TY - JOUR
T1 - Memory Inflation during Chronic Viral Infection Is Maintained by Continuous Production of Short-Lived, Functional T Cells
AU - Snyder, Christopher M.
AU - Cho, Kathy S.
AU - Bonnett, Elizabeth L.
AU - van Dommelen, Serani
AU - Shellam, Geoffrey R.
AU - Hill, Ann B.
N1 - Funding Information:
This work was supported by the National Institutes of Health, grant RO1 A I47206, and the American Foundation for Aging Research (A.B.H.), as well as by a postdoctoral training grant from the American Heart Association (no. 0725786Z) awarded to C.M.S. The authors declare that they have no competing financial interests.
PY - 2008/10/17
Y1 - 2008/10/17
N2 - During persistent murine cytomegalovirus (MCMV) infection, the T cell response is maintained at extremely high intensity for the life of the host. These cells closely resemble human CMV-specific cells, which compose a major component of the peripheral T cell compartment in most people. Despite a phenotype that suggests extensive antigen-driven differentiation, MCMV-specific T cells remain functional and respond vigorously to viral challenge. We hypothesized that a low rate of antigen-driven proliferation would account for the maintenance of this population. Instead, we found that most of these cells divided only sporadically in chronically infected hosts and had a short half-life in circulation. The overall population was supported, at least in part, by memory T cells primed early in infection, as well as by recruitment of naive T cells at late times. Thus, these data show that memory inflation is maintained by a continuous replacement of short-lived, functional cells during chronic MCMV infection.
AB - During persistent murine cytomegalovirus (MCMV) infection, the T cell response is maintained at extremely high intensity for the life of the host. These cells closely resemble human CMV-specific cells, which compose a major component of the peripheral T cell compartment in most people. Despite a phenotype that suggests extensive antigen-driven differentiation, MCMV-specific T cells remain functional and respond vigorously to viral challenge. We hypothesized that a low rate of antigen-driven proliferation would account for the maintenance of this population. Instead, we found that most of these cells divided only sporadically in chronically infected hosts and had a short half-life in circulation. The overall population was supported, at least in part, by memory T cells primed early in infection, as well as by recruitment of naive T cells at late times. Thus, these data show that memory inflation is maintained by a continuous replacement of short-lived, functional cells during chronic MCMV infection.
KW - CELL_IMMUNO
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U2 - 10.1016/j.immuni.2008.07.017
DO - 10.1016/j.immuni.2008.07.017
M3 - Article
C2 - 18957267
AN - SCOPUS:53549106627
SN - 1074-7613
VL - 29
SP - 650
EP - 659
JO - Immunity
JF - Immunity
IS - 4
ER -