Autoimmune Rheumatic Disease Does Not Influence Immune Response Against COVID-19


Research indicates that patients with autoimmune rheumatic diseases (AIRD) did not differ from the general population in terms of protective antibody responses against COVID-19.

Despite suspicions that patients with autoimmune rheumatic diseases (AIRD) may have worse immune responses against COVID-19, research indicates that this patient population did not differ from the general population in terms of protective antibody responses, according to a study published in Springer.1

Protective antibodies support a robust immune system response. Most notably, spike protein (S) and nucleocapsid protein (N) have been shown to protect from reinfection and symptomatic disease. Alternatively, non-neutralizing antibodies may be able to predict more severe reactions.

“The present study shows that patients with AIRD, despite their underlying immune defects and current immunosuppression, mount adequate antibody responses similar to those of healthy controls,” explained investigators. “This is very reassuring considering that there was a widespread fear that patients on immunosuppressants may not mount an adequate immune response and may be vulnerable to reinfection with COVID-19.”

A sample of 50 patients with AIRD (mean age 45.9 ± 13; 76% females) who developed COVID-19 were matched with 50 controls (mean age 45.9 ± 13; 76% females) with COVID-19. Investigators matched for age, sex, and COVID-19 severity, which was determined using the National Institutes of Health’s Coronavirus Disease (COVID-19) Treatment Guidelines. In the AIRD cohort, patients were included if they were on disease-modifying anti-rheumatic drugs (DMARDs) or immunosuppressants for a minimum of 3 months and had reverse transcription polymerase chain reaction (RT-PCR) or rapid antigen positivity for SARS-CoV-2. The most common AIRDs were rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), and spondyloarthritis. Comorbidities were balanced between the 2 groups.

Approximately 30 days after the RT-PCR test, serum was collected and kept at -80°. Immunoglobulin G (IgG) antibodies were assessed using electrochemiluminescence immunoassay (ECLIA).

Anti-N IgG was positive in 80% (40) of patients with AIRD and 90% (45) of controls and anti-S IgG was positive in 82% (41) patients with AIRD and 86% (43) of COVID-19 cases in the control cohort. Neutralizing antibodies were negative in 14% (7) of patients in the AIRD cohort and 10% (5) in the control group. Patients with AIRD displayed adequate protective antibody responses to COVID-19 at 30 days post-infection. Female participants in both groups had the highest proportion of the protective antibody.

Investigators also hypothesized that if patients had an adequate response to natural infection while on immunosuppressants, they would most likely have a similar response to the COVID-19 vaccination.

The study was minorly limited by only including antibody responses, a limited sample size, and the mixture of AIRD patients on a variety of drugs. However, the one-to-one control group removes many confounders, such as age, sex, and disease severity. Further, the antibody responses studied were not inferior to the control group and anti-N and anti-S antibodies in fact protect from severe COVID-19. While sample size was limited, it was the largest cohort to date in which investigators determined the correlation between rheumatic disease and specific protective antibodies.

“Though patients were heterogeneous with different diagnoses, what was common was that all patients had a systemic inflammatory disease and were on some form of immunosuppression,” concluded investigators. “Thus, this data has important implication for rheumatologists in a real-life scenario to provide them with the confidence that such patients still have adequate humoral immune responses to SARS-CoV-2 despite the immunosuppressant drugs.”


Shenoy P, Ahmed S, Shanoj KC, et al. Antibody responses after documented COVID-19 disease in patients with autoimmune rheumatic disease [published online ahead of print, 2021 Jun 22]. Clin Rheumatol. 2021;1-6. doi:10.1007/s10067-021-05801-9

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