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Articles by F He
Total Records ( 3 ) for F He
  T Kawli , F He and M. W. Tan
  Trupti Kawli, Fanglian He, and Man-Wah Tan

The innate immune response is evoked as a consequence of interactions between invading foreign infectious agents and host immune cells. A successful innate immune response is pivotal in maintaining the delicate balance between health and disease; an insufficient response results in infection, whereas an excessive response results in prolonged inflammation and tissue damage. Alterations in the state and function of the nervous system influence the immune response. The nervous system regulates innate immune responses through the release of neurotransmitters, neuropeptides and neurohormones. However, many questions related to the molecular and cellular mechanisms involved, the physiological role of the link between the immune and the nervous system, and the biological significance of neuro-immune interactions remain unresolved. The interactions between the nematode Caenorhabditis elegans and its pathogens provide insights into mechanisms of neuroendocrine regulation of immunity and address many outstanding issues related to neuro-immune interactions.

  B Hu , K Lefort , W Qiu , B. C Nguyen , R. D Rajaram , E Castillo , F He , Y Chen , P Angel , C Brisken and G. P. Dotto
 

Epithelial–mesenchymal interactions are key to skin morphogenesis and homeostasis. We report that maintenance of the hair follicle keratinocyte cell fate is defective in mice with mesenchymal deletion of the CSL/RBP-J gene, the effector of "canonical" Notch signaling. Hair follicle reconstitution assays demonstrate that this can be attributed to an intrinsic defect of dermal papilla cells. Similar consequences on hair follicle differentiation result from deletion of Wnt5a, a specific dermal papilla signature gene that we found to be under direct Notch/CSL control in these cells. Functional rescue experiments establish Wnt5a as an essential downstream mediator of Notch–CSL signaling, impinging on expression in the keratinocyte compartment of FoxN1, a gene with a key hair follicle regulatory function. Thus, Notch/CSL signaling plays a unique function in control of hair follicle differentiation by the underlying mesenchyme, with Wnt5a signaling and FoxN1 as mediators.

  Y. C Wang , X. B Hu , F He , F Feng , L Wang , W Li , P Zhang , D Li , Z. S Jia , Y. M Liang and H. Han
 

Dendritic cells (DCs) are professional antigen presenting cells to initiate immune response against pathogens, but mechanisms controlling the maturation of DCs are unclear. Here we report that, in the absence of recombination signal binding protein-J (RBP-J, the transcription factor mediating Notch signaling), lipopolysaccharide-stimulated monocyte-derived DCs are arrested at a developmental stage with few dendrites, low major histocompatibility complex II (MHC II) expression, and reduced motility and antigen presentation ability. RBP-J null DCs had lower expression of CXCR4. Transduction with a CXCR4-expressing lentivirus rescued developmental arrest of RBP-J-deficient DCs. Activation of Notch signaling in DCs up-regulated CXCR4 expression and increased the outgrowth of dendrites and the expression of MHC II. These effects were abrogated by a CXCR4 inhibitor. Therefore, Notch signaling is essential for DCs to transit from a dendritelowMHC IIlow immature state into a dendritehighMHC IIhigh mature state, during the lipopolysaccharide-induced DC maturation, most likely through the up-regulation of CXCR4.

 
 
 
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