| Summary: | <p>The capacity of the mammalian adaptive immune response to generate immunological memory has for years been exploited by systemic vaccination strategies to protect large populations from infectious diseases. Recently, evidence has emerged for the establishment of memory B cells in tissues prone to antigen exposure. These tissue-resident B cells (Brm) may be adapted toward rapid reactivation at local sites – reducing the need for systemic intervention when fighting recurring pathogens.</p>
<p>Here, I utilize cytometry, microscopy, and transcriptomic sequencing approaches to explore the dynamics of Brm residence in the lung and their response to secondary influenza virus infections. I propose that the induction of C-X-C motif chemokine ligands 9 and 10 (CXCL9, CXCL10) early after rechallenge are important for Brm migration and accumulation at sites of infection. Innate immune cells, including alveolar macrophages, bridge the inflammatory and adaptive immune systems in part by inducing the expression of these two chemokines.</p>
<p>The recruitment of Brm at sites of viral infection is associated with the rapid appearance of antibody-producing cells in the same niche. This enables the prompt delivery of antibodies in a highly localized manner at sites of viral replication. Defining the protection granted by Brm towards recurring antigens has important implications for developing immunization strategies against respiratory viruses such as influenza.</p>
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