Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Expression Data from BALB/c and Stat6-deficient bone marrow derived macrophages (BMDM)


ABSTRACT: We used microarrays to find Stat6 dependent genes in control and IL-4 exposed bone marrow derived macrophages. Alternatively activated macrophages (AAM) accumulate in tissues during Th2-associated immune responses like helminth infections and allergic disorders. These cells possess potent inhibitory activity against T cells. The differentiation of AAM depends on IL-4/IL-13-mediated activation of the transcription factor Stat6. Stat6 is also required in AAM to induce several genes, such as YM1, FIZZ1 and Arginase1. Macrophages were differentiated from bone marrow cells in supplemented RPMI 1640 for 7 days in the presence of 10% supernatant from the M-CSF producing fibroblast cell line L929. After removal of nonadherent cells, macrophages were detached using 5mM EDTA treatment, washed, counted, and replated at a density of 10x6 cells/mL. Macrophages were cultured for 24 hours in medium (control) or in the presence of IL-4 (10mg/mL). F4/80 positive macrophages were sorted with a purity of 99% and RNA was isolated (Trizol/Chloroform) according to the manufacturer's instructions. RNA was labeled (biotin), fragmented, and hybridized to the arrays according to the manufacturer's recommendations.

ORGANISM(S): Mus musculus

SUBMITTER: Silke Huber 

PROVIDER: E-GEOD-20030 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Alternatively activated macrophages inhibit T-cell proliferation by Stat6-dependent expression of PD-L2.

Huber Silke S   Hoffmann Reinhard R   Muskens Femke F   Voehringer David D  

Blood 20100712 17


Alternatively activated macrophages (AAM) accumulate in tissues during Th2-associated immune responses like helminth infections and allergic disorders. These cells differentiate in response to interleukin 4 (IL-4)/IL-13-mediated activation of Stat6 and possess potent inhibitory activity against T cells. The molecular mechanism that leads to T-cell suppression remains unclear and could involve soluble factors or inhibitory ligands. Microarray analysis revealed that the inhibitory ligand, programm  ...[more]

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