The inactivated influenza vaccine (IIV) is known to activate B cells and T follicular helper (TFH) cells and, via these, leads to antibody secretion and serum antibody titres. However, the cellular events that precede this generation of protective immunity are still not fully understood. The authors examined B and T cell immune responses to IIV in 35 healthy adults by using recombinant haemagglutinin (rHA) probes to analyse the quantity, phenotype and isotype of influenza-specific B cells against A/California09/H1N1, A/Switzerland/H3N2 and B/Phuket. The authors found that vaccination induces a three-pronged B cell response comprising a transient CXCR5-CXCR3+ antibody-secreting B cell population, CD21hiCD27+ memory B cells and CD21loCD27+ B cells. The activation of circulating TFH cells correlated with the development of both CD21lo and CD21hi memory B cells. However, the authors also found that preexisting antibodies can limit increases in serum antibody titres. IIV had no marked effect on CD8+, mucosal-associated invariant T, γδ T and natural killer cell activation. In addition, vaccine-induced B cells were not maintained in peripheral blood 1 year following vaccination. When examining rHA-specific B cells across seven human tissue compartments, the authors found that influenza-specific memory (CD21hiCD27+) B cells primarily reside within secondary lymphoid tissues and the lungs. Therefore the design of universal vaccines needs to consider these circulating TFH cells, preexisting serological memory and tissue compartmentalisation in order to achieve effective B cell immunity, as well as to improve targeting of cellular T cell immunity.
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