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Objectives/Hypothesis: Adenoid cystic carcinoma of the head and neck (ACCHN) is characterized by late recurrence and frequent distant metastasis. Tumor attack by cytotoxic T lymphocytes and macrophages is mediated by the interaction of leukocyte function‐associated antigen (LFA)‐1 on lymphocytes with intercellular adhesion molecule (ICAM)‐1 on the tumor surface. Thus, the reduced expression of ICAM‐1 on tumor cells could contribute to their escape from host immune surveillance. To investigate the relationship between the clinical features of ACCHN and host immune surveillance, the expression of ICAM‐1 and infiltration of T/natural killer (NK) cells and macrophages were immunohistochemically examined. Study Design: Retrospective analysis of immunohistochemical tumor characteristics and clinical outcome. Methods: Immunohistochemical study of ICAM‐1, T/NK cells, and macrophages was performed on paraffin sections of 42 patients with ACCHN. The expression of T/NK cells and macrophages was represented by T‐cell‐restricted antigen (TIA)‐1 and CD68 expression, respectively. The expression of these molecules and clinical features were analyzed. Results: Of 42 ACCHN cases, 15,9, and 15 patients were classified as ICAM‐1 high, TIA‐1 high, and CD68 high, respectively. The TIA‐1 expression scores in ICAM‐1‐low patients were significantly lower than those in ICAM‐1‐high patients (1.3 ± 3.7 vs. 8.3 ± 12.7, P = .0031). The CD68 expression scores in ICAM‐1‐low patients were also significantly lower than those in ICAM‐1‐high patients (9.6 ± 9.G vs. 21.1 ± 17.6, P = .0047). Moreover, ICAM‐1‐high patients had a significantly better disease‐free survival rate (P = .043). Conclusions: Reduced expression of ICAM‐1 may promote immune evasion and metastasis, resulting in poor prognosis in ACCHN.

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