Amin Alirezaylavasani, Ingrid Marie Egner, Børresdatter Dahl, Adity Chopra, Taissa de Matos Kasahara, Guro Løvik Goll, Jørgen Jahnsen, Gunnveig Grødeland, John Torgils Vaage, Fridtjof Lund-Johansen, Jan Cato Holter, Bente Halvorsen, Kristin Kaasen Jørgensen, Ludvig A Munthe, Hassen Kared
{"title":"Deficient SARS-CoV-2 hybrid immunity during inflammatory bowel disease.","authors":"Amin Alirezaylavasani, Ingrid Marie Egner, Børresdatter Dahl, Adity Chopra, Taissa de Matos Kasahara, Guro Løvik Goll, Jørgen Jahnsen, Gunnveig Grødeland, John Torgils Vaage, Fridtjof Lund-Johansen, Jan Cato Holter, Bente Halvorsen, Kristin Kaasen Jørgensen, Ludvig A Munthe, Hassen Kared","doi":"10.1016/j.clim.2024.110404","DOIUrl":null,"url":null,"abstract":"<p><p>Patients with Inflammatory Bowel Disease (IBD) undergoing immunosuppressive therapies face heightened susceptibility to severe COVID-19. An in-depth understanding of systemic inflammation and cellular immune responses after SARS-CoV-2 vaccination and breakthrough infections (BTI) is required for optimizing vaccine strategies in this population. While the prevalence of high serological responders post- third COVID-19 vaccine dose was lower, and the antibody waning was higher in IBD patients than in healthy donors (HD), IBD patients showed an increase in anti-RBD Wild Type IgG levels and cross-reactive Spike -specific memory B cells following BTI. However, there was no significant enhancement in cellular immune responses against anti-SARS-CoV-2 post-BTI, with responses instead characterized by activation of SARS-CoV-2 specific and also bystander CD8 T cells. These results suggest a complex interaction between chronic inflammation in IBD and the generation of new immune responses, highlighting the need for tailored vaccine regimens and anti-inflammatory therapies to boost cellular immunity against SARS-CoV-2.</p>","PeriodicalId":10392,"journal":{"name":"Clinical immunology","volume":" ","pages":"110404"},"PeriodicalIF":4.5000,"publicationDate":"2024-12-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Clinical immunology","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1016/j.clim.2024.110404","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"IMMUNOLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
Patients with Inflammatory Bowel Disease (IBD) undergoing immunosuppressive therapies face heightened susceptibility to severe COVID-19. An in-depth understanding of systemic inflammation and cellular immune responses after SARS-CoV-2 vaccination and breakthrough infections (BTI) is required for optimizing vaccine strategies in this population. While the prevalence of high serological responders post- third COVID-19 vaccine dose was lower, and the antibody waning was higher in IBD patients than in healthy donors (HD), IBD patients showed an increase in anti-RBD Wild Type IgG levels and cross-reactive Spike -specific memory B cells following BTI. However, there was no significant enhancement in cellular immune responses against anti-SARS-CoV-2 post-BTI, with responses instead characterized by activation of SARS-CoV-2 specific and also bystander CD8 T cells. These results suggest a complex interaction between chronic inflammation in IBD and the generation of new immune responses, highlighting the need for tailored vaccine regimens and anti-inflammatory therapies to boost cellular immunity against SARS-CoV-2.
期刊介绍:
Clinical Immunology publishes original research delving into the molecular and cellular foundations of immunological diseases. Additionally, the journal includes reviews covering timely subjects in basic immunology, along with case reports and letters to the editor.