B-cell receptor specific for influenza A hemagglutinin epitopes (HA-specific BCR)

B-cell receptors (BCRs) specific for influenza A hemagglutinin (HA) epitopes are specialized membrane-bound immunoglobulins that serve as the primary sensors for the adaptive immune response against influenza viruses [Nature, 2013]. These receptors recognize and bind to specific antigenic sites on the HA protein, which is the major surface glycoprotein of the virus responsible for cell attachment and entry [Acta Naturae, 2016]. Upon antigen binding, the BCR initiates signaling pathways that drive B-cell activation, proliferation, and the eventual secretion of neutralizing antibodies that provide protection against infection [JCI Insight, 2019]. Research has demonstrated that the influenza virus can also utilize these specific BCRs to infect and eliminate the very B cells intended to neutralize it, particularly in the respiratory tract, thereby hindering the early immune response [Nature, 2013]. Therapeutic strategies, such as the development of universal influenza vaccines, aim to modulate the BCR repertoire by focusing the immune response on conserved epitopes, such as those found in the HA stalk region [Frontiers in Immunology, 2021]. Monitoring the frequency and functional state of HA-specific B cells is a critical biomarker for evaluating vaccine efficacy and the breadth of immunity across different influenza strains [JCI, 2023].

Other names

Hemagglutinin-specific B-cell receptorHA-specific BCRAnti-HA B-cell receptorInfluenza A hemagglutinin-specific B-cell receptor

Vaccines containing influenza hemagglutinin (HA) antigens bind to and cross-link HA-specific B-cell receptors (BCRs), triggering intracellular signaling cascades that lead to B-cell activation, clonal expansion, and differentiation into memory B cells and antibody-secreting plasma cells [NIH, 2024; JCI Insight, 2019]. Additionally, the influenza A virus can exploit these specific BCRs as an alternative entry receptor to infect and kill the B cells, a process that can delay the host's protective immune response [Nature, 2013].