9/ 🙌 Huge thanks to our awesome team: Anna Cole (1st author), Hannah Knochelmann (co-1st), Megan Wyatt, @megen-w.bsky.social Megen Wittling, Natalie Horvat, Aubrey Smith, Guillermo Rangel Rivera, Sound Kumaresan, Pawel Muranski, Ayana Ruffin, Jeremy Boss, & MPI Greg Lesinski. #CancerImmunotherapy

8/💡From cells to cures: @meganmw.bsky.social Megan Wyatt in our lab is developing a TIL-based therapy leveraging Th17 cells for checkpoint-refractory tumors.
Stay tuned @winshipcancer.emory.edu. Thanks to collaborations w/@lesinskilab.bsky.social and support @thevfoundation.bsky.social, NCI $ more!

7/ 🧠Why does this matter? Because T cell therapies often ignore B cells. Our data say: stop doing that.
CD4+ Th17 cells provide the help B cells need to generate potent antitumor antibodies. It’s a team sport.

6/ 🔬IL-21 production by Th17 cells is essential. Block the IL-21 receptor and the B cell response crashes (Fig 7).
Reduced germinal centers. Less plasma cells. No sustained immunity. IL-21 is the handshake between these two arms.

5/ 🧠Here’s the kicker: If we transfer serum from cured mice into naive mice, they resist metastatic challenge. Passive transfer of protection. See the lungs in Fig 8F + quant in 8G. The antibodies *work*.

4/ 🧪Mice cured with Th17 therapy have tons of class-switched, tumor-binding antibodies in serum (IgG1, IgG2a, IgG2b). Shown in Fig 8A-C. Not just any antibody — it’s tumor-specific and persistent.

3/ 💥 Depleting B cells with αCD20 or using muMT mice abolishes the effect of Th17 therapy. Survival plummets. B cells aren’t passengers here — they’re co-drivers of durable immunity.

2/ 🐭Want to keep tumors away for good?
Check out this weeks @cp-cancercell.bsky.social
You’ll need both T cells *and* B cells.
Th17 therapy fails in mice genetically deficient in B cells or in mice antibody depleted of B cells.
Bottom line:No host T/B cells, no cure!
See survival curves (Fig 3).