Stepwise B-cell-dependent expansion of T helper clonotypes diversifies the T-cell response

Julia Merkenschlager, Mickaël J. Ploquin, Urszula Eksmond, Rakieb Andargachew, Georgina Thorborn, Andrew Filby, Marion Pepper, Brian Evavold and George Kassiotis ()
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Julia Merkenschlager: Retroviral Immunology, The Francis Crick Institute, Mill Hill Laboratory
Mickaël J. Ploquin: Retroviral Immunology, The Francis Crick Institute, Mill Hill Laboratory
Urszula Eksmond: Retroviral Immunology, The Francis Crick Institute, Mill Hill Laboratory
Rakieb Andargachew: Emory University School of Medicine
Georgina Thorborn: Retroviral Immunology, The Francis Crick Institute, Mill Hill Laboratory
Andrew Filby: Retroviral Immunology, The Francis Crick Institute, Mill Hill Laboratory
Marion Pepper: University of Washington
Brian Evavold: Emory University School of Medicine
George Kassiotis: Retroviral Immunology, The Francis Crick Institute, Mill Hill Laboratory

Nature Communications, 2016, vol. 7, issue 1, 1-13

Abstract: Abstract Antigen receptor diversity underpins adaptive immunity by providing the ground for clonal selection of lymphocytes with the appropriate antigen reactivity. Current models attribute T cell clonal selection during the immune response to T-cell receptor (TCR) affinity for either foreign or self peptides. Here, we report that clonal selection of CD4+ T cells is also extrinsically regulated by B cells. In response to viral infection, the antigen-specific TCR repertoire is progressively diversified by staggered clonotypic expansion, according to functional avidity, which correlates with self-reactivity. Clonal expansion of lower-avidity T-cell clonotypes depends on availability of MHC II-expressing B cells, in turn influenced by B-cell activation. B cells clonotypically diversify the CD4+ T-cell response also to vaccination or tumour challenge, revealing a common effect.

Date: 2016
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DOI: 10.1038/ncomms10281

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