Dependence of Lymphoma Growth on &amp;lsquo;Reversed Immunological Surveillance&amp;rsquo;

Ponzio, Nicholas M.; Alonso, A. Mateo; Alisauskas, Rita

doi:10.1159/000157038

Cited by 14 publications

(3 citation statements)

References 20 publications

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“…Conversely, limited growth potential displayed by human lymphoma in vitro [323] and in vivo [324] in the absence of growth factors or T cells might suggest that clonal B-cells are probably not capable of autonomous growth, particularly in the earlier stages of lymphomagenesis. The phenomena of B-cell clone accompanied by an abundant infiltration of T cells, mainly CD4 cells, is also observed in the spontaneous follicular lymphomas of the SJL mice [325,326]. It is also shown that the intact immune components of the recipient animals is an absolute requirement for the transplantability and in vivo growth of these lymphoma cells in syngeneic mice [327].…”

Section: Contribution Of T Cells and Other Microenvironmental Factorsmentioning

confidence: 76%

Lymphoma and the Control of B Cell Growth and Differentiation

Goodnow²

2006

CMM

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It is now widely accepted that lymphomagenesis is a multistep transformation process. A number of genetic changes and environmental and infectious factors contributing to the development and malignant progression of B-cell lymphoproliferative disorders are well documented. Reciprocal chromosomal translocations involving the immunoglobulin loci are a hallmark of most mature B cell lymphomas and lead to dysregulated expression of proto-oncogenes (c-myc) important for cell proliferation or genes involved in cell cycle progression (cyclin D1), differentiation block (bcl-6, PAX5) and cell survival (bcl-2, NF-kappaB). In addition, genetic alterations that inactivate tumor suppressor genes (p53, p16) have been frequently detected in some lymphoma tissues. Many of these genes are normally regulated by signals from the B cell antigen receptor. The high prevalence of bacterial and viral infection in lymphoma patients supports the hypothesis that infectious agents may play a contributory role in the development and evolution of B cell lymphoproliferative disorders by either directly inducing polyclonal B cell hyperactivation (EBV, HCV), or providing a chronic antigenic stimulus (EBV, HCV, HBV, H. pylori), or mimicking B cell antigen receptor signaling (EBV, HCV, HHV8), although whether these are causative factors or they are secondary to genetic changes in lymphomagenesis remains to be defined. Stimulatory signals from reactive T cells, local cytokines and growth factors can also contribute, to some extent, to the progression of transformation. Modulation of B cell antigen receptor signaling therefore emerges as a potentially powerful strategy for controlling the growth of certain B cell lymphomas.

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Section: Contribution Of T Cells and Other Microenvironmental Factorsmentioning

confidence: 76%

Lymphoma and the Control of B Cell Growth and Differentiation

Goodnow²

2006

CMM

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“…The response of SJL T cells to RCS is inhibited by anti-I-AS and by anti-CD4 (Brown et al, 1983;Ponzio et al, 1987). Recently, we have shown that the syngeneic T cell response to RCS is exhibited primarily by V,316-bearing T cells (Tsiagbe et al, 1993), suggesting that this is a superantigen-like response, resembling the response to Mlslike determinants.…”

Section: Introductionmentioning

confidence: 94%

Linkage of superantigen-like stimulation of syngeneic T cells in a mouse model of follicular center B cell lymphoma to transcription of endogenous mammary tumor virus.

