Table 1.

Immune modulators and proposed benefits for sepsis-induced apoptosis therapy

Immune modulator	Effects	Reference
G-CSF	Improve neutrophils and monocyte production and release	194
GM-CSF	Activate and induce production of neutrophils and monocytes or macrophages and reduce cell death	195, 196
IFN-γ	Increase monocyte expression of HLA-DR, increase numbers of IL-17 producing CD4+ T cells	197, 198
PD-1/PD-L1	Anti-apoptotic effects to prevent loss of protective function of NK cells Prevent lymphocyte apoptosis and reverse monocyte dysfunction	132, 133, 199, 200
IL-7	Blockade of sepsis-induced apoptosis depletion, increase production of CD4+ T and CD8 T cells Enhance trafficking of T cells to sites of infection	1, 156, 201
IL-15	Restrain sepsis-induced apoptosis of CD8 T cells, NK cells, and DCs	130
Tim-2-specific antibody	Decrease lymphocyte apoptosis and reverse the macrophage function	202, 203
Ulinastatin	Increase apoptotic rate of Treg cells and reduce the percentage through NF-κB pathway, ameliorate mortality	188
CTLA-4-specific antibody	Improve overall sepsis-induced lymphocyte apoptosis and survival of secondary fungal infections	163, 204

G-CSF granulocyte colony-stimulating factor, GM-CSF granulocyte-macrophage colony-stimulating factor, IFN-γ interferon gamma, PD-1 programmed cell death-1, IL interleukin, CTLA-4 cytotoxic T lymphocyte antigen-4