Ficus iidaiana Rehder et Wilson

原著和名: オホヤマイチヂク科名: クワ科 = Moraceae採集地: 東京都 小笠原村 母島 (小笠原村 母島)採集日: 1971/3/30採集者: 萩庭丈壽整理番号: JH045375国立科学博物館整理番号: TNS-VS-99537

Network of direct and indirect gene connections between >2-fold downregulated genes.

<p>Network of direct and indirect gene connections as predicted by Ingenuity Pathway Analysis software. >2-fold downregulated mouse genes were uploaded on the IPA platform to establish a network of their published connections.</p

Comparison between the regulated pathways of the pEAE dataset with presymptomatic and active EAE (clinical score 3) monocyte derived macrophages, as well as with presymptomatic and active EAE microglial derived macrophages.

<p>(A) Venn diagrams of each comparison set. (B) Venn diagram of the unique canonical pathways regulated only in pEAE mice identified from the comparison of the chronic relapsing and secondary progressive EAE dataset with the macrophage populations.</p

Genetic deletion of Autotaxin from CD11b+ cells decreases the severity of experimental autoimmune encephalomyelitis.

Autotaxin (ATX) is a secreted lysophospholipase D catalyzing the extracellular production of lysophosphatidic acid (LPA), a growth factor-like signaling lysophospholipid. ATX and LPA signaling have been incriminated in the pathogenesis of different chronic inflammatory diseases and various types of cancer. In this report, deregulated ATX and LPA levels were detected in the spinal cord and plasma of mice during the development of experimental autoimmune encephalomyelitis (EAE). Among the different sources of ATX expression in the inflamed spinal cord, F4/80+ CD11b+ cells, mostly activated macrophages and microglia, were found to express ATX, further suggesting an autocrine role for ATX/LPA in their activation, an EAE hallmark. Accordingly, ATX genetic deletion from CD11b+ cells attenuated the severity of EAE, thus proposing a pathogenic role for the ATX/LPA axis in neuroinflammatory disorders

Network of direct and indirect gene connections between >3-fold upregulated genes.

<p>Network of direct and indirect gene connections as predicted by Ingenuity Pathway Analysis software. >3-fold upregulated mouse genes were uploaded on the IPA platform to establish a network of their published connections.</p

Comparison between the differentially upregulated and downregulated genes in the pEAE mice and MS susceptibility genes.

<p>(A) Venn diagram depicting the common genes between MS susceptibility genes (Hoppmann et al., [<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0157754#pone.0157754.ref074" target="_blank">74</a>]) and upregulated EAE genes (34) and the common genes between the MS susceptibility genes and downregulated EAE genes (4). (B) List of the common genes as identified in the Venn diagram.</p

Most significantly upregulated genes (>16 fold change) with non-immunological functions.

<p>Most significantly upregulated genes (>16 fold change) with non-immunological functions.</p

Identification of differentially expressed genes.

<p>(A) MA plot representing the ratio of FPKM expression values between chronic relapsing secondary progressive EAE samples and control samples plotted against their average. All 14,373 genes are plotted with significantly regulated genes (q<0.05) plotted in red. (B) Volcano plot presenting the 14,373 genes, with genes over the significance cut off at <i>p</i> <0.0072 (-log <i>p</i> <2.1426) plotted in grey. The statistically significant genes with >2-fold change in expression are plotted in red.</p

Most significantly downregulated genes (>4 fold change).

<p>Most significantly downregulated genes (>4 fold change).</p