H₁R expression by CD11B⁺ cells is not required for susceptibility to experimental allergic encephalomyelitis

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• 作者：Naresha Saligrama^a ; Rajkumar Noubade^a ; Laure K. Case^a ; Matthew E. Poynter^a ; ^c ; Cory Teuscher^a ; ^b ; ^d ; ^{C.Teuscher@uvm.edu}
• 关键词：APCs ; antigen presenting cells ; DCs ; dendritic cells ; HA ; histamine ; EAE ; experimental allergic encephalomyelitis ; MS ; multiple sclerosis ; BBB ; blood brain barrier ; PE ; peritoneal exudate ; DLN ; draining lymph node ; MOG35&ndash ; 55 ; myelin oligodendrocyte g
• 刊名：Cellular Immunology
• 出版年：2012
• 出版时间：July-August, 2012
• 年：2012
• 卷：278
• 期：1-2
• 页码：27-34
• 全文大小：797 K

文摘

The histamine H₁ receptor (Hrh1/H₁R) was identified as an autoimmune disease gene in experimental allergic encephalomyelitis (EAE), the principal autoimmune model of multiple sclerosis (MS). Previously, we showed that selective re-expression of H₁R by endothelial cells or T cells in H₁RKO mice significantly reduced or complemented EAE severity and cytokine responses, respectively. H₁R regulates innate immune cells, which in turn influences peripheral and central nervous system CD4⁺ T cell effector responses. Therefore, we selectively re-expressed H₁R in CD11b⁺ cells of H₁RKO mice to test the hypothesis that H₁R signaling in these cells contributes to EAE susceptibility. We demonstrate that transgenic re-expression of H₁R by H₁RKO-CD11b⁺ cells neither complements EAE susceptibility nor T cell cytokine responses highlighting the cell-specific effects of Hrh1 in the pathogenesis of EAE and MS, and the need for cell-specific targeting in optimizing therapeutic interventions based on such genes.