SOCS2 expression in bone marrow derived dendritic cells is a positive regulator of T cell activation
© Hu et al; licensee BioMed Central Ltd. 2012
Published: 28 November 2012
After a completed T cell response the activation of DCs needs to be terminated to avoid harmful inflammation or autoimmune disease. Besides the negative regulation of JAK/STAT signaling pathway on growth hormone and prolactin for suppressor of cytokine signaling (SOCS) 2 , murine SOCS2-/- DCs are recently found to be hyper-responsive to microbial stimuli and refractory to the inhibitory actions of the anti-inflammatory mediator LXA4 . Thus, we investigate the role of SOCS2 in DC antigen presentation.
Materials and methods
Mice: SOCS2 deficient mice and transgenic OT-II mice. Mouse bone marrow-derived dendritic cells (BMDCs): Mouse bone marrow cells were incubated 7 days with 20 ng/ml GM-CSF and 20 ng/ml IL-4 to create mouse BMDCs. Quantitative RT-PCR: Real-time PCR was used to measure pro-inflamatory cytokines gene expression. CFSE proliferation assay: BMDCs were incubated with 100 ng/ml LPS and 50 ng/ml OVA323-339 peptide. The next day CD90+ splenocytes from OT-II mice were labeled with CFSE and added to the BMDC culture for 5 days. Then cells were stained for CD4 and read by FACS.
SOCS2 is complex regulator of DC effecter functionality, with an overall positive regulatory function on T cell activation.
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