized by the expansion of only effector, not memory, T cells. The enhancement of CD8 T cells in the setting of B cell depletion suggests a regulatory mechanism between B and CD8 T cell vaccine responses. |
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| MeSH term(s) | Humans ; COVID-19 Vaccines ; Multiple Sclerosis ; RNA, Viral ; COVID-19/prevention & control ; SARS-CoV-2 ; RNA, Messenger |
| Chemical Substances | COVID-19 Vaccines ; RNA, Viral ; RNA, Messenger |
| Language | English |
| Publishing date | 2024-04-05 |
| Publishing country | United States |
| Document type | Journal Article |
| ISSN | 2573-7732 |
| ISSN (online) | 2573-7732 |
| DOI | 10.4049/immunohorizons.2300108 |
| Database | MEDical Literature Analysis and Retrieval System OnLINE |
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