PubMed · 8934513
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M Levin, D J Roberts, L B Holmes, C Tabin. 1996-11-28. Laterality defects in conjoined twins.. https://doi.org/10.1038/384321a0
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Follicular helper T cells (TFH cells) are CD4(+) T cells specialized in helping B cells and are associated both with protective antibody responses and autoimmune diseases. The promise of targeting TFH cells therapeutically has been limited by fragmentary understanding of extrinsic signals that regulate the differentiation of human TFH cells. A screen of a human protein library identified activin A as a potent regulator of TFH cell differentiation. Activin A orchestrated the expression of multiple genes associated with the TFH program, independently or in concert with additional signals. TFH cell programming by activin A was antagonized by the cytokine IL-2. Activin A's ability to drive TFH cell differentiation in vitro was conserved in non-human primates but not in mice. Finally, activin-A-induced TFH programming was dependent on signaling via SMAD2 and SMAD3 and was blocked by pharmacological inhibitors.
Gene transcripts differentially expressed in activin-induced human prostatic LNCaP apoptotic cells have been discovered by an improved subtractive hybridization method, uracil-DNA subtraction assay (USA), which involves digestion with uracil-DNA glycosylase and mung-bean nuclease. Among the five up-regulated and seven down-regulated genes, we have identified six known (>95% homology and similar size; p16, p53, Siva, RHAMM, Pax2, and eIF-4a1), three homologues (>95% homology but different size; myosin, a helicase motif, and a kinase motif), and three novel genes (no homology). In addition, anti-sense knock-out of a resulting novel kinase-like gene was found to abolish the apoptotic DNA fragmentation in activin-treated LNCaP cells. These findings indicate a new potential mechanism in DNA fragmentation of activin-induced cell-cycle arresting and apoptosis.
Vertebrate germ layer development is an intricately interwoven process with the organism operating as an integrated whole. To examine these processes we have used embryonic stem (ES) cell in vitro differentiation in a serum-free, chemically defined medium (CDM). In CDM, ES cells differentiate as embryoid bodies to neuroectoderm with upregulation of pax-6, without commensurate expression of Brachyury. In the presence of Activin A, pax-6 and Brachyury mRNAs are readily detectable, suggestive of both neuroectoderm and mesoderm formation, while in the presence of BMP-4 a process resembling primitive streak formation at the molecular level occurs. Neuroectoderm development in CDM alone is consistent with the view that this process can occur by default, as reported in Xenopus, due to the absence or sequestration of mesoderm-inducing factors. Additionally, these data show that BMP-4 alone is capable of instigating a process resembling primitive streak formation in ES cells and possibly in vivo.