Particularly prominent in the RNA - Seq analysis was the up - regulation of a number
of granzymes, a group of proteinases secreted by immune cells that were originally thought to be involved in killing (via apoptosis) virus infected cells or other target cells.
Further, although we could detect enhancement
of granzyme B production in DKO T cells relative to WT, DGKζ − / −, or Cbl - b − / − T cells at early time points (Fig. 3B, upper panels), we did not observe enhanced granzyme B production in DKO relative to DGKζ − / − or Cbl - b − / − T cells at later time points (Fig. 3B, lower panels), at higher or lower concentrations of anti-CD3 Ab, or with addition of anti-CD28 Ab (Supplemental Fig. 2B).
Deletion of DGKζ or Cbl - b comparably enhanced CD8 + T cell functional responses, such as proliferation, production of IFN - γ, and generation
of granzyme B when compared with wild type T cells.
Not exact matches
Not only do controllers have more CD8 T cells, each cell produces greater quantities
of perforin and
granzymes, which stimulate apoptosis, or cell death.
Lieberman, Dotiwala and their team were particularly struck by how much the
granzyme - sparked cascade resembles apoptosis, a controlled form
of cellular suicide that helps eliminate damaged or potentially cancerous cells.
They kill cells by releasing small cytoplasmic granules
of proteins called perforin and
granzyme that cause the target cell to die by apoptosis (programmed cell death).
Perforin pores in the endosomal membrane trigger the release
of endocytosed
granzyme B into the cytosol
of target cells.
(C) Intracellular
granzyme B was measured from purified T cells gated from CD8 + populations after 24 and 72 h
of stimulation with 0.3 μg / ml anti-CD3 stimulation.