Induction of recipient cell-specific donor T-cell anergy by UV-C-irradiated recipient immature monocyte-derived dendritic cells

Tochiki, Nozomi; Narita, Miwako; Zheng, Zhi; Lu, Chengfang; Saitoh, Anri; Watanabe, Norihiro; Satoh, Noriyuki; Furukawa, Tatsuo; Toba, Kenji; Fuse, Ichiro; Aizawa, Yoshifusa; Takahashi, Miho

doi:10.1038/bmt.2008.28

Cited by 2 publications

(1 citation statement)

References 21 publications

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“…4 SEB stimulation of T-cells lead either to an outburst of cytokines ('cytokine storm' or sepsis), [5][6][7][8][9] cellular anergy or apoptosis depending on the nature of antigen-presenting cells (APCs), secreted cytokines and receptor T-cells. 10 For example, in vivo anergized APCs such as monocytes with suppressed HLA-DR 11 and radiation-exposed dendritic cells 12 shown to form unstable immunological synapses in vitro and failed to initiate T-cell activation leading to T-cell anergy. These findings suggest that anergy in compromised accessory molecules of APCs induces defects in the earliest events of T-cell activation, immunological synapse formation and T-cell receptor (TCR)-mediated signaling.…”

Section: Introductionmentioning

confidence: 98%

Stress-caused anergy of leukocytes towards Staphylococcal enterotoxin B and exposure transcriptome signatures

et al. 2015

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Leucocytes from soldiers exposed to battlefield-like stress (RASP: Rangers Assessment and Selection Program) were exposed in vitro to Staphylococcal enterotoxin B (SEB). We assayed SEB-induced regulation of gene expression, both in the presence and absence of severe stress, to generate two sets of gene profiles. One set of transcripts and microRNAs were specific to post-RASP SEB exposure, and another set were signatures of SEB exposure common to both the pre- and post-RASP leucocytes. Pathways and upstream regulatory analyses indicated that the post-RASP SEB-signature transcripts were manifestation of the anergic state of post-RASP leucocytes. These were further verified using expression-based predictions of cellular processes and literature searches. Specificity of the second set of transcripts to SEB exposure was verified using machine-learning algorithms on our and four other (Gene Expression Omnibus) data sets. Cell adhesion, coagulation, hypoxia and vascular endothelial growth factor-mediated vascular leakage were SEB-specific pathways even under the background of severe stress. Hsa-miR-155-3p was the top SEB exposure predictor in our data set, and C-X-C motif chemokine ligand 9 was SEB specific in all the analyzed data sets. The SEB-signature transcripts (which also showed distinct expression signatures from Yersinia pestis and dengue virus) may serve as potential biomarkers of SEB exposure even under the background of stress.

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