scholarly journals Intestinal Immune System and Amplification of Mouse Mammary Tumor Virus

2022 ◽  
Vol 11 ◽  
Author(s):  
Lankai Chen ◽  
Xipeng Zhang ◽  
Guisheng Liu ◽  
Shuo Chen ◽  
Minying Zheng ◽  
...  
Keyword(s):  
Breast Cancer ◽  
T Cells ◽  
Mammary Tumor ◽  
Mouse Mammary Tumor Virus ◽  
Mammary Tumor Virus ◽  
Source Of Infection ◽  
Mouse Mammary Tumor ◽  
Intestinal Immune System ◽  
Tumor Virus

Mouse mammary tumor virus (MMTV) is a virus that induces breast cancer in mice. During lactation, MMTV can transmit from mother to offspring through milk, and Peyer’s patches (PPs) in mouse intestine are the first and specific target organ. MMTV can be transported into PPs by microfold cells and then activate antigen-presenting cells (APCs) by directly binding with Toll-like receptors (TLRs) whereas infect them through mouse transferrin receptor 1 (mTfR1). After being endocytosed, MMTV is reversely transcribed and the cDNA inserts into the host genome. Superantigen (SAg) expressed by provirus is presented by APCs to cognate CD4+ T cells via MHCII molecules to induce SAg response, which leads to substantial proliferation and recruitment of related immune cells. Both APCs and T cells can be infected by MMTV and these extensively proliferated lymphocytes and recruited dendritic cells act as hotbeds for viral replication and amplification. In this case, intestinal lymphatic tissues can actually become the source of infection for the transmission of MMTV in vivo, which results in mammary gland infection by MMTV and eventually lead to the occurrence of breast cancer.

scholarly journals Heregulin Co-opts PR Transcriptional Action Via Stat3 Role As a Coregulator to Drive Cancer Growth

2015 ◽  
Vol 29 (10) ◽  
pp. 1468-1485 ◽  
Author(s):  
Cecilia J. Proietti ◽  
Franco Izzo ◽  
María Celeste Díaz Flaqué ◽  
Rosalía Cordo Russo ◽  
Leandro Venturutti ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Signaling Pathways ◽  
Mammary Tumor ◽  
Mouse Mammary Tumor Virus ◽  
Cancer Growth ◽  
Mammary Tumor Virus ◽  
Mouse Mammary Tumor ◽  
Tumor Virus ◽  
Virus Promoter

Abstract Accumulated findings have demonstrated the presence of bidirectional interactions between progesterone receptor (PR) and the ErbB family of receptor tyrosine kinases signaling pathways in breast cancer. We previously revealed signal transducer and activator of transcription 3 (Stat3) as a nodal convergence point between said signaling pathways proving that Stat3 is activated by one of the ErbBs' ligands, heregulin (HRG)β1 via ErbB2 and through the co-option of PR as a signaling molecule. Here, we found that HRGβ1 induced Stat3 recruitment to the promoters of the progestin-regulated cell cycle modulators Bcl-XL and p21CIP1 and also stimulated Stat3 binding to the mouse mammary tumor virus promoter, which carries consensus progesterone response elements. Interestingly, HRGβ1-activated Stat3 displayed differential functions on PR activity depending on the promoter bound. Indeed, Stat3 was required for PR binding in bcl-X, p21CIP1, and c-myc promoters while exerting a PR coactivator function on the mouse mammary tumor virus promoter. Stat3 also proved to be necessary for HRGβ1-induced in vivo tumor growth. Our results endow Stat3 a novel function as a coregulator of HRGβ1-activated PR to promote breast cancer growth. These findings underscore the importance of understanding the complex interactions between PR and other regulatory factors, such as Stat3, that contribute to determine the context-dependent transcriptional actions of PR.

scholarly journals Peripheral T cell activation and deletion induced by transfer of lymphocyte subsets expressing endogenous or exogenous mouse mammary tumor virus.

