There is still much to learn! Is there a role for IL-12 in severe infection? Is there interplay with innate immunity? How is this response negatively regulated? How can it be shut off when it causes too much damage? Does IL-12 influence B cell memory?

We are excited about new questions raised by these studies, discussed in Inaki Sanz’s N&V https://t.co/3wnYcIKBTq. EF responses are prominent in autoimmune diseases including SLE, and infection-associated immunopathogenesis including COVID-19.

IL-12 and IFNg act together to induce a unique gene regulatory network that promotes the EF response. We speculate that this shift helps focus immune resources on antibody and TH1 production to fight infection, saving GC for after infection is resolved.

In our @NatImmunol paper, we found that IL-12 shifts the B cell response to extrafollicular (EF) plasmablast production, suppressing germinal centers (GC). IL-12 gets the ball rolling by inducing IFNg production from B cells.

Check out the N&V in @NatImmunol by Inaki Sanz about our recent paper on how B cell intrinsic IL-12 promotes EF and suppresses GC responses via an autocrine positive feedback loop with IFNg. https://t.co/3wnYcIKBTq

Fauna Smith, Nicole Baumgarth @nbaumgarth and colleagues @ucdavis identify important previously unknown characteristics of the natural IgM pool. https://t.co/2jlbdW15IG #InfectiousDisease #HostDefense