Expression of major histocompatibility complex class II antigens and interleukin-1 by epithelial cells of Warthin's tumor

Abstract

The immunoreactivity for class II antigens of the major histocompatibility complex and interleukin-1 (IL-1) in Warthin's tumor (WT) cells was studied. In addition to macrophages, dendritic cells, and capillary endothelia, the luminal tumor cells and some keratinocytes in the metaplastic squamous foci exhibited immunoreactivity for both class II antigens and IL-1. The distribution of the class II antigens in the luminal tumor cells was limited to their basolateral membrane. These data, together with previous findings, strongly suggest that the luminal tumor cells of WT introduce the luminal antigen to the underlying lymphoid tissue and, thus, act as an antigen-presenting cell.

Tissue that has lost its track: Warthin’s tumour

“…In this context, further similarities between the lymphoid components of the tumour and the lymphoid tissue of the intestinal mucosa were found [15]. The subepithelial infiltrates consist mainly of B-cells containing a large number of IgA producing subpopulations.…”

Steroid hormone receptors in parotid gland cystadenolymphoma (Warthin's tumour)

“…In most surveys, the assumption prevails that this tumour has its origin in heterotopic salivary parenchymal inclusions in the intra‐ and peri‐glandular lymph nodes of the parotid gland 7,8 . Other studies discussed the importance of immunological reactions during the formation of the tumour 9–11 …”

“…7,8 Other studies discussed the importance of immunological reactions during the formation of the tumour. [9][10][11] The great majority of cystadenolymphomas (approximately 70%) occur in men at a peak age between the fourth and seventh decades of life. [12][13][14] The incidence in women of this tumour seems to be rising.…”

The prognostic impact of human leukocyte antigen (HLA) class I antigen abnormalities in salivary gland cancer. A clinicopathological study of 288 cases

“…prostate cancer 1 and colorectal cancer, 2,3 are extremely difficult to establish in SGC treatment, owing to the low frequency of the disease and the lack of comprehensive knowledge of tumour immune escape mechanisms, including alterations of components of the antigen processing machinery (APM) in SGC. To date, only two studies have addressed the expression of proteins of the human leukocyte antigen (HLA) complex in SGC, both focusing on HLA-DR, 4,5 and two other studies have analyzed HLA complex expression in Warthin's tumour 6 and pleomorphic adenoma. 7 Effective CD8 + cytotoxic T-lymphocyte responses require adequate surface expression of the major histocompatibility complex (MHC) class I antigens.…”