SARS-CoV-2 vaccines and autoimmune diseases amidst the COVID-19 crisis

Abstract

Coronavirus disease 2019 (COVID-19) pandemic has become challenging even for the most durable healthcare systems. It seems that vaccination, one of the most effective public-health interventions, presents a ray of hope to end the pandemic by achieving herd immunity. In this review, we aimed to cover aspects of the current knowledge of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) vaccines and vaccine candidates in the light of autoimmune inflammatory diseases (AIIDs) and to analyze their potential in terms of safety and effectiveness in patients with AIIDs. Therefore, a focused narrative review was carried out to predict the possible implications of different types of SARS-CoV-2 vaccines which confer distinct immune mechanisms to establish immune response and protection against COVID-19: whole virus (inactivated or weakened), viral vector (replicating and non-replicating), nucleic acid (RNA, DNA), and protein-based (protein subunit, virus-like particle). Still, there is uncertainty among patients with AIIDs and clinicians about the effectiveness and safety of the new vaccines. There are a variety of approaches towards building a protective immunity against SARS-CoV-2. Only high-quality clinical trials would clarify the underlying immunological mechanisms of the newly implemented vaccines/adjuvants in patients living with AIIDs.

Keywords: Autoimmune diseases; COVID-19; COVID-19 vaccines; Messenger RNA; Rheumatic diseases; SARS-CoV-2; Vaccination.

Fig. 1

The immune processes involved in the mechanism of mRNA vaccines—activation of T helper cells (CD4+) via MHC I molecules and processed viral antigen in antigen-presenting cells in the lymph node; stimulation of T cytotoxic cells (CD8+) via MHC class II molecules and processed viral antigen and B cell by native viral antigens. In antigen-presenting cells, mRNA sense TLR7 and 8, leading to activation of down cascade and production and secretion of proinflammatory cytokines and type I interferons. Some of the mechanisms are simplified in the figure by omitting (i.e., the inflammasome, the proteasome, secondary messengers, etc.)