About this Research Topic
Recent studies have shown the complementary immunological functions of Mucosal-associated invariant T (MAIT), T follicular helper (Tfh), and B cells in the production of IgA. Indeed, studies from our research team showed the involvement of B cell responses in modulating MAIT cell responses. For instance, B cell upregulation of HLA-G expression downregulates the inhibitory HLA-G receptor CD85j on MAIT cells, thereby resulting in their loss. On the other hand, another group demonstrated ex vivo and in vivo the effect of MAIT cells on B cell differentiation into IgA-secreting plasmablasts. More recently, using a mouse model of influenza infection, others found that MAIT cells activate dendritic cells to promote Tfh cell differentiation and antigen specific SIgA responses. Despite these observations, much remains unknown regarding the contribution of MAIT, T follicular helper, and B cells in the events that influence SIgA production in the mucosal sites. In our research Topic, we plan to review the current understanding of the functions of MAIT, Tfh, and B cells in the production of SIgA, and how these functions may be altered during homeostasis disruption.
We will welcome Original Research, Review, Mini-Review, and Perspective articles providing diverse overviews regarding, but not limited to:
• The functions of MAIT, Tfh, and B cells in the production of SIgA during homeostasis, disease, and after vaccination.
• Molecular events underlying MAIT, Tfh, and B cell crosstalk and the induction of SIgA in the mucosal tissues.
• SIgA association with vaccine protection against causative agents of enteric and respiratory diseases.
Keywords: Mucosal-associated Invariant T cells, T follicular helper cells, B cells, and Secretory Immunoglobulin A
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