NDLI: Truncated form of TGF-ßRII, but not its absence, induces memory CD8+ T cell expansion and lymphoproliferative disorder in mice.

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Truncated form of TGF-ßRII, but not its absence, induces memory CD8+ T cell expansion and lymphoproliferative disorder in mice.

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What is and what should always have been: long-lived plasma cells induced by T cell-independent antigens.

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Truncated form of TGF-ßRII, but not its absence, induces memory CD8+ T cell expansion and lymphoproliferative disorder in mice.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Sanjabi, Shomyseh Ishigame, Harumichi Mosaheb, Munir M. Flavell, Richard A.
Description	Country affiliation: United States Author Affiliation: Ishigame H ( Department of Immunobiology, Yale University School of Medicine, New Haven, CT 06520, USA.)
Abstract	Inflammatory and anti-inflammatory cytokines play an important role in the generation of effector and memory CD8(+) T cells. We used two different models, transgenic expression of truncated (dominant negative) form of TGF-ßRII (dnTGFßRII) and Cre-mediated deletion of the floxed TGF-ßRII to examine the role of TGF-ß signaling in the formation, function, and homeostatic proliferation of memory CD8(+) T cells. Blocking TGF-ß signaling in effector CD8(+) T cells using both of these models demonstrated a role for TGF-ß in regulating the number of short-lived effector cells but did not alter memory CD8(+) T cell formation and their function upon Listeria monocytogenes infection in mice. Interestingly, however, a massive lymphoproliferative disorder and cellular transformation were observed in Ag-experienced and homeostatically generated memory CD8(+) T cells only in cells that express the dnTGFßRII and not in cells with a complete deletion of TGF-ßRII. Furthermore, the development of transformed memory CD8(+) T cells expressing dnTGFßRII was IL-7- and IL-15-independent, and MHC class I was not required for their proliferation. We show that transgenic expression of the dnTGFßRII, rather than the absence of TGF-ßRII-mediated signaling, is responsible for dysregulated expansion of memory CD8(+) T cells. This study uncovers a previously unrecognized dominant function of the dnTGFßRII in CD8(+) T cell proliferation and cellular transformation, which is caused by a mechanism that is different from the absence of TGF-ß signaling. These results should be considered during both basic and translational studies where there is a desire to block TGF-ß signaling in CD8(+) T cells.
ISSN	00221767
e-ISSN	15506606
DOI	10.4049/jimmunol.1300397
Journal	The Journal of Immunology
Issue Number	12
Volume Number	190
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2013-06-15
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Cd8-positive T-lymphocytes Immunology Immunologic Memory Lymphoproliferative Disorders Protein-serine-threonine Kinases Receptors, Transforming Growth Factor Beta Signal Transduction Adoptive Transfer Animals Metabolism Flow Cytometry Listeriosis Lymphocyte Activation Mice Mice, Inbred C57bl Mice, Transgenic Real-time Polymerase Chain Reaction Reverse Transcriptase Polymerase Chain Reaction Transforming Growth Factor Beta Research Support, Non-u.s. Gov't Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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