T cell infiltration is associated with increased Lyme arthritis in TLR2-/- mice
T cell infiltration is associated with increased Lyme arthritis in TLR2-/- mice
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DOI：
10.1111/j.1574-695x.2007.00356.x
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发表时间：
2008-01-01
影响因子：
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通讯作者：
Weis, Janis J.
中科院分区：
文献类型：
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作者：
Wang, Xiaohui;Ma, Ying;Weis, Janis J.
TLR 2缺陷的C57 BL/6小鼠在感染伯氏疏螺旋体后比野生型C57 BL/6小鼠发展更严重的关节炎，并且这种增加被同时存在的scid突变抑制。这表明在TLR 2（-/-）小鼠中亚急性莱姆关节炎的发展中需要淋巴细胞，这一特征通常与这种关节炎无关。B的病理学增加。Burgdorferi感染的TLR 2（-/-）小鼠也伴随单核细胞浸润的增加。在这项研究中，T细胞被发现是负责感染TLR 2（-/-）C3 H小鼠单核细胞的增加。因此，IFN-诱导型T细胞趋化因子CXCL 9和CXCL 10的转录物在TLR 2（-/-）小鼠的关节组织中大大增强，原型IFN-诱导型基因IFN-γ诱导的GTP酶（igtp）的转录物也是如此。用超声处理的B处理小鼠滑膜细胞。burgdorferi导致趋化因子和其它IFN诱导基因的转录物的诱导，而不管TLR 2的存在。T淋巴细胞的存在大大增强了滑膜细胞的转录反应。这些结果表明TLR 2（-/-）C3 H小鼠中炎症细胞浸润的增加是T细胞吸引趋化因子局部过量产生的结果。
C57BL/6 mice deficient in TLR2 develop more severe arthritis following infection with Borrelia burgdorferi than do wild-type C57BL/6 mice, and this increase is suppressed by the simultaneous presence of the scid mutation. This suggested a requirement for lymphocytes in the development of subacute Lyme arthritis in TLR2(-/-) mice, a feature not commonly associated with this arthritis. The increased pathology of B. burgdorferi-infected TLR2(-/-) mice was also accompanied by an increase in mononuclear cell infiltration. In this study, T cells were found to be responsible for the increase in mononuclear cells in infected TLR2(-/-) C3H mice. Accordingly, transcripts for the IFN-inducible T cell chemokines, CXCL9 and CXCL10, were greatly enhanced in joint tissue from TLR2(-/-) mice, as were transcripts for a prototypical IFN-inducible gene IFN-gamma-induced GTPase (igtp). Treatment of murine synovial cells with sonicated B. burgdorferi resulted in induction of transcripts for chemokines and other IFN-inducible genes, irrespective of the presence of TLR2. The presence of T lymphocytes greatly enhanced the transcriptional response of synovial cells. These results suggest that the increased inflammatory cell infiltration in TLR2(-/-) C3H mice is the result of localized overproduction of T cell attracting chemokines.