hexacosa-2,4,6,8,10,12,14,16,18,20,22,24-dodecaene | 2423-64-5

• 分子结构分类: 有机化合物 - 碳氢化合物 - 不饱和烃
• 英文名称: hexacosa-2,4,6,8,10,12,14,16,18,20,22,24-dodecaene
• 英文别名: Hexacosa-2,4,6,8,10,12,14,16,18,20,22,24-dodecaen
• CAS: 2423-64-5
• 化学式: C₂₆H₃₀
• 分子量: 342.524
• InChiKey: GUBLYMFLRLBOBF-ZEEDBMCGSA-N

反应信息

• 作为产物：
  描述：

  alkaline earth salt of/the/ methylsulfuric acid 在 四氢呋喃 、 lithium aluminium tetrahydride 作用下， 生成 hexacosa-2,4,6,8,10,12,14,16,18,20,22,24-dodecaene
  参考文献：
  名称：

  Investigation of a Mechanism for Accelerated Breakdown of Immune Tolerance to the Primary Biliary Cirrhosis–Associated Autoantigen, Pyruvate Dehydrogenase Complex

  摘要：

  Primary biliary cirrhosis (PBC) is an autoimmune liver disease characterized by autoreactive T- and B-cell responses to the highly conserved enzyme pyruvate dehydrogenase complex (PDC). In this study we have examined the breakdown of T-cell tolerance to self-PDC using a mouse model. Female SJL/J mice were sensitized intraperitoneally with foreign-PDC (bovine) and/or self-PDC (murine) in complete Freund's adjuvant, and serum, spleen, and liver tissue was taken 8 weeks later. Animals sensitized with foreign-PDC produced IgG antibodies that were reactive with both foreign and self-PDC, but splenic T cells from these animals only responded to stimulation with foreign PDC. Sensitization with self-PDC elicited neither antibodies nor reactive T cells. Significantly, cosensitization with mixed self-PDC and foreign-PDC resulted in a full breakdown of self-tolerance, with generation of both antibody and T-cell responses to self-PDC of the type seen exclusively in human PBC patients. Mild bile duct lesions deficient in CD8(+) T cells were seen 8 weeks after sensitization with either foreign or self-PDC. However, after sensitization with mixed self-PDC and foreign-PDC, these lesions were significantly larger and heavily infiltrated by CD8(+) T cells. Liver-infiltrating T cells derived from the self-PDC and foreign-PDC cosensitized but not from control animals showed reactivity with self-PDC, suggesting a possible role for autoreactive PDC-specific T-cell responses in the pathogenesis of the observed histologic changes. It is likely that B-cell cross-reactivity between foreign and self-PDC enhances the potential for breakdown of T-cell self-tolerance by allowing efficient presentation of self-antigens in the inoculum. This model may provide a useful system for investigating the etiology and treatment of PBC.

  DOI：

  10.1038/labinvest.3780413