SARS-CoV-2 spike protein-specific B cell receptor (SARS-CoV-2 S-BCR)

SARS-CoV-2 spike protein-specific B cell receptors (BCRs) and related immune recognition molecules, such as T cell receptors (TCRs), are the primary sensors of the adaptive immune system that identify the SARS-CoV-2 virus. BCRs are membrane-bound immunoglobulins on B lymphocytes that bind directly to the viral spike (S) protein, particularly the receptor-binding domain (RBD), initiating signaling cascades that lead to B cell activation and the production of neutralizing antibodies (Gaebler et al., 2021; Pinto et al., 2020). These antibodies provide protection by preventing the virus from attaching to the host's ACE2 receptor. Concurrently, S-specific TCRs recognize processed spike peptides presented by Major Histocompatibility Complex (MHC) molecules, coordinating the cellular immune response and the killing of infected cells (Sette & Crotty, 2021). In the context of drug development, these recognition molecules are the fundamental physiological targets of COVID-19 vaccines, which aim to expand the repertoire of S-specific B and T cells to establish long-term immunity (Sakharkar et al., 2021). Furthermore, the characterization and cloning of high-affinity BCRs from convalescent patients have directly enabled the engineering of therapeutic monoclonal antibodies used for passive immunization (Robbiani et al., 2020).

Other names

Anti-SARS-CoV-2 spike BCRSpike-reactive B cell receptorSARS-CoV-2 S-specific BCRCOVID-19 spike-specific BCRSARS-CoV-2 spike-specific T cell receptorSARS-CoV-2 spike-specific immune recognition molecules

Vaccines deliver the SARS-CoV-2 spike protein or its genetic code to stimulate these receptors, triggering B cell differentiation into antibody-secreting plasma cells and long-lived memory B cells (Turner et al., 2021; Gaebler et al., 2021). Therapeutic monoclonal antibodies are engineered versions of the high-affinity binding domains of these receptors, designed to neutralize the virus by blocking its interaction with the host ACE2 receptor (Robbiani et al., 2020).