B cells display a range of effector and memory phenotypes, antibody isotypes and affinities. We show that during malaria parasite infection, individual, activated clones commonly combine early, class-switch recombination, clonal expansion, effector fate bifurcation and somatic hypermutation to rapidly diversify in vivo.
Taylor, J. J.
et al. Humoral hmmunity: apoptosis and antigen affinity limit effector cell differentiation of a single naïve B cell.
Science 347 , 784–787 (2015). This study uses single-cell transfer to explore effector fate outcomes in naive B cells.
Horton, M. B.
et al. Lineage tracing reveals B cell antibody class switching is stochastic, cell-autonomous, and tuneable.
Immunity 55 , 1843–1855 (2022). This study shows that class-switching is stochastic and orthogonal to effector fate.
Nkumama, I. N.
et al. Breadth of Fc-mediated effector function correlates with clinical immunity following human malaria challenge.
Immunity 57 , 1215–1224 (2024). This study shows that antibody diversity correlates with anti-parasitic immunity in humans living in malaria-endemic areas.
Tellier, J. et al.
Unraveling the diversity and functions of tissue-resident plasma cells. Nat Immunol.
25 , 330–342 (2024).
Nature Immunology published a clinical update in Infectious Disease on 16 Jun 2026.
The item focuses on B cell clones combine overlapping mechanisms to diversify during infection.
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