1993 ◽  
Vol 177 (5) ◽  
pp. 1359-1366 ◽  
Author(s):  
G A Waanders ◽  
A N Shakhov ◽  
W Held ◽  
O Karapetian ◽  
H Acha-Orbea ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
Mammary Tumor ◽  
Mouse Mammary Tumor Virus ◽  
Lymphocyte Subsets ◽  
Mammary Tumor Virus ◽  
Mouse Mammary Tumor ◽  
Tumor Virus ◽  
Cell Deletion

Murine T cell reactivity with products of the minor lymphocyte stimulatory (Mls) locus correlates with the expression of particular variable (V) domains of the T cell receptor (TCR) beta chain. It was recently demonstrated that Mls antigens are encoded by an open reading frame (ORF) in the 3' long terminal repeat of either endogenous or exogenous mouse mammary tumor virus (MMTV). Immature thymocytes expressing reactive TCR-V beta domains are clonally deleted upon exposure to endogenous Mtv's. Mature T cells proliferate vigorously in response to Mls-1a (Mtv-7) in vivo, but induction of specific anergy and deletion after exposure to Mtv-7-expressing cells in the periphery has also been described. We show here that B cells and CD8+ (but not CD4+) T cells from Mtv-7+ mice efficiently induce peripheral deletion of reactive T cells upon transfer to Mtv-7- recipients, whereas only B cells stimulate specific T cell proliferation in vivo. In contrast to endogenous Mtv-7, transfer of B, CD4+, or CD8+ lymphocyte subsets from mice maternally infected with MMTV(SW), an infectious homologue of Mtv-7, results in specific T cell deletion in the absence of a detectable proliferative response. Finally, we show by secondary transfers of infected cells that exogenous MMTV(SW) is transmitted multidirectionally between lymphocyte subsets and ultimately to the mammary gland. Collectively our data demonstrate heterogeneity in the expression and/or presentation of endogenous and exogenous MMTV ORF by lymphocyte subsets and emphasize the low threshold required for induction of peripheral T cell deletion by these gene products.

scholarly journals Nucleosome-mediated disruption of transcription factor-chromatin initiation complexes at the mouse mammary tumor virus long terminal repeat in vivo.

1994 ◽  
Vol 14 (1) ◽  
pp. 32-41 ◽  
Author(s):  
H L Lee ◽  
T K Archer
Keyword(s):  
Mammary Tumor ◽  
Dna Sequences ◽  
Mouse Mammary Tumor Virus ◽  
Binding Protein ◽  
Tata Binding Protein ◽  
Mammary Tumor Virus ◽  
Mouse Mammary Tumor ◽  
Tumor Virus ◽  
Nuclear Factor 1

Glucocorticoid induction of mouse mammary tumor virus (MMTV) is short lived, returning to base levels within 24 h despite the continued presence of hormone. MMTV DNA sequences assembled as chromatin require hormone for binding by nuclear factor 1 (NF1) and octamer proteins (OCT). However, in the same cells, NF1 and OCT factors are bound to transiently introduced DNA in the absence of hormone. In contrast, recruitment of the TATA-binding protein and a novel DNA-binding protein, which we have designated FDT, for factor downstream of the TATA-binding protein, is hormone dependent for both stable and transient templates. Furthermore, transient DNA templates, but not nucleosomal templates, retain these transcription factors over the course of 24 h. This finding suggests that MMTV chromatin structure contributes to activation and cessation of transcription in vivo.

