T-cell intrinsic expression of MyD88 is required for sustained expansion of the virus-specific CD8+ T-cell population in LCMV-infected mice
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T-cell intrinsic expression of MyD88 is required for sustained expansion of the virus-specific CD8+ T-cell population in LCMV-infected mice. / Bartholdy, Christina; Christensen, Jeanette Erbo; Grujic, Mirjana; Christensen, Jan P; Thomsen, Allan R.
In: Journal of General Virology, Vol. 90, No. Pt 2, 2009, p. 423-31.Research output: Contribution to journal › Journal article › Research › peer-review
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TY - JOUR
T1 - T-cell intrinsic expression of MyD88 is required for sustained expansion of the virus-specific CD8+ T-cell population in LCMV-infected mice
AU - Bartholdy, Christina
AU - Christensen, Jeanette Erbo
AU - Grujic, Mirjana
AU - Christensen, Jan P
AU - Thomsen, Allan R
PY - 2009
Y1 - 2009
N2 - Acute infection with lymphocytic choriomeningitis virus (LCMV) normally results in robust clonal expansion of virus-specific CD8(+) T cells, which in turn control the primary infection. However, similar infection of myeloid differentiation factor 88 (MyD88)-deficient mice leads to a markedly impaired T-cell response and chronic infection. It has been found previously that impairment of the innate immune response is not sufficient to explain this profound change in outcome. Using adoptive transfer of CD8(+) T cells, this study demonstrated unequivocally that T-cell expression of MyD88 is critical for a normal T-cell response to LCMV. In addition, it was found that expression of MyD88 is superfluous during early activation and proliferation of the antigen-activated CD8(+) T cells, but plays a critical role in the sustained expansion of the antigen-specific CD8(+) T-cell population during the primary T-cell response. Interestingly, a critical role for MyD88 was evident only under conditions of systemic infection with virus capable of causing prolonged infection, suggesting that MyD88 expression may function as an internal regulator of the threshold for antigen-driven, exhaustive differentiation.
AB - Acute infection with lymphocytic choriomeningitis virus (LCMV) normally results in robust clonal expansion of virus-specific CD8(+) T cells, which in turn control the primary infection. However, similar infection of myeloid differentiation factor 88 (MyD88)-deficient mice leads to a markedly impaired T-cell response and chronic infection. It has been found previously that impairment of the innate immune response is not sufficient to explain this profound change in outcome. Using adoptive transfer of CD8(+) T cells, this study demonstrated unequivocally that T-cell expression of MyD88 is critical for a normal T-cell response to LCMV. In addition, it was found that expression of MyD88 is superfluous during early activation and proliferation of the antigen-activated CD8(+) T cells, but plays a critical role in the sustained expansion of the antigen-specific CD8(+) T-cell population during the primary T-cell response. Interestingly, a critical role for MyD88 was evident only under conditions of systemic infection with virus capable of causing prolonged infection, suggesting that MyD88 expression may function as an internal regulator of the threshold for antigen-driven, exhaustive differentiation.
U2 - 10.1099/vir.0.004960-0
DO - 10.1099/vir.0.004960-0
M3 - Journal article
C2 - 19141452
VL - 90
SP - 423
EP - 431
JO - Journal of General Virology
JF - Journal of General Virology
SN - 0022-1317
IS - Pt 2
ER -
ID: 9745744