IL-4-Secreting secondary Tfh cells arise from memory T cells, not persisting 
Tfh cells, not persisting Tfh cells, through a B cell dependent mechanism

Fairfax, Keke C.; Everts, Bart; Amiel, Eyal; Smith, Amber M.; Schramm, Gabriele; Haas, Helmut; Randolph, Gwendalyn J.; Taylor, Justin J.; Pearce, Edward J.

doi:10.4049/jimmunol.1401225

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IL-4-Secreting secondary Tfh cells arise from memory T cells, not persisting Tfh cells, not persisting Tfh cells, through a B cell dependent mechanism

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Pearce, Edward J.
Department Immunometabolism, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

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https://www.jimmunol.org/content/194/7/2999
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Citation

Fairfax, K. C., Everts, B., Amiel, E., Smith, A. M., Schramm, G., Haas, H., et al. (2015). IL-4-Secreting secondary Tfh cells arise from memory T cells, not persisting Tfh cells, not persisting Tfh cells, through a B cell dependent mechanism. The Journal of Immunology, 194, 2999-3010. doi:10.4049/jimmunol.1401225.

Cite as: https://hdl.handle.net/21.11116/0000-0006-A4DC-9

Abstract

Humoral immunity requires crosstalk between T follicular helper (Tfh) and B cells. Nevertheless, a detailed understanding of this intercellular interaction during secondary immune responses is lacking. We examined this by focusing on the response to a soluble, unadjuvanted, pathogen-derived Ag (SEA) that induces type 2 immunity. We found that activated Tfh cells persisted for long periods within germinal centers following primary immunization. However, the magnitude of the secondary response appeared not to depend on pre-existing Tfh cells. Instead, Tfh cell populations expanded through a process dependent on memory T cells recruited into the reactive LN, and the participation of B cells. We found that during the secondary response, IL-4 was critical for the expansion of a population of plasmablasts that correlated with increased SEA-specific IgG1 titers. Additionally, following immunization with SEA (but not with an Ag that induced type 1 immunity), IL-4 and IL-21 were co-produced by individual Tfh cells, revealing a potential mechanism through which appropriate class-switching can be coupled to plasmablast proliferation to enforce type 2 immunity. Our findings demonstrate a pivotal role for IL-4 in the interplay between T and B cells during a secondary Th2 response and have significant implications for vaccine design.