A Mouse Mammary Tumor Virus-Like Long Terminal Repeat Superantigen in Human Breast Cancer

2004 ◽  
Vol 64 (12) ◽  
pp. 4105-4111 ◽  
Author(s):  
Yue Wang ◽  
Jian-Dong Jiang ◽  
Dongping Xu ◽  
Yan Li ◽  
Chunfeng Qu ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Long Terminal Repeat ◽  
Mammary Tumor ◽  
Mouse Mammary Tumor Virus ◽  
Human Breast Cancer ◽  
Terminal Repeat ◽  
Human Breast ◽  
Mammary Tumor Virus ◽  
Mouse Mammary Tumor ◽  
Tumor Virus

scholarly journals Bone marrow stromal cell antigen 2 (BST-2) restricts mouse mammary tumor virus (MMTV) replication in vivo

Retrovirology ◽  
2012 ◽  
Vol 9 (1) ◽  
pp. 10 ◽  
Author(s):  
Philip H Jones ◽  
Harshini V Mehta ◽  
Martina Maric ◽  
Richard J Roller ◽  
Chioma M Okeoma
Keyword(s):  
Bone Marrow ◽  
Mammary Tumor ◽  
Mouse Mammary Tumor Virus ◽  
Stromal Cell ◽  
Bone Marrow Stromal Cell ◽  
Mammary Tumor Virus ◽  
Marrow Stromal Cell ◽  
Mouse Mammary Tumor ◽  
Tumor Virus

scholarly journals A Novel Block to Mouse Mammary Tumor Virus Infection of Lymphocytes in B10.BR Mice

2007 ◽  
Vol 82 (3) ◽  
pp. 1314-1322 ◽  
Author(s):  
Chioma M. Okeoma ◽  
Ming Shen ◽  
Susan R. Ross
Keyword(s):  
T Cells ◽  
T Cell ◽  
Mammary Tumor ◽  
Mouse Mammary Tumor Virus ◽  
Cell Activation ◽  
Mouse Strains ◽  
Mammary Tumor Virus ◽  
Mouse Mammary Tumor ◽  
Tumor Virus ◽  
Mhc Locus

ABSTRACT Classic studies on C57BL-derived mouse strains showed that they were resistant to mouse mammary tumor virus (MMTV) infection. Although one form of resistance mapped to the major histocompatibility complex (MHC) locus, at least one other, unknown gene was implicated in this resistance. We show here that B10.BR mice, which are derived from C57BL mice but have the same MHC locus (H-2 k ) as susceptible C3H/HeN mice, are resistant to MMTV, and show a lack of virus spread in their lymphoid compartments but not their mammary epithelial cells. Although in vivo virus superantigen (Sag)-mediated activation of T cells was similar in C3H/HeN and B10.BR mice, T cell-dependent B-cell and dendritic cell activation was diminished in the latter. Ex vivo, B10.BR T cells showed a diminished capacity to proliferate in response to the MMTV Sag. The genetic segregation of the resistance phenotype indicated that it maps to a single allele. These data highlight the role of Sag-dependent T-cell responses in MMTV infection and point to a novel mechanism for the resistance of mice to retroviral infection that could lead to a better understanding of the interplay between hosts and pathogens.

scholarly journals No association between Epstein-Barr Virus and Mouse Mammary Tumor Virus with Breast Cancer in Mexican Women

2013 ◽  
Vol 3 (1) ◽  
Author(s):  
Abigail Morales-Sánchez ◽  
Tzindilú Molina-Muñoz ◽  
Juan L. E. Martínez-López ◽  
Paulina Hernández-Sancén ◽  
Alejandra Mantilla ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Mammary Tumor ◽  
Mouse Mammary Tumor Virus ◽  
Epstein Barr Virus ◽  
Mexican Women ◽  
Mammary Tumor Virus ◽  
Barr Virus ◽  
Mouse Mammary Tumor ◽  
Tumor Virus ◽  
Epstein Barr

Increased incidence of mouse mammary tumor virus-related antigen in tunisian patients with breast cancer

1984 ◽  
Vol 33 (3) ◽  
pp. 305-308 ◽  
Author(s):  
P. H. Levine ◽  
R. Mesa-Tejada ◽  
I. Keydar ◽  
F. Tabbane ◽  
S. Spiefelman ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Mammary Tumor ◽  
Mouse Mammary Tumor Virus ◽  
Mammary Tumor Virus ◽  
Mouse Mammary Tumor ◽  
Tunisian Patients ◽  
Tumor Virus
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