Superantigen-induced immune stimulation amplifies mouse mammary tumor virus infection and allows virus transmission

Held, Werner; Waanders, Gary A.; Shakhov, Alexander N.; Scarpellino, Léonardo; Acha‐Orbea, Hans; MacDonald, H. Robson

doi:10.1016/0092-8674(93)80054-i

Cited by 173 publications

(187 citation statements)

References 51 publications

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“…MMTV is known to replicate in B-and T-lymphoid cells during the transmission of virus from mother's milk in the newborn murine gut to target epithelial cells in the mammary gland (9,24,29). We have shown previously that MMTV expression is repressed by the homeodomain protein SATB1, and we have proposed that SATB1 restricts MMTV expression in many tissues other than the mammary gland, particularly T cells (40,41).…”

Section: Fig 8 Stable Transfections Of Mmtv Ltr-reporter Gene Constmentioning

confidence: 99%

CDP Is a Repressor of Mouse Mammary Tumor Virus Expression in the Mammary Gland

Zhu

Gregg

Lozano

et al. 2000

J Virol

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Section: Fig 8 Stable Transfections Of Mmtv Ltr-reporter Gene Constmentioning

confidence: 99%

CDP Is a Repressor of Mouse Mammary Tumor Virus Expression in the Mammary Gland

Zhu

Gregg

Lozano

et al. 2000

J Virol

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“…Several naturally MMTV-resistant mouse strains have been described. Expression of an endogenous Mtv-SAg in the thymus and periphery leads to deletion of the SAg-reactive T cells and therefore prevents amplification of virus-infected B cells and chronic infection (29,30). A second genetic mechanism of protection is the lack of expression of I-E molecules because I-A molecules are unable to efficiently present several MMTV SAg (10).…”

Section: Viral Infection and Tumor Development In The Absence Of Neutmentioning

confidence: 99%

The role of neutralizing antibodies for mouse mammary tumor virus transmission and mammary cancer development

Finke

Luther²,

Acha‐Orbea³

2002

Proc. Natl. Acad. Sci. U.S.A.

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Mouse mammary tumor virus (MMTV) infection establishes chronic germinal centers and a lifelong neutralizing Ab response. We show that removal of the draining lymph node after establishment of the germinal center reaction led to complete loss of neutralizing Abs despite comparable infection levels in peripheral lymphocytes. Importantly, in the absence of neutralization, only the exocrine organs mammary gland, salivary gland, pancreas, and skin showed strikingly increased infection, resulting in accelerated mammary tumor development. Induction of stronger neutralization did not influence chronic infection levels of peripheral lymphoid organs but strongly inhibited mammary gland infection and virus transmission to the next generation. Taken together, we provide evidence that a tight equilibrium in virus neutralization allows limited infection of exocrine organs and controls cancer development in susceptible mouse strains. These experiments show that a strong neutralizing Ab response induced after infection is not able to control lymphoid MMTV infection. Strong neutralization, however, is capable of blocking amplification of mammary gland infection, tumor development, and virus transmission to the next generation. The results also indicate a role of neutralization in natural resistance to MMTV infection.

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“…Mtv-6, -8, and -9 were detected by PCR of tail DNA (35). Mtv-7 was detected by Southern blot analysis of tail DNA, as described elsewhere (33).…”

Section: Pcr and Southern Blottingmentioning

confidence: 99%

Requirement for a Complex Array of Costimulators in the Negative Selection of Autoreactive Thymocytes In Vivo

Page

2001

The Journal of Immunology

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Autoreactive thymocytes can be deleted at an immature stage of their development by Ag-induced apoptosis or negative selection. In addition to Ag, negative selection also requires costimulatory signals from APC. We recently used a fetal thymus organ culture system to show that CD5, CD28, and TNF cooperatively regulate deletion of autoreactive thymocytes. Although these experiments provided strong evidence for the action of several costimulators in negative selection, we wished to demonstrate a role for these molecules in a physiologically natural model where thymocytes are deleted in vivo by endogenously expressed Ags. Accordingly, we examined thymocyte deletion in costimulator-null mice in three models of autoantigen-induced negative selection. We compared CD5−/− CD28−/− mice to CD40L−/− mice, which exhibited a profound block in negative selection in all three systems. Surprisingly, only one of the three models revealed a requirement for the CD5 and CD28 costimulators in autoantigen-induced deletion. These results suggest that an extraordinarily complex array of costimulators is involved in negative selection. We predict that different sets of costimulators will be required depending on the timing of negative selection, the Ag, the signal strength, the APC, and whether Ag presentation occurs on class I or class II MHC molecules.

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Superantigen-induced immune stimulation amplifies mouse mammary tumor virus infection and allows virus transmission

Cited by 173 publications

References 51 publications

CDP Is a Repressor of Mouse Mammary Tumor Virus Expression in the Mammary Gland

CDP Is a Repressor of Mouse Mammary Tumor Virus Expression in the Mammary Gland

The role of neutralizing antibodies for mouse mammary tumor virus transmission and mammary cancer development

Requirement for a Complex Array of Costimulators in the Negative Selection of Autoreactive Thymocytes In Vivo

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