Communication between pathogenic T cells and myeloid cells in neuroinflammatory disease

被引:61
作者
Codarri, Laura [1 ]
Greter, Melanie [1 ]
Becher, Burkhard [1 ]
机构
[1] Univ Zurich, Inst Expt Immunol, CH-8091 Zurich, Switzerland
基金
瑞士国家科学基金会;
关键词
multiple sclerosis; experimental autoimmune encephalomyelitis; T helper cells; cytokines; granulocyte-macrophage colony-stimulating factor; interleukin-23; myeloid cells; macrophages; dendritic cells; CENTRAL-NERVOUS-SYSTEM; COLONY-STIMULATING FACTOR; EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS; EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS; NECROSIS-FACTOR-ALPHA; CYTOKINE GM-CSF; MULTIPLE-SCLEROSIS; DENDRITIC CELLS; IN-VIVO; IMMUNE INVASION;
D O I
10.1016/j.it.2012.09.007
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Clinical and experimental data suggest that T helper (T-H) cells are involved in the pathogenicity of experimental autoimmune encephalomyelitis (EAE) and multiple sclerosis (MS), but it is unlikely that they are directly responsible for the observed demyelination and axonal loss. Instead, the cell population that targets the destruction of oligodendrocytes and axons, and the mechanism exploited by central nervous system (CNS)invading encephalitogenic T-H cells to instruct these cells to mediate tissue damage, are still under debate. Mature myeloid cells form a prominent component of the neuroinflammatory infiltrates and are the suspected culprits behind the CNS injury due to their arsenal of toxic factors. Here, we describe the process of encephalitogenic T-H cell activation followed by their entry into the CNS and discuss how pathogenic T-H cells influence the myeloid compartment.
引用
收藏
页码:114 / 119
页数:6
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