B cell depleting therapies effectively treat #MultipleSclerosis, yet our understanding of why remains limited. How does loss of B cells impact the immune system in MS? See our multicohort study employing high-dimensional single-cell immunophenotyping:

Check out our most recent work resolving a longstanding controversy: which phagocyte subset drives oxidative damage in neuroinflammation? Thank you for the support and the mentoring @SarahMundt5. Thanks to Mundtlab, @BecherLab and all coauthors! Link:

Twin study dissects CXCR3+ memory B cells as non-heritable feature in multiple sclerosis - read the recent study between @FlorianIngelfi1, @BecherLab & the van Luijn lab in @MedCellPress #AAI2024

What if we could measure time in single cell RNA seq data? Check out our most recent study spearheaded by the fantastic @D_Birschenkaum and our time traveler crew @CuriousKX, @kathleenabadie, Yonathan, @AssafWeiner from the @IdoAmitLab to uncover temporal immune escape in GBM!

I would like to thank our collaborators and everyone involved including @FlorianIngelfi1 @burkhard_becher @EdoGal89. Also, my heartfelt gratitude to all the patients for their invaluable contributions to science.

Therapy success therefore, may partially stem from the disruption of interactions between B and T helper cells when B cells are depleted. Thus our study links the mechanism of B cell depleting therapies to the prognostic biomarker sCD27.

Considering our findings and the fact that CD27 on the surface of T helper cells interacts with CD70 on the surface of APCs. We propose a mechanism by which B and T cell interactions through the CD27/CD70 axis contribute to MS pathophysiology.

Using publicly available data we show that the highest CD70 expression within the CSF of MS patients is in B cells. Our immunohistological analysis reveals the co-localization of CD70-expressing B cells and CD27-expressing T helper cells to lesion sites in MS.

The most striking effect of the treatment was an increase in surface levels of CD27 within the T helper cell compartment. The soluble form of the molecule, released by T cells upon sustained signaling with its ligand CD70, is a prognostic biomarker in MS.

Very proud that we made it to the cover page of @ScienceTM It was a great team-effort of @ThomasLook_ @AmitLab @BecherLab @Philogen Many thanks to the editor @ScienceTM, the reviewers and the patients. We are excited to move this forward in a randomized multicenter setting

➡️The link to the full manuscript / El enlace al manuscrito completo👇🏽 https://t.co/ch88T1KD44

What an amazing special issue on @NeuroCellPress!! Super grateful for the opportunity to contribute with our Perspective on #CNS phagocytes with @burkhard_becher and Melanie Greter (still not on Twitter…). Looking forward to read all the other articles! https://t.co/chQtLvKSZZ

𝘿𝙤𝙣'𝙩 𝙗𝙡𝙖𝙢𝙚 𝙞𝙩 𝙤𝙣 𝘽 𝙘𝙚𝙡𝙡𝙨!🚫🙅🧪 Production of antibodies by B-1 cells is heavily impaired in 𝘣𝘶𝘮𝘣𝘭𝘦 mice (KO for the disease CVID-associated gene IκBNS), and one might think that the B cell is to blame. 1/2

This study would have been impossible without @FlorianIngelfi1 @burkhard_becher @EdoGal89 et al. Thanks for this amazing collaboration!

We propose a mechanism by which B and T cell interactions through the CD27/CD70 axis contribute to MS pathophysiology. Compromise of this signaling pathway by B cell depleting therapies would lead to higher surface CD27 as the molecule is not released in soluble form.

Surface levels of the costimulatory molecule CD27 were elevated in follicular and memory T helper cells upon treatment. The soluble form of the molecule, released by T cells upon sustained signaling with its ligand CD70, is a prognostic biomarker in MS.

Main impacts of the therapies are localized to the helper T cell compartment. CD4 T cells become more naïve in phenotype as the naïve-to-memory ratio increases. T follicular helper cells, reported to be involved in the disease, are reduced in the peripheral blood after treatment.

B cell depleting therapies are an unexplained success story of #MultipleSclerosis treatment. How does the loss of B cells impact the immune system in MS? Checkout our longitudinal multicohort study employing high-dimensional single-cell immunophenotyping:

Excited to share our paper on ILC1 and NK cell ontogeny. Embryonic ILC1s persist and mature in the liver, forming cytotoxic effectors - postnatal wave brings first NK cells and more ILC1s. Now in @SciImmunology https://t.co/eaW5zBNTqs