Transcriptomic analysis of NFAT5- deficient macrophages revealed the molecular networks defining cell survival and proliferation.

An in vitro functional study demonstrated that NFAT5- deficient macrophages were more susceptible to apoptotic death.

Surprisingly, Syk- deficient macrophages were impaired in the ability to survive or proliferate on plastic petri dishes.

Passive adoptive transfer of NFATc3 deficient macrophages conferred protection against LPS induced ALI in wild type mice.

Our in vitro studies demonstrate that MCMV replicates to dramatically higher titers in Tyk2- deficient macrophages compared with wild-type cells.

In vitamin D- deficient macrophages, activation of ER stress increased adhesion and adhesion molecule expression and induced an M2-predominant phenotype.

In a flow cytometry-based phagocytic assay, uPAR- deficient macrophages displayed significant defect in internalization but not tethering of apoptotic cells.

Studies using STAT6- deficient macrophages indicated that the increase in IGF-I expression was dependent on STAT6.

Mechanistic studies revealed that CaMKIIγ- deficient macrophages and atherosclerotic lesions lacking myeloid CaMKIIγ had increased expression of the transcription factor ATF6.

Analysis of mammary glands from mice with STAT5- deficient macrophages demonstrates delayed ductal elongation, enhanced ductal branching and increased epithelial proliferation.

Blockade of glycolysis normalizes the differential expression of pro-inflammatory cytokines between control and SLC37A2 deficient macrophages.

We identified a number of cytokines and chemokines that were differentially expressed in wild type versus NOD2- deficient macrophages in response to gonococcal infection.

Coculture with WT peritoneal macrophages significantly increased proliferation of MCA205 cells but decreased in the presence of CD163- deficient macrophages.

Moreover, after intra-articular injection, NFAT5- deficient macrophages were more susceptible to apoptosis and less efficient at promoting joint destruction than were NFAT5-sufficient macrophages.

While TLR9 expression was not altered, the intensity of internalized CpG DNA was increased in CCR4- deficient macrophages when compared to WT macrophages.