Cellular and Humoral Immune Responses to SARS-CoV-2 Vaccination in Inflammatory Bowel Disease Patients

Abstract

Background and Aims Knowledge on the immunogenicity of anti-SARS-CoV-2 vaccines in inflammatory bowel disease (IBD) patients is limited. Therefore, SARS-CoV-2-specific T-cell response and antibodies were analyzed in 60 IBD vaccine recipients and 30 controls. Methods SARS-CoV-2 IgG antibodies against the viral spike protein were measured at baseline and at 8 and 26 weeks after the second vaccine dose. SARS-CoV-2 IgG antibodies against the nucleocapsid antigens were measured at week 26. SARS-CoV-2 interferon-gamma released assay (IGRA) was performed in all vaccinees at week 26. Results At weeks 0 and 8, no differences were found in anti-spike antibodies between cohorts. At week 26, the decrease in antibody levels was more significant in the IBD cohort compared to the healthy cohort, and anti-nucleocapsid antibodies were not detected in either group. At week 26, 16 of 90 (18 %) vaccinated individuals had a negative IGRA test result, 7 of 90 (8 %) were borderline, and 67 (74 %) had a positive IGRA result; 22 of the 23 individuals with negative or borderline IGRA results belonged to the IBD cohort. However,the overall functional ability of T-lymphocytes to produce interferon-gamma after the unspecific mitogen stimulation was lower in IBD patients. In vaccinees with low or borderline IGRA, treatment with TNF-alpha inhibitors was the most frequent. In individuals with a significant drop in anti-spike antibody levels, plasmatic interferon-gamma concentrations after the specific SARS-CoV-2 stimulation were also insufficient. Conclusions Simple humoral and cellular post-vaccination monitoring is advisable in IBD patients so that repeated vaccine doses may be scheduled.

Higher Cell-Mediated Immune Responses in Patients With Inflammatory Bowel Disease on Anti-TNF Therapy After COVID-19 Vaccination

“…Among 60 patients with IBD from the Czech Republic, the CMIR, measured 26 weeks after the second dose with the IFN- γ–released assay response, was absent in 18% of patients, who were more likely to be on anti-TNF therapy. 29 Similar to the CLARITY IBD study, the study found an agreement between CMIR and antibody concentrations. In contrast, 2 other studies observed that most patients with IBD had a measurable CMIR.…”

“… 31 Whether an inadequate CMIR also warrants an additional dose to the primary series for most patients with IBD is unknown. 12 , 29 After primary immunization, boosters should be administered as recommended for the general population. In fact, studies have shown robust antibody responses after 3 doses of COVID-19 vaccines in patients with IBD, with antibody concentrations being higher after the third dose than after the 2-dose primary series.…”

Systemic and T cell‐associated responses to SARS‐CoV‐2 immunisation in gut inflammation (STAR SIGN study): effects of biologics on vaccination efficacy of the third dose of mRNA vaccines against SARS‐CoV‐2

“…Recently, another study reported that after two doses, a higher proportion of IBD patients lacked adequate SARS‐CoV‐2‐directed IFN‐γ secretion, when compared to healthy controls. 52 Importantly, this is the first study to demonstrate impaired functional T cell immunity in anti‐TNF‐treated IBD patients after three doses of SARS‐CoV‐2 mRNA vaccines. Interestingly, no correlation between humoral and T cell immunity was detected in this study (Figure 7A,B ).…”

COVID-19 Vaccine Booster Shot Preserves T Cells Immune Response Based on Interferon-Gamma Release Assay in Inflammatory Bowel Disease (IBD) Patients on Anti-TNFα Treatment

“…Despite T lymphocytes being the key orchestrators of adaptive immune responses and conferring long-lasting protection through immune memory [ 29 , 30 ], their role in this setting is not well defined. In particular, the effects of immune-modifying treatments on cellular immune response in IBD patients following COVID-19 vaccination were poor and often controversial [ 31 , 32 , 33 , 34 , 35 ]. The imbalance of anti-SARS-CoV-2 vaccine effectiveness among two branches of adaptive immune responses could be due to the complexity of gold standard assays, which are unsuitable for clinical laboratory application.…”