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Title: Myeloid Cell Arg1 Inhibits Control of Arthritogenic Alphavirus Infection by Suppressing Antiviral T Cells
Authors: Burrack K.S.
Tan J.J.L.
McCarthy M.K.
Her Z.
Berger J.N.
Ng L.F.P. 
Morrison T.E.
Keywords: alpha interferon
beta interferon
C reactive protein
gamma interferon inducible protein 10
interleukin 10
interleukin 6
Arg1 protein, mouse
arginase I, human
Alphavirus infection
animal cell
animal experiment
animal model
animal tissue
arthritogenic alphaviral infection
bone marrow cell
controlled study
flow cytometry
gene expression
polymerase chain reaction
real time polymerase chain reaction
reverse transcription polymerase chain reaction
RNA isolation
T cell depletion
T lymphocyte
transcription regulation
virus immunity
virus isolation
virus load
Western blotting
adoptive transfer
Alphavirus infection
bone marrow cell
C57BL mouse
Chikungunya virus
lymphocyte activation
Ross River virus
Adoptive Transfer
Alphavirus Infections
Blotting, Western
Chikungunya Fever
Chikungunya virus
Flow Cytometry
Lymphocyte Activation
Mice, Inbred C57BL
Myeloid Cells
Polymerase Chain Reaction
Ross River virus
Viral Load
Issue Date: 2015
Citation: Burrack K.S., Tan J.J.L., McCarthy M.K., Her Z., Berger J.N., Ng L.F.P., Morrison T.E. (2015). Myeloid Cell Arg1 Inhibits Control of Arthritogenic Alphavirus Infection by Suppressing Antiviral T Cells. PLoS Pathogens 11 (10) : e1005191. ScholarBank@NUS Repository.
Rights: Attribution 4.0 International
Abstract: Arthritogenic alphaviruses, including Ross River virus (RRV) and chikungunya virus (CHIKV), are responsible for explosive epidemics involving millions of cases. These mosquito-transmitted viruses cause inflammation and injury in skeletal muscle and joint tissues that results in debilitating pain. We previously showed that arginase 1 (Arg1) was highly expressed in myeloid cells in the infected and inflamed musculoskeletal tissues of RRV- and CHIKV-infected mice, and specific deletion of Arg1 from myeloid cells resulted in enhanced viral control. Here, we show that Arg1, along with other genes associated with suppressive myeloid cells, is induced in PBMCs isolated from CHIKV-infected patients during the acute phase as well as the chronic phase, and that high Arg1 expression levels were associated with high viral loads and disease severity. Depletion of both CD4 and CD8 T cells from RRV-infected Arg1-deficient mice restored viral loads to levels detected in T cell-depleted wild-type mice. Moreover, Arg1-expressing myeloid cells inhibited virus-specific T cells in the inflamed and infected musculoskeletal tissues, but not lymphoid tissues, following RRV infection in mice, including suppression of interferon-? and CD69 expression. Collectively, these data enhance our understanding of the immune response following arthritogenic alphavirus infection and suggest that immunosuppressive myeloid cells may contribute to the duration or severity of these debilitating infections. ? 2015 Burrack et al.
Source Title: PLoS Pathogens
ISSN: 15537366
DOI: 10.1371/journal.ppat.1005191
Rights: Attribution 4.0 International
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