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Articles by C Moon
Total Records ( 3 ) for C Moon
  Y Wang , M Zhang , C Moon , Q Hu , B Wang , G Martin , Z Sun and H. Wang
 

FE65 is expressed predominantly in the brain and interacts with the C-terminal domain of β-amyloid precursor protein (APP). We examined hippocampus-dependent memory and in vivo long-term potentiation (LTP) at the CA1 synapses with isoform-specific FE65 knockout (p97FE65–/–) mice. When examined using the Morris water maze, p97FE65–/– mice were impaired for the hidden platform task but showed normal performance in the probe test. To further discriminate the role of FE65 in acquisition and memory consolidation, we examined p97FE65–/– mice with temporal dissociative passive avoidance (TDPA) and contextual fear conditioning (CFC). p97FE65–/– mice showed impaired short-term memory for both TDPA and CFC when tested 10 min after training. After multiple TDPA training sessions, the crossover latency of some p97FE65–/– mice reached the cutoff value, but it significantly decayed in 8 d. At the Schaffer collateral-CA1 synapses, p97FE65–/– mice showed defective early-phase LTP (E-LTP). These results demonstrate novel roles of FE65 in synaptic plasticity, acquisition, and retention for certain forms of memory formation.

  B. T Edelson , W KC , R Juang , M Kohyama , L. A Benoit , P. A Klekotka , C Moon , J. C Albring , W Ise , D. G Michael , D Bhattacharya , T. S Stappenbeck , M. J Holtzman , S. S. J Sung , T. L Murphy , K Hildner and K. M. Murphy
 

Although CD103-expressing dendritic cells (DCs) are widely present in nonlymphoid tissues, the transcription factors controlling their development and their relationship to other DC subsets remain unclear. Mice lacking the transcription factor Batf3 have a defect in the development of CD8+ conventional DCs (cDCs) within lymphoid tissues. We demonstrate that Batf3–/– mice also lack CD103+CD11b DCs in the lung, intestine, mesenteric lymph nodes (MLNs), dermis, and skin-draining lymph nodes. Notably, Batf3–/– mice displayed reduced priming of CD8 T cells after pulmonary Sendai virus infection, with increased pulmonary inflammation. In the MLNs and intestine, Batf3 deficiency resulted in the specific lack of CD103+CD11b DCs, with the population of CD103+CD11b+ DCs remaining intact. Batf3–/– mice showed no evidence of spontaneous gastrointestinal inflammation and had a normal contact hypersensitivity (CHS) response, despite previous suggestions that CD103+ DCs were required for immune homeostasis in the gut and CHS. The relationship between CD8+ cDCs and nonlymphoid CD103+ DCs implied by their shared dependence on Batf3 was further supported by similar patterns of gene expression and their shared developmental dependence on the transcription factor Irf8. These data provide evidence for a developmental relationship between lymphoid organ–resident CD8+ cDCs and nonlymphoid CD103+ DCs.

 
 
 
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