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⁻, αβTCR⁺, NKRP‐1⁻, specific to Aa) and G2 (CD4⁻ CD8⁻, αβTCR⁺, 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 non‐infected), 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.