One of the key cell types behind both the acute and resolution phase of inflammation is the macrophage. However, the roles and functions of macrophages are diverse and sometimes opposing in different phases of inflammation. This contradiction was addressed by the M1/M2 macrophage polarization paradigm, which explains that macrophages are plastic, heterogenous and represent various, functionally diverse phenotypes. Nuclear receptor PPARγ is part of the Peroxisome Proliferator-activated Receptor subfamily, and has been known as a key regulator of lipid metabolism. Recent findings connected PPARγ to the M2/alternative activation pathway of macrophages. Our hypothesis is that the development and function of the M2 cellular phenotype at the gene expression level is mediated be the lipid ligand inducible (PPARγ) and lineage specific (RXRα) transcription factors. Our goal is focused around the identification of the network of cistromic and transcriptional interactions and key effectors that determine the M2 cellular immunophenotype in human macrophages. For our experiments, we isolated CD14+ monocytes from Buffy coats and differentiated them using M-CSF and IL-4 into macrophages. Using FACS experiments we confirmed that a 24h-72h stimulation of IL-4 resulted in a cell population strongly expressing M2 macrophage markers (CD206). Using this method, we were able to generate M2 cells for further experiments. ChIP-qPCR experiments were carried out on these cells. The results showed an important enrichment of the promoter regions of known PPARγ targets (ANGPL4, CCL26, LXRα, CD36). To confirm whether this enrichment translates into increased mRNA levels of said genes, we isolated RNA from M2 cells and performed a qPCR. The results confirmed that the mRNA levels of known PPARγ targets were also induced in our M2 cells. Using genomics and transcriptomics we confirmed that our proposed model is working as intended. These results encouraged us to perform genome-wide analysis of PPARγ targets using ChIP-seq, and to determine the mRNA profile changes using RNA-seq. The ChIP-seq analysis showed that we failed to obtain peaks for several of the well-known targets of PPARg. The strongest immunoprecipitated promoters obtained were those of MANA1A, ZIC3 and GALC, whose function do not necessarily correlate with immune function or metabolism. We conclude that this is are promising results but we are currently working on a new set of samples that are already be sent for ChIP-sequencing.