Deficient SARS-CoV-2 hybrid immunity during inflammatory bowel disease

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

Deficient SARS-CoV-2 hybrid immunity during inflammatory bowel disease

Clin Immunol. 2024 Dec 5:271:110404. doi: 10.1016/j.clim.2024.110404. Online ahead of print.

Authors

Amin Alirezaylavasani¹, Ingrid Marie Egner¹, Børresdatter Dahl², Adity Chopra³, Taissa de Matos Kasahara⁴, Guro Løvik Goll⁵, Jørgen Jahnsen⁶, Gunnveig Grødeland⁷, John Torgils Vaage⁷, Fridtjof Lund-Johansen³, Jan Cato Holter⁸, Bente Halvorsen⁹, Kristin Kaasen Jørgensen¹⁰, Ludvig A Munthe¹¹, Hassen Kared¹²

Affiliations

¹ Department of Immunology, Oslo University Hospital, Oslo, Norway; KG Jebsen Centre for B cell Malignancies, Institute of Clinical Medicine, University of Oslo, Norway; Precision Immunotherapy Alliance, University of Oslo, Oslo, Norway.
² Research Institute of Internal Medicine, Oslo University Hospital, Oslo, Norway.
³ Department of Immunology, Oslo University Hospital, Oslo, Norway; Precision Immunotherapy Alliance, University of Oslo, Oslo, Norway; ImmunoLingo Convergence Center, University of Oslo, Oslo, Norway.
⁴ Department of Immunology, Oslo University Hospital, Oslo, Norway.
⁵ Division of Rheumatology and Research, Diakonhjemmet Hospital, Oslo, Norway; Institute of Health and Society, Faculty of Medicine, University of Oslo, Oslo, Norway.
⁶ Department of Gastroenterology, Akershus University Hospital, Lørenskog, Norway; Institute of Clinical Medicine, University of Oslo, Oslo, Norway.
⁷ Department of Immunology, Oslo University Hospital, Oslo, Norway; Institute of Clinical Medicine, University of Oslo, Oslo, Norway.
⁸ Institute of Clinical Medicine, University of Oslo, Oslo, Norway.; Department of Microbiology, Oslo University Hospital, Oslo, Norway.
⁹ Research Institute of Internal Medicine, Oslo University Hospital, Oslo, Norway; Institute of Clinical Medicine, University of Oslo, Oslo, Norway.
¹⁰ Department of Gastroenterology, Akershus University Hospital, Lørenskog, Norway.
¹¹ Department of Immunology, Oslo University Hospital, Oslo, Norway; KG Jebsen Centre for B cell Malignancies, Institute of Clinical Medicine, University of Oslo, Norway; Precision Immunotherapy Alliance, University of Oslo, Oslo, Norway. Electronic address: [email protected].
¹² Department of Immunology, Oslo University Hospital, Oslo, Norway; KG Jebsen Centre for B cell Malignancies, Institute of Clinical Medicine, University of Oslo, Norway; Precision Immunotherapy Alliance, University of Oslo, Oslo, Norway. Electronic address: [email protected].

PMID: 39645159
DOI: 10.1016/j.clim.2024.110404

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.

Keywords: Activation; Antibody waning; Hybrid immunity; IBD; Inflammation; TNF inhibitors.