NDLI: Cutting edge: Asymmetric memory T cell division in response to rechallenge.

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Cutting edge: Asymmetric memory T cell division in response to rechallenge.

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Cutting edge: Asymmetric memory T cell division in response to rechallenge.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Burkhardt, Janis K. Reiner, Steven L. Barnett, Burton E. Ciocca, Maria L. Chang, John T.
Description	Country affiliation: United States Author Affiliation: Ciocca ML ( Abramson Family Cancer Research Institute, University of Pennsylvania, Philadelphia, PA 19104, USA.)
Abstract	Clonal selection of a T cell for use in the immune response appears to necessitate proliferative expansion and terminal effector differentiation of some cellular progeny, while reserving other progeny as less-differentiated memory cells. It has been suggested that asymmetric cell division may promote initial cell diversification. Stem cell-like models of adaptive immunity might predict that subsequent encounters with a pathogen would evoke reiterative, self-renewing, asymmetric division by memory T cells. In this study, we show that murine memory CD8(+) T cells can divide asymmetrically in response to secondary encounter with pathogen. Critical regulators of signaling and transcription are partitioned to one side of the mitotic spindle in rechallenged memory T cells, and two phenotypically distinct populations of daughter cells are evident from the earliest divisions. Memory T cells may thus use asymmetric cell division to generate cellular heterogeneity when faced with pathogen rechallenge.
ISSN	00221767
e-ISSN	15506606
DOI	10.4049/jimmunol.1200176
Journal	The Journal of Immunology
Issue Number	9
Volume Number	188
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2012-05-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Cd8-positive T-lymphocytes Immunology Cell Division Immunologic Memory Lymphocytic Choriomeningitis Lymphocytic Choriomeningitis Virus Signal Transduction Animals Genetics Mice Mice, Transgenic Transcription, Genetic Research Support, N.i.h., Extramural Research Support, Non-u.s. Gov't Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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Cutting edge: Expression of FcÎ³RIIB tempers memory CD8 T cell function in vivo.

Protein energy malnutrition impairs homeostatic proliferation of memory CD8 T cells.

FoxO1 controls effector-to-memory transition and maintenance of functional CD8 T cell memory.

Cutting edge: resident memory CD8 T cells occupy frontline niches in secondary lymphoid organs.

Differential T cell responses to residual viral antigen prolong CD4+ T cell contraction following the resolution of infection.

MyD88 plays a critical T cell-intrinsic role in supporting CD8 T cell expansion during acute lymphocytic choriomeningitis virus infection.

B cell depletion curtails CD4+ T cell memory and reduces protection against disseminating virus infection.

Disparate roles for STAT5 in primary and secondary CTL responses.

CD8+ memory T cells appear exhausted within hours of acute virus infection.

Cutting edge: Asymmetric memory T cell division in response to rechallenge.

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Cutting edge: Expression of FcÎ³RIIB tempers memory CD8 T cell function in vivo.

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FoxO1 controls effector-to-memory transition and maintenance of functional CD8 T cell memory.

Cutting edge: resident memory CD8 T cells occupy frontline niches in secondary lymphoid organs.

Differential T cell responses to residual viral antigen prolong CD4+ T cell contraction following the resolution of infection.

MyD88 plays a critical T cell-intrinsic role in supporting CD8 T cell expansion during acute lymphocytic choriomeningitis virus infection.

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CD8+ memory T cells appear exhausted within hours of acute virus infection.

Cutting edge: Asymmetric memory T cell division in response to rechallenge.