In:
The Journal of Immunology, The American Association of Immunologists, Vol. 198, No. 1_Supplement ( 2017-05-01), p. 124.14-124.14
Abstract:
Transcription of IL-1β activity has been extensively studied in stimulated myeloid cells, but not in lymphoid-derived CD4 T cells, the primary cellular target for infection by HIV. Most CCR5+ CD4 T cells in lymphoid tissues are non-permissive for productive HIV infection and die by Caspase-1-mediated pyroptosis, in which proInterleukin 1β (proIL-1β) precursor is converted to highly active mature IL-1β. It is unclear whether expression of proIL-1β protein in CCR5+ CD4 T cells is derived from active transcription of the IL1B gene, or from previously transcribed mRNA and/or stored protein. Our results reveal that despite very low amounts of IL1B mRNA, CCR5+ CD4 T cells accumulate intracellular proIL-1β protein at levels higher than that of both unstimulated myeloid THP-1 cells and CCR5− CD4 T cells. Further, we observe that the chromatin from CCR5+, but not CCR5− CD4 T cells, contain RNA polymerase II and bivalent H3K4me3 and H3K27me3 nucleosomes at the IL1B promoter, consistent with developmentally regulated constitutive gene expression. This observation contrasts with the rapidly activated and extremely robust H3K4me3 monovalent IL1B gene promoter in TLR4-activated monocytes. This unique phenomenon of CCR5+ CD4 T cells is important to understanding how non-myeloid lineage cells express and release significant levels of IL-1β in the apparent absence of transcription induction.
Type of Medium:
Online Resource
ISSN:
0022-1767
,
1550-6606
DOI:
10.4049/jimmunol.198.Supp.124.14
Language:
English
Publisher:
The American Association of Immunologists
Publication Date:
2017
detail.hit.zdb_id:
1475085-5
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