HuR regulates Th17 cell and Th1-like Th17 cell differentiation.
HuR directly and indirectly modulates expression of RUNX1 and RORt, respectively.
Targeting HuR by its inhibitor reduces severity of autoimmune neuroinflammation.
Myeloid cells are the dominant cell type expressing DNase1L3 in human blood cells.
Homeostatic stimuli may be a key driver of DNase1L3 production in myeloid cells.
Monocytes from MDS patients display low phagocytic activity.
MDS monocyte-derived DCs show morphological alterations and low expression of HLA-DR.
Monocytes from MDS patients downregulate genes that trigger immune responses.
Free ISG15 causes tissue alert in the skin upon therapeutic vaccination in mice.
Free ISG15 is a potent adjuvant for the CTL response, acting, in part, via NK cells.
Free ISG15 function in mice requires amino acids defining ligand function in humans.
SCFβ-TrCP E3 ubiquitin ligase governs TIPE2 protein stability.
TAK1 phosphorylates Ser3 to trigger TIPE2 for ubiquitination and degradation.
The amount of TIPE2 determines the strength of LPS-induced signaling.
TLR stimulation of B cells into Ig-secreting plasma cells requires NOX-dependent ROS.
The high secretion of IgG per cell results in excessive ROS-dependent ER stress.
NAC selectively inhibits the secretion of IgG and not that of IgM.
The chromatin modifying BAP complex regulates Drosophila immune mechanisms.
Transcriptome analysis of osa RNAi flies indicates a role for Osa in metabolism.
Osa negatively regulates immunity and enhances expression of metabolic genes.
ADAR1 depletion from early developmental stages impairs T cell development in mice.
Concurrent MDA5 deletion partially ameliorates aberrant thymocyte development.
The RNA-editing–independent function of ADAR1 is required for early T cell development.
RhCMV/HBV vectors engender MHC-E–restricted CD8+ T cell responses in RM.
HD and RM PH express MHC-E.
PH present HBV Ag to MHC-E–restricted CD8+ T cells from RhCMV/HBV-inoculated RM.
IL-10 antagonizes IL-17 in determining clinical disease phenotypes of periodontitis.
IL-10 dampens an IL-17–mediated inflammatory response in innate immune cells.
Bone loss in Il10–/– mice is associated with an M1-skewing macrophage phenotype.
