DYSFUNCTION OF DENDRITIC CELLS FOLLOWING TRAUMA MEDIATES SUPPRESSION OF DELAYED TYPE HYPERSENSITIVITY RESPONSE IN MICE

Abstract

Dendritic cells (DCs) participate in the afferent (sensitization) phase of delayed type hypersensitivity (DTH) response, which is suppressed after severe injury. However, whether DCs functions alter after severe injury remains unclear. Herein BALB/c mice were underwent severe injury and then sensitized with 2,4-dinitrofluorobenzene (DNFB) at different time-point post-injury, 5 days later mice were challenged with DNFB and then (24 h later) DTH response was determined. The results showed that DTH response on day 1 post-injury was most significantly decreased and draining lymph nodes (DLN) cells proliferation and IL-2, IL-12 and IFN-gamma production were reduced, whereas IL-6, IL-10 production were augmented. After 24 h sensitization of DNFB, purified DCs from DLN of 1 day post-injury showed lower percentage of MHCII+CD11c+cells, less IL-12 secretion and weaker transferring ability for DTH to recipient mice than that of sham-injured mice. After 6d sensitization of DNFB, DLN cells from injured mice also showed suppressed transferring ability for DTH. Supplementation of sensitized DCs from DLN of sham-injured or injured mice, in the meantime of skin sensitization of DNFB, could partially restore reduced DTH response of injured mice. These data strongly suggested that dysfunction of dendritic cells following trauma mediates suppression of delayed type hypersensitivity response in mice and supplementation of sensitized DCs, regardless of from injured or control host, into injured mice can alleviate this immunosuppression.