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Data availability The data that support the plots within this paper and other findings of this study are available from the corresponding author upon request. The bulk and single-cell RNA-seq data are available as part of the Gene Expression Omnibus (GEO) SuperSeries GSE134691. Author contributions S.C. and A.G. designed the study, performed experiments, interpreted results and wrote the manuscript. J.Á.N.-Á. designed the study and experiments and interpreted data.

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Basic helix-loop-helix (bHLH) transcription factors are important regulators of retinal neurogenesis. In the developing retina, proneural bHLH genes have highly defined expressions, which are influenced by pattern formation and cell-specification pathways. We report here that the tissue-specific bHLH transcription factor Ptf1a (also known as PTF1-p48) is expressed from embryonic day 12.5 of gestation (E12.5)to postnatal day 3 (P3) during retinogenesis in the mouse. Using recombination-based lineage tracing, we provide evidence that Ptf1ais expressed in precursors of amacrine and horizontal cells. Inactivation of Ptf1a in the developing retina led to differentiation arrest of amacrine and horizontal precursor cells in addition to partial transdifferentiation of Ptf1a-expressing precursor cells to ganglion cells. Analysis of late cell-type-specific markers revealed the presence of a small population of differentiated amacrine cells, whereas GABAergic and glycinergic amacrine cells, as well as horizontal cells, were completely missing in Ptf1a-knockout retinal explants. We conclude that Ptf1a contributes to the differentiation of horizontal cells and types of amacrine cells during mouse retinogenesis.

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Monomeric serum immunoglobulin A (IgA) can contribute to the development of various autoimmune diseases, but the regulation of serum IgA effector functions is not well defined. Here, we show that the two IgA subclasses (IgA1 and IgA2) differ in their effect on immune cells due to distinct binding and signaling properties. Whereas IgA2 acts pro-inflammatory on neutrophils and macrophages, IgA1 does not have pronounced effects. Moreover, IgA1 and IgA2 have different glycosylation profiles, with IgA1 possessing more sialic acid than IgA2. Removal of sialic acid increases the pro-inflammatory capacity of IgA1, making it comparable to IgA2. Of note, disease-specific autoantibodies in patients with rheumatoid arthritis display a shift toward the pro-inflammatory IgA2 subclass, which is associated with higher disease activity. Taken together, these data demonstrate that IgA effector functions depend on subclass and glycosylation, and that disturbances in subclass balance are associated with autoimmune disease.

Research within the anatomical sciences often relies on human cadaveric tissues. Without the good will of these donors who allow us to use their bodies to push