et al. 1993

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The MHC class II I‐A(s) positive B cell lymphomas reticulum cell sarcoma (RCS) that arise in > 90% of SJL mice by the age of 12 months have superantigen‐like stimulating properties. In the present study, therefore, RCS cell lines were examined for abnormal expression of endogenous mouse mammary tumor virus (MMTV) proviruses. Extraordinarily high expression of a 1.8 kb mRNA hybridizing with the long terminal repeat (LTR) of MMTV was found in both primary lymphomas and in vitro RCS lines, but not in an SJL B cell lymphoma, NJ101, that does not stimulate syngeneic T cells, or in LPS activated SJL B cells. A cDNA was cloned from cRCS‐2 and sequenced. A 31mer oligonucleotide probe, prepared based on the unique C‐terminal sequence of this RCS‐Mtv LTR, detected the 1.8 kb mRNA in all RCS lymphomas, while a similar probe for the C‐terminal sequence of Mtv‐8 LTR hybridized with the larger mRNA present in normal B cells and in NJ101. Preincubation with 19mer antisense S‐oligonucleotides, prepared based on the sequences of the first two potential translation initiation sites common to both Mtv‐8 and the RCS‐Mtv LTR, significantly reduced the ability of RCS cells to stimulate syngeneic T cells. Moreover, transfection of NJ101 cells with the cloned RCS‐MMTV cDNA conferred V beta 16 T cell stimulating properties on to these cells. It is concluded that expression of the product of this MMTV‐LTR mRNA provides RCS with the strong T cell stimulating properties that it needs for its growth. These results thus identify a novel oncogenic property of MMTV‐LTR.

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“…This is particularly true for the I-E ϩ MA/My mice, where V␤16 ϩ T cells (our unpublished observation), in addition to V␤5.1 ϩ , V␤11 ϩ , and V␤12 ϩ T cells, are deleted. Moreover, although the need for CD4 T cells in promoting in vivo growth of SJL and C57L lymphomas was clearly established in previous studies (7,20,25,37), this information is not yet available for the MA/My or the SW ϫ J-1 lymphomas studied here.…”

Section: Discussionmentioning

confidence: 79%

META-Controlled env-Initiated Transcripts Encoding Superantigens of Murine Mtv29 and Mtv7 and Their Possible Role in B Cell Lymphomagenesis

Sen

Simmons²,

Thomas

et al. 2001

The Journal of Immunology

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Spontaneous germinal center (GC)-derived B cell lymphomas of SJL mice (RCS) transcribe a 1.8-kb Mtv-29 mRNA under control of the META-env promoter. The encoded vSAg29 stimulates syngeneic Vβ16+ CD4+ T cells, thereby acquiring T cell help necessary for RCS growth. Other strains of B cell lymphoma-prone mice include Mtv29+ C57L and MA/MyJ, and the Mtv29− Mtv7+-recombinant inbred strain, SW × J-1. The lymphomas of these mice produce similar mouse mtv-vSAg-encoding mRNA, as characterized by Northern blotting, PCR, and RNase protection. A 1.8-kb mRNA in C57L/J and MA/MyJ lymphomas hybridized with an Mtv29-specific oligonucleotide, whereas SW × J-1 lymphomas produced 1.8-kb transcripts hybridizing with an Mtv7-specific oligonucleotide. Similar META-env-initiated transcripts were absent from LPS-activated B cells from any strain examined but were detected in Peyer’s patch RNA from SJL mice. Like typical SJL-derived RCS, all these lymphomas stimulated syngeneic CD4+ T cells and Vβ16+ T hybridoma cells. Immunohistochemical staining of primary tumors showed the presence of peanut agglutinin binding (PNA+) highly mitotic lymphoblasts, suggesting their GC derivation. The findings indicate that this novel mRNA for Mtv29 is present in B cell lymphomas from several Mtv29+ mouse strains. Additionally, this is the first description of the ability of Mtv7 to produce transcripts that are controlled and spliced identically to those of Mtv29 and that are expressed in SW × J-1, I-As+, lymphomas that also stimulate Vβ16+ T cells. Our results suggest an important role for mouse mtv-vSAgs and Vβ16 T cell stimulation in the development of GC-derived murine B cell lymphomas.

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Dependence of Lymphoma Growth on ‘Reversed Immunological Surveillance’

Cited by 14 publications

References 20 publications

Lymphoma and the Control of B Cell Growth and Differentiation

Lymphoma and the Control of B Cell Growth and Differentiation

Linkage of superantigen-like stimulation of syngeneic T cells in a mouse model of follicular center B cell lymphoma to transcription of endogenous mammary tumor virus.

META-Controlled env-Initiated Transcripts Encoding Superantigens of Murine Mtv29 and Mtv7 and Their Possible Role in B Cell Lymphomagenesis

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