Expression of MHC class II antigens in human B-cell leukaemia and non-Hodgkin's lymphoma

Guy, Keith; Krajewski, A. S.; Dewar, A E

doi:10.1038/bjc.1986.31

Cited by 47 publications

(24 citation statements)

References 57 publications

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“…Interestingly, loss of human leukocyte antigen (HLA) class I and class II expression has been described in a subset of aggressive B-cell lymphomas (consisting primarily of DLBCLs), and this loss correlated with extranodal disease 71 and poor survival. [72][73][74] Similarly, a recent study of 258 DLBCLs found extensive loss of heterozygosity within the HLA region on the p arm of chromosome 6, primarily in extranodal lymphomas. 75 The authors of this study also speculated that a structural loss of HLA class I and II gene expression might contribute to escape of aggressive B-cell lymphomas from immune surveillance.…”

Section: Expression Profiling Of T(14;18)-positive Cell Lines 131mentioning

confidence: 89%

Microarray Analysis of B-Cell Lymphoma Cell Lines with the t(14;18)

Robetorye

Bohling

Morgan

et al. 2002

The Journal of Molecular Diagnostics

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The t(14;18) is the most common genetic alteration in follicular lymphoma, and is detectable in a subset of diffuse large B-cell lymphomas (DLBCL), resulting in over-expression of the anti-apoptotic protein BCL-2. Although the t(14;18)-induced over-expression of BCL-2 is an important step in lymphomagenesis,The t(14;18) is a frequent chromosomal alteration in nonHodgkin's lymphomas (NHL), occurring in up to 90% of follicular lymphomas 1 and 20 to 30% of diffuse large B-cell lymphomas (DLBCL). 2,3 This translocation is acquired early in B-cell development and results in juxtaposition of the bcl-2 gene on chromosome 18 with the immunoglobulin heavy-chain locus on chromosome 14, resulting deregulated expression of a structurally intact BCL-2 protein. 4 -8 BCL-2 is located in the inner mitochondrial membrane and functions as an anti-apoptotic protein that inhibits programmed cell death, 9 resulting in accumulation of B-lymphocytes by virtue of increased cell survival. 9 -11 Although the t(14;18)-induced over-expression of bcl-2 is an important step in lymphomagenesis, this alteration alone is not sufficient to produce malignant lymphoma. This has been demonstrated in in vitro gene transfer experiments using cell lines and transgenic mice studies in which forced over-expression of bcl-2 was insufficient to cause lymphoma. 12,13 Indeed, low numbers of t(14; 18)-carrying cells can be detected in benign lymphoid tissues such as follicular hyperplasias and the hyperplastic tonsils of young children. 14 These studies indicate that cumulative genetic and cellular alterations superimposed on the t(14;18) are necessary for the development of lymphoma and underscore the need for further analysis of t(14;18)-containing DLBCLs to identify additional genes involved in lymphomagenesis and progression.cDNA microarray technology allows large scale parallel analyses of gene expression and permits simultaneous comparison of the relative gene expression levels of several thousand genes in different cell types. 15,16 This approach has now been used successfully by a number

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Section: Expression Profiling Of T(14;18)-positive Cell Lines 131mentioning

confidence: 89%

Microarray Analysis of B-Cell Lymphoma Cell Lines with the t(14;18)

Robetorye

Bohling

Morgan

et al. 2002

The Journal of Molecular Diagnostics

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“…The study of the epigenetic regulation of the Master Regulator CIITA is clinically relevant, as aberrant expression of CIITA leads to inappropriate expression of MHC II proteins. [26][27][28] Dysregulated expression of MHC II is associated with various disorders and diseases; in sum, overexpression of MHC II is correlated with autoimmune diseases, while suppression of MHC II expression leads to tumor development and immune deficiency syndromes.…”

