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Department of Surgery (Immunology), Brigham and Women’s Hospital and Harvard Medical School, Boston, MA 02115
Major injury initiates a systemic inflammatory response that can be detrimental to the host. We have recently reported that burn injury primes innate immune cells for a progressive increase in TLR4 and TLR2 agonist-induced proinflammatory cytokine production and that this inflammatory phenotype is exaggerated in adaptive immune system-deficient (Rag1–/–) mice. The present study uses a series of adoptive transfer experiments to determine which adaptive immune cell type(s) has the capacity to control innate inflammatory responses after injury. We first compared the relative changes in TLR4- and TLR2-induced TNF-
, IL-1
, and IL-6 production by spleen cell populations prepared from wild-type (WT), Rag1–/–, CD4–/–, or CD8–/– mice 7 days after sham or burn injury. Our findings indicated that splenocytes prepared from burn-injured CD8–/– mice displayed TLR-induced cytokine production levels similar to those in WT mice. In contrast, spleen cells from burn-injured CD4–/– mice produced cytokines at significantly higher levels, equivalent to those in Rag1–/– mice. Moreover, reconstitution of Rag1–/– or CD4–/– mice with WT CD4+ T cells reduced postinjury cytokine production to WT levels. Additional separation of CD4+ T cells into CD4+CD25+ and CD4+CD25– subpopulations before their adoptive transfer into Rag1–/– mice showed that CD4+CD25+ T cells were capable of reducing TLR-stimulated cytokine production levels to WT levels, whereas CD4+CD25– T cells had no regulatory effect. These findings suggest a previously unsuspected role for CD4+CD25+ T regulatory cells in controlling host inflammatory responses after injury.
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