Kawai T, Shimauchi H, Eastcott J W, Smith D J, Taubman M A
Department of Immunology, Forsyth Dental Center, Boston, MA 02115, USA.
Immunology. 1998 Jan;93(1):11-9. doi: 10.1046/j.1365-2567.1998.00408.x.
This study was performed to investigate T-cell traffic to periodontal tissues during infection with a periodontal pathogen Actinobacillus actinomycetemcomitans (Aa). Rowett rat T-cell clones, A3 (CD4+ CD8-, alpha beta TCR+, NKRP-1-, specific to Aa) and G2 (CD4- CD8-, alpha beta TCR+, NKRP-1+, which reacts to Aa, Gram-negative and -positive bacteria), both expressed the same prominent adhesion molecules (LFA-1, VLA-4) to the same extent. Binding of both T-cell clones to rat endothelial cells in vitro was blocked by antibody to VLA-4. Rowett rats were infected with Aa and infused with Aa-stimulated, isogenic T-clone lymphocytes that had been labelled in vitro with 125IUdR. Radioactivity associated with recovery of clone A3, but not G2, was significantly elevated in the gingivae of infected rats, suggesting migration to infected animals' gingival tissues. Migration of radioactive Aa-specific A3 clone cells traced by autoradiography reached a maximum at 24 hr (1.2% of total lymphocytes as radiolabelled cells in infected gingiva versus 0.6% in noninfected), indicating an apparent antigen-directed retention in infected rats' gingival tissues. The G2 clone was not retained in the gingival tissues (0.20% of total lymphocytes as radiolabelled cells in infected gingiva versus 0.26% in non-infected). However, the possibility of A3 retention directed by inflammation or tissue-selective homing could not be excluded. In further experiments, other adoptively transferred T-clone lymphocytes [clones G23 (Th1) and F13 (Th2)] with specificity for the 29,000 MW outer membrane protein of Aa with the same prominent adhesion molecules could be recovered from rat gingivae previously challenged with this antigen. However, transferred T-clone lymphocytes [clone G26 (Th1)] with specificity for a different Aa antigen were not recovered. Therefore, the dynamics of cell entry into periodontal lesions vary for activated T lymphocytes with different antigenic specificities, indicating the significance of antigen in lymphocyte traffic to periodontal tissues.
本研究旨在调查在感染牙周病原体伴放线放线杆菌(Aa)期间T细胞向牙周组织的迁移情况。罗威特大鼠T细胞克隆A3(CD4 + CD8 - ,αβTCR + ,NKRP - 1 - ,对Aa特异)和G2(CD4 - CD8 - ,αβTCR + ,NKRP - 1 + ,对Aa、革兰氏阴性和阳性细菌均有反应),二者表达相同的主要粘附分子(LFA - 1、VLA - 4),且程度相同。体外实验中,两种T细胞克隆与大鼠内皮细胞的结合均被抗VLA - 4抗体阻断。将罗威特大鼠感染Aa,并注入经Aa刺激的、体外已用125IUdR标记的同基因T克隆淋巴细胞。与克隆A3而非G2的回收相关的放射性在感染大鼠的牙龈中显著升高,提示其迁移至感染动物的牙龈组织。通过放射自显影追踪放射性Aa特异性A3克隆细胞的迁移,在24小时达到峰值(感染牙龈中作为放射性标记细胞的总淋巴细胞的1.2%,而未感染牙龈中为0.6%),表明在感染大鼠的牙龈组织中有明显的抗原导向性滞留。G2克隆未滞留在牙龈组织中(感染牙龈中作为放射性标记细胞的总淋巴细胞的0.20%,而未感染牙龈中为0.26%)。然而,不能排除A3滞留是由炎症或组织选择性归巢所导向的可能性。在进一步实验中,其他对Aa的29,000MW外膜蛋白具有特异性且具有相同主要粘附分子的过继转移T克隆淋巴细胞[克隆G23(Th1)和F13(Th2)],可从先前用该抗原攻击过的大鼠牙龈中回收。然而,对不同Aa抗原具有特异性的过继转移T克隆淋巴细胞[克隆G26(Th1)]未被回收。因此,具有不同抗原特异性的活化T淋巴细胞进入牙周病变的动态过程各不相同,这表明抗原在淋巴细胞向牙周组织迁移中的重要性。