Section: O N O T D I S T R I B U T Ementioning

confidence: 99%

Early epigenetic events regulate the adaptive immune response gene CIITA

Mehta¹,

Truax²,

Boyd³

et al. 2011

Epigenetics

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“…In contrast, E-myc tumors express very low levels of MHC II (supplemental Figure 1), consistent with aberrant MHC II expression in many human B-cell malignancies. 40 In this regard, E-myc tumor immunogenicity more closely resembles human B-cell lymphomas than A20 tumors. Similarly, it is unclear why CD8 T cells were critical for inhibition of E-myc but not A20 tumor growth after vaccination, but this may also be explained by the differences in MHC class I expression.…”

mentioning

confidence: 99%

NKT cell adjuvant-based tumor vaccine for treatment of myc oncogene-driven mouse B-cell lymphoma

Mattarollo

West

Steegh

et al. 2012

Blood

121

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Immunomodulators are effective in controlling hematologic malignancy by initiating or reactivating host antitumor immunity to otherwise poorly immunogenic and immune suppressive cancers. We aimed to boost antitumor immunity in B-cell lymphoma by developing a tumor cell vaccine incorporating ␣-galactosylceramide IntroductionHematologic malignancies typically express the necessary machinery for eliciting antitumor immunity, such as costimulatory molecules, yet many tumors are poorly immunogenic. Therapeutic vaccination strategies that incorporate immune adjuvants are likely to enhance immune recognition and targeting of hematologic cancers, an example being in mice vaccinated against mouse lymphomas with whole tumor cells loaded with CpG adjuvant. 1 Natural killer T (NKT) lymphocytes represent an immune regulatory population with recognized capacity for inducing innate (eg, NK cells) and adaptive (eg, CD8 T cell) antitumor immunity, [2][3][4] by their unique ability to rapidly produce large quantities of cytokines on TCR ligation, in particular IFN-␥. 5,6 As a result, the synthetic CD1d-dependent NKT cell ligand ␣-galactosylceramide (␣-GalCer) has been used for its NKT cell-mediated immune adjuvant properties in anticancer therapies. [7][8][9][10] Initial attempts to stimulate NKT cells in situ were to simply infuse soluble ␣-GalCer, which briefly inhibited the tumor growth, but had limited effects on survival. 11,12 In addition, multiple injections of ␣-GalCer led to deleterious effects including long-term NKT cell functional anergy or unresponsiveness. 12 Subsequently, ␣-GalCer was loaded onto dendritic cells (DCs) as a vaccine. This approach induced more potent antitumor effects than soluble ␣-GalCer injections, mainly by prolonging NKT cell IFN-␥ production and preventing induction of NKT cell anergy, and was able to significantly improve the activity of the DC vaccine if coadministered with tumor antigens. 10,13,14 The cumbersome nature of inducing and expanding DC from patients' peripheral blood monocytes for autologous ␣-GalCerpulsed DC therapy stimulated the use of irradiated tumor cells as a vehicle to deliver ␣-GalCer in vivo. [15][16][17] Here a full complement of tumor antigens (including undefined ones) and ␣-GalCer are codelivered, thus allowing generation of innate immunity and potentially long-term tumor-specific T-cell adaptive immunity. In a prophylactic setting, whole tumor cells loaded with ␣-GalCer were able to protect mice against subsequent challenge with live tumor cells 15,16 and were also shown to be partially effective at inhibiting growth of established solid tumors 17 (S.R.M., K.S., M. Li, H.D., S.F. Ngiow, M.J.S., Transient Foxp3 ϩ regulatory T cell depletion enhances therapeutic anticancer vaccination targeting the immunestimulatory properties of NKT cells, manuscript submitted, August 2012), demonstrating the ability of this vaccine to work successfully in a The online version of this article contains a data supplement.The publication costs of this article were defrayed in part by ...

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Expression of MHC class II antigens in human B-cell leukaemia and non-Hodgkin's lymphoma

Cited by 47 publications

References 57 publications

Microarray Analysis of B-Cell Lymphoma Cell Lines with the t(14;18)

Microarray Analysis of B-Cell Lymphoma Cell Lines with the t(14;18)

Early epigenetic events regulate the adaptive immune response gene CIITA

NKT cell adjuvant-based tumor vaccine for treatment of myc oncogene-driven mouse B-cell lymphoma

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