Expression analysis of classic and non-classic HLA molecules before interferon alfa-2b treatment of melanoma

Wagner, Stephan N.; Rebmann, Vera; Willers, Christoph; Grosse‐Wilde, H.; Goos, M.

doi:10.1016/s0140-6736(00)02486-7

Cited by 103 publications

(75 citation statements)

References 3 publications

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“…13,39,[48][49][50][51] Such an observation deserves particular attention in the context of IFN-based immunotherapy or anti-tumor chemotherapy using demethylating drugs such as decitabine in melanoma patients whose immune system may be inhibited by the boosted expression of HLA-G1. 6,7 Interestingly, in our study, the HLA-G switch from HLA-G1 to HLA-G2 was strong enough to prevent reexpression of HLA-G1 mRNA and protein even following treatment with cytokines and DNA demethylating agent.…”

Section: Discussionmentioning

confidence: 48%

“…1 HLA-G is normally absent on healthy tissues except trophoblast, 2 thymus 3 and cornea. 4 Interestingly, both HLA-G transcription and protein expression are up-regulated on various tumors cells, as demonstrated in biopsies from patients with melanoma, [5][6][7] breast cancer, 8 renal carcinoma, 9,10 primary cutaneous lymphoma, 11 lung cancer, 12 glioma, 13 epithelial cutaneous malignant lesions 14 and colorectal cancer. 15 .…”

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confidence: 99%

“…Moreover, the immunotolerant role of HLA-G has been emphasized by its involvement in the resistance to IFN-based therapies that is observed in some melanoma patients. 6,7 In contrast to these data obtained with surgically removed tumor lesions, the detection of HLA-G on in vitro established tumor cell lines has been mainly unsuccessful (reviewed in 1). To date, only a few tumor cell lines, other than choriocarcinoma cell lines, have been found to express cell-surface HLA-G: 4 renal carcinoma cell lines, 9,16,17 4 glioma cell lines 13 and 9 short-term ovarian carcinoma cell lines.…”

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confidence: 99%

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Switch ofHLA-G alternative splicing in a melanoma cell line causes loss of HLA-G1 expression and sensitivity to NK lysis

et al. 2005

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these points by studying a melanoma cell line derived from a surgically-removed HLA-G-positive melanoma lesion. We show that HLA-G expression in melanoma cells can be regulated at the mRNA splicing level. Indeed, melanoma cells rapidly switched from cell-surface HLA-G1 to intra-cellular HLA-G2 expression. This mechanism restored tumor sensitivity to NK lysis. Moreover, switch from HLA-G1 to HLA-G2 was strong enough to prevent re-expression of immunoprotective HLA-G1 even following treatments with cytokines and DNA demethylating agent. Modulating HLA-G at the mRNA splicing level would be an efficient way of lifting in vivo HLA-G-mediated tumor immune escape. ' 2005 Wiley-Liss, Inc.

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Section: Discussionmentioning

confidence: 48%

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confidence: 99%

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confidence: 99%

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Switch ofHLA-G alternative splicing in a melanoma cell line causes loss of HLA-G1 expression and sensitivity to NK lysis

et al. 2005

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“…Whether the nonclassical HLA-G molecule is upregulated during IFN treatment or plays a role in favoring or impairing immune responses to such therapeutic approaches also remains an interesting issue. Indeed, analysis of aberrant expression of HLA-G combined with loss of classical HLA mol-ecules on melanoma cells could have important practical implications for the selection of patients likely not to benefit from interferon ␣ therapy (61).…”

Section: Figmentioning

confidence: 99%

A Specific Interferon (IFN)-stimulated Response Element of the Distal HLA-G Promoter Binds IFN-regulatory Factor 1 and Mediates Enhancement of This Nonclassical Class I Gene by IFN-β

Lefebvre

Berrih‐Aknin

Adrián

et al. 2001

Journal of Biological Chemistry

106

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“…10,11 HLA-G expression was initially found to be restricted to placenta. More recently, its expression has been detected in thymic epithelial cells, 12 various malignant cells, [13][14][15] and peripheral blood monocytes activated by IL-10. 16 HLA-G is known to inhibit cytotoxic activity of T lymphocytes and natural killer cells (NK), 17,18 which are essential effector cells in graft rejection.…”

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Human Leukocyte Antigen-G Expression After Heart Transplantation Is Associated With a Reduced Incidence of Rejection

et al. 2002

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Background — Human leukocyte antigen (HLA)-G, a nonclassic major histocompatibility complex class I molecule expressed in the extravillous cytotrophoblast at the feto-maternal interface, is known to protect the fetus from maternal cellular immunity. In a preliminary study, we showed that HLA-G is expressed in the hearts of some patients after heart transplantation. Methods and Results — In the present study, a larger number of patients was investigated to confirm this finding and to look for possible correlations between HLA-G expression and the number and types of rejection. Expression of HLA-G in endomyocardial biopsy specimens was investigated by immunohistochemical analysis, and detection of the soluble HLA-G in the serum was performed by immunoprecipitation followed by Western blot analysis. HLA-G was detected in the biopsy specimens and serum of 9 of 51 patients (18%). The number of episodes of acute rejection was significantly lower in HLA-G-positive patients (1.2±1.1) as compared with HLA-G-negative patients (4.5±2.8) ( P <0.001). No chronic rejection was observed in HLA-G-positive patients, whereas 15 HLA-G-negative patients had chronic rejection ( P <0.032). A longitudinal study of these patients reveals that the status of HLA-G expression was maintained after 6 months both in serum and in biopsy specimens. During this period, HLA-G-positive patients did not have chronic rejection. Conclusions — There is a significant correlation between rejection and HLA-G expression in the heart after transplantation. HLA-G expression and its effect in reducing the incidence and severity of rejection seem to be stable throughout the evolution.

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Expression analysis of classic and non-classic HLA molecules before interferon alfa-2b treatment of melanoma

Cited by 103 publications

References 3 publications

Switch ofHLA-G alternative splicing in a melanoma cell line causes loss of HLA-G1 expression and sensitivity to NK lysis

Switch ofHLA-G alternative splicing in a melanoma cell line causes loss of HLA-G1 expression and sensitivity to NK lysis

A Specific Interferon (IFN)-stimulated Response Element of the Distal HLA-G Promoter Binds IFN-regulatory Factor 1 and Mediates Enhancement of This Nonclassical Class I Gene by IFN-β

Human Leukocyte Antigen-G Expression After Heart Transplantation Is Associated With a Reduced Incidence of Rejection

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