MHC class I down-regulation: tumour escape from immune surveillance? (Review)

Bubenı́k, Jan

doi:10.3892/ijo.25.2.487

Cited by 105 publications

(104 citation statements)

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“…34 An altered expression of antigen-presenting molecule in different stages of the disease has also been reported in other types of cancer. 35 Based on these observations, it has been proposed that in the initial preclinic phase of many tumors, an increased expression of HLA-I molecules due to immunological signaling (ie by g-IFN)…”

Section: Discussionmentioning

confidence: 99%

Clonal plasma cells from monoclonal gammopathy of undetermined significance, multiple myeloma and plasma cell leukemia show different expression profiles of molecules involved in the interaction with the immunological bone marrow microenvironment

et al. 2005

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The immunological bone marrow (BM) microenvironment plays a major role in controlling growth and survival of clonal plasma cells (PC); this might translate into different patterns of expression of molecules involved in immune responses on PC from different types of monoclonal gammopathies (MG). We have studied the expression of a group of nine such molecules on both BMPC and the plasma of 61 newly diagnosed MG patients (30 MG of undetermined significance (MGUS), 27 multiple myeloma (MM) and four plasma cell leukemia (PCL)) and five normal individuals. Clonal PC from all MG displayed significantly increased levels of CD56, CD86 and CD126, and decreased amounts of CD38 (Po0.001). Additionally, HLA-I and b2-microglobulin were abnormally highly expressed in MGUS, while CD40 expression was decreased in MM and PCL (Po0.05). Interestingly, a progressive increase in the soluble levels of b2-microglobulin was found from MGUS to MM and PCL patients (P ¼ 0.03). In contrast, all groups showed similar surface and soluble amounts of CD126, CD130 and CD95, except for increased soluble levels of CD95 observed in PCL. Overall, those phenotypic differences are consistent with increased antigen presentation and costimulatory capacities in MGUS, which progressively deteriorate in malignant MG (MM and PCL).

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Section: Discussionmentioning

confidence: 99%

Clonal plasma cells from monoclonal gammopathy of undetermined significance, multiple myeloma and plasma cell leukemia show different expression profiles of molecules involved in the interaction with the immunological bone marrow microenvironment

et al. 2005

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“…Thus, the MHC class I levels on tumour cells participate in determining which part of the immune system (adaptive or innate) can interact with tumour cells and how these parts can co-operate in the immunity development (1-3). Among tumour escape routes, alteration of MHC class I cell surface expression is the mechanism used in a wide variety of human solid tumours, including cervical carcinoma (4)(5)(6)(7)(8).…”

Section: Introductionmentioning

confidence: 99%

NK1.1+ cells are important for the development of protective immunity against MHC I-deficient, HPV16-associated tumours

Indrová

Šímová²,

Bieblová³

et al. 2010

Oncol Rep

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“…ancer cells often down-regulate expression of cell surface MHC class I molecules (1)(2)(3)(4). This helps them evade immunosurveillance mediated by conventional T lymphocytes that express ␣␤ T cell receptors recognizing peptide/ MHC complexes (5).…”

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confidence: 99%

Complex Interplay of Activating and Inhibitory Signals Received by Vγ9Vδ2 T Cells Revealed by Target Cell β2-Microglobulin Knockdown

Trichet

Benezech

Dousset

et al. 2006

The Journal of Immunology

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Tumor cells often escape immunosurveillance by down-regulating MHC class I molecule expression. For human Vγ9Vδ2 T cells, a major peripheral blood T cell subset with broad antitumor reactivity, this down-regulation can affect signals transmitted by both the inhibitory and the activating MHC class I and Ib-specific NK receptors (NKRs) that these lymphocytes frequently express. To assess the overall impact of MHC down-regulation on Vγ9Vδ2 T cell activation, we used stable β2-microglobulin knockdown to generate tumor cells with a ∼10-fold down-modulation of all MHC class I molecules. This down-modulation had little effect on T cell proliferation or cytokine production, but modified tumor cell killing efficiency. Ab-blocking studies identified ILT2 as an important inhibitor of tumor cell killing by Vγ9Vδ2 T cells. Down-modulation of MHC class I and Ib molecules severely reduced ILT2 inhibitory signaling, but still allowed signaling by activating CD94-based receptors. It also unveiled a frequent enhancing effect of NKG2D on tumor killing by Vγ9Vδ2 T cells. Current models suggest that activating NKRs have less affinity for their MHC ligands than homologous inhibitory NKRs. Our results show that, despite this, activating NKRs recognizing MHC class I molecules play an important role in the increased killing by Vγ9Vδ2 T cells of tumor cells with down-regulated MHC class I molecule expression, and suggest that these T cells will best lyse tumor cells combining MHC class I molecule expression down-regulation with up-regulated NKG2D ligand expression.

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MHC class I down-regulation: tumour escape from immune surveillance? (Review)

Cited by 105 publications

References 0 publications

Clonal plasma cells from monoclonal gammopathy of undetermined significance, multiple myeloma and plasma cell leukemia show different expression profiles of molecules involved in the interaction with the immunological bone marrow microenvironment

Clonal plasma cells from monoclonal gammopathy of undetermined significance, multiple myeloma and plasma cell leukemia show different expression profiles of molecules involved in the interaction with the immunological bone marrow microenvironment

NK1.1+ cells are important for the development of protective immunity against MHC I-deficient, HPV16-associated tumours

Complex Interplay of Activating and Inhibitory Signals Received by Vγ9Vδ2 T Cells Revealed by Target Cell β2-Microglobulin Knockdown

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