Abstract
BackgroundTumors avoid destruction by cytotoxic T cells (CTL) and natural killer (NK) cells by downregulation of classical human leukocyte antigens (HLA) and overexpression of non-classical HLA. This is the first...
Highlights
Tumors avoid destruction by cytotoxic T cells (CTL) and natural killer (NK) cells by downregulation of classical human leukocyte antigens (HLA) and overexpression of non-classical HLA
HLA class I expression in primary cervical cancer and paired metastatic lymph node (LN) HLA class I expression in paired primary tumor and LN metastasis samples of squamous cell carcinoma (SCC) and AC was analyzed by immunohistochemistry for HLA-A, HLA-B/C, HLA-E and HLA-G
Comparison of HLA class I expression between SCC and AC When complete loss and weak expression of HLA-A were compared between the histological subtypes, we found a trend toward more complete loss in primary SCC (P = 0.053, Chi2 test - pairwise) and SCC metastatic LN (P = 0.081, Chi2 test - pairwise) (Fig. 4a)
Summary
Tumors avoid destruction by cytotoxic T cells (CTL) and natural killer (NK) cells by downregulation of classical human leukocyte antigens (HLA) and overexpression of non-classical HLA. This is the first study to investigate HLA expression in relation to histology (squamous cell carcinoma (SCC) vs adenocarcinoma (AC)), clinicopathological parameters and survival in a large cervical cancer patient cohort. One of the mechanisms by which tumor cells can escape immune destruction, is downmodulaton of classical human leukocyte antigens (HLA) class I (HLA-A, -B, and -C) expression These molecules are responsible for tumor-associated antigen presentation at the cell surface for recognition by cytotoxic T cells (CTLs) and targeted cell lysis [2,3,4,5,6]. HLA-E can bind the stimulatory CD94/NKG2C receptor of NK cells, this might have less impact because of a 6-fold lower affinity as compared to the inhibitory receptors [13]
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