期刊
JOURNAL OF CLINICAL INVESTIGATION
卷 119, 期 10, 页码 2990-2999出版社
AMER SOC CLINICAL INVESTIGATION INC
DOI: 10.1172/JCI39780
关键词
-
资金
- NIH [NIH R01 NS047175, NIH R03 NS0SS871, P30-NS04S7S8]
Traumatic injury to the mammalian spinal cord activates B cells, which culminates in the synthesis of auto-antibodies. The functional significance of this immune response is unclear. Here, we show that locomotor recovery was improved and lesion pathology was reduced after spinal cord injury (SCI) in mice lacking B cells. After SCI, antibody-secreting B cells and Igs were present in the cerebrospinal fluid and/or injured spinal cord of WT mice but not mice lacking B cells. In mice with normal B cell function, large deposits of antibody and complement component 1q (C1q) accumulated at sites of axon pathology and demyelination. Antibodies produced after SCI caused pathology, in part by activating intraspinal complement and cells bearing Fc receptors. These data indicate that B cells, through the production of antibodies, affect pathology in SCI. One or more components of this pathologic immune response could be considered as novel therapeutic targets for minimizing tissue injury and/or promoting repair after SCI.
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