Baker P J, Garneau J, Howe L, Roopenian D C
Biology Department, Bates College, Lewiston, Maine 04210, USA.
Acta Odontol Scand. 2001 Aug;59(4):222-5. doi: 10.1080/00016350152509247.
We have previously shown that mice lacking CD4+, but not CD8+, T cells lose less alveolar bone loss in response to oral infection with Porphyromonas gingivalis than do immunocompetent mice of the same genetic background, indicating that CD4+ T cells contribute to bone resorption. The CD4+ and CD8+ T-cell knockouts were produced by targeted deletions of, respectively, major histocompatibility complex II (MHCII) or beta2-microglobulin (producing non-expression of MHCI). Because MHC deletions can have other effects in addition to those on T-cell selection, we wanted to confirm that the lessened bone loss was truly an effect of the lack of T cells. Consequently, we repeated our experiments with C57B1 /6J-Tcra mice that have a targeted deletion of the alpha chain of the T-cell receptor (Tcra). Six weeks after oral infection with P. gingivalis ATCC 53977 the total bone loss at buccal maxillary sites was 0.28 mm in infected immunocompetent mice (P=0.002 compared with sham-infected mice), whereas in Tcra knockouts the bone loss was only 0.08 mm (P=0.04 compared with shams). The T-cell-deficient mice thus lost 70% less bone after infection than did genetically matched immunocompetent mice (P =0.003). These experiments confirm that T cells, and their responses to oral infection with P. gingivalis, help to push bone remodeling in the direction of net loss of bone.
我们之前已经表明，缺乏CD4⁺而非CD8⁺ T细胞的小鼠，在受到牙龈卟啉单胞菌口腔感染时，与具有相同遗传背景的免疫活性小鼠相比，牙槽骨丧失较少，这表明CD4⁺ T细胞有助于骨吸收。CD4⁺和CD8⁺ T细胞敲除小鼠分别是通过靶向缺失主要组织相容性复合体II（MHCII）或β2-微球蛋白（导致MHCI不表达）产生的。由于MHC缺失除了对T细胞选择有影响外还可能有其他作用，我们想确认骨丧失减少确实是缺乏T细胞的结果。因此，我们用靶向缺失T细胞受体α链（Tcra）的C57B1 /6J-Tcra小鼠重复了我们的实验。在用牙龈卟啉单胞菌ATCC 53977进行口腔感染六周后，感染的免疫活性小鼠上颌颊侧部位的总骨丧失为0.28毫米（与假感染小鼠相比，P = 0.002），而在Tcra敲除小鼠中骨丧失仅为0.08毫米（与假感染小鼠相比，P = 0.04）。因此，T细胞缺陷小鼠在感染后比基因匹配的免疫活性小鼠少丧失70%的骨（P = 0.003）。这些实验证实，T细胞及其对牙龈卟啉单胞菌口腔感染的反应有助于推动骨重塑朝着骨净丧失的方向发展。
