We describe a case of cutaneous lymphadenoma, which is known to be infiltrated with various types of lymphocytes [1
]. In this report, we employed immunohistochemical staining to verify the tumor-composing lymphocytes, especially focusing on the profiles of the T cell subsets.
Cutaneous lymphadenoma is a rare neoplasm that arises mainly on the skin of the head and neck [1
]. The exact pathogenesis remains unknown and the histogenesis is uncertain. Clinically, the tumor presents as a slow growing, skin colored papule, nodule, or plaque without erythema or other signs of tumor-associated inflammation [5
]. The histological differential diagnosis includes clear cell BCC, clear cell syringoma, trichoepithelioma, dermal thymus and malignant lymphoepithelioma-like carcinoma [8
]. However, a lymphoid cell infiltrate within the tumor lobules is not prominent in such tumors.
Previously, several reports suggested that, in cutaneous lymphadenoma, cells within both the lobules and interstitial area consist of CD1a+
Langerhans cells, CD30+
T or B cells, and CD3+
T cells [1
]. More detailed investigation has not been performed yet. In our case, immunohistochemical staining for CD3, CD4, CD8, TIA-1, CD20, CD68, Foxp3 and CD56 was found in the phenotypic analysis of the cutaneous lymphadenoma-infiltrating cells. We investigated the expression of CD45RA and CD45Ro on infiltrating lymphocytes, and found that, in cutaneous lymphadenoma, infiltrating cells mainly consist of memory T cells. We also detected prominent infiltration of Foxp3+
Treg cells, as we previously reported in other types of skin tumors [9
]. In addition, we also focused on the tumor stroma. In our case, the tumor lobules consisted of AE1/AE3+
cells, and within the lobules, stroma is mainly positive for AE1/AE3. In contrast, on the outside of the lobules, the stroma showed abundant mucin deposits. As we previously reported the profiles of TILs in metastatic malignant melanomas [10
], normally in malignant tumor microenvironment, specific lymphocytes such as Tregs, cytotoxic T lymphocytes, etc. are increasing. In the present case, there is no tendency of increasing numbers of effector T cells, suppressor cells, nor antigen-presenting cells. These observations may be because cutaneous lymphadenoma is not a malignant tumor but a benign neoplasm of follicular or lymphoepithelial differentiation. Our present case suggested that the pathogenesis of tumor-infiltrating cells in cutaneous lymphadenoma is different from TILs in malignant skin tumors. Though we could not further assess the functions of these infiltrating cells, our present study suggests, at least, that these varieties of lymphocytes may have played roles in tuning and maintaining the homeostasis of this tumor.