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de Jesus ER, Isidro RA, Cruz ML, et al. Adoptive Transfer of Dendritic Cells Expressing Fas Ligand Modulates Intestinal Inflammation in a Model of Inflammatory Bowel Disease. J Clin Cell Immunol. 2016;7(2)doi: 10.4172/2155-9899.1000411.
de Jesus, E. R., Isidro, R. A., Cruz, M. L., Marty, H., & Appleyard, C. B. (2016). Adoptive Transfer of Dendritic Cells Expressing Fas Ligand Modulates Intestinal Inflammation in a Model of Inflammatory Bowel Disease. Journal of clinical & cellular immunology, 7(2), . https://doi.org/10.4172/2155-9899.1000411
de Jesus, Edelmarie Rivera, et al. "Adoptive Transfer of Dendritic Cells Expressing Fas Ligand Modulates Intestinal Inflammation in a Model of Inflammatory Bowel Disease." Journal of clinical & cellular immunology vol. 7,2 (2016). doi: https://doi.org/10.4172/2155-9899.1000411
de Jesus ER, Isidro RA, Cruz ML, Marty H, Appleyard CB. Adoptive Transfer of Dendritic Cells Expressing Fas Ligand Modulates Intestinal Inflammation in a Model of Inflammatory Bowel Disease. J Clin Cell Immunol. 2016 Apr;7(2). doi: 10.4172/2155-9899.1000411. Epub 2016 Apr 29. PMID: 27274906; PMCID: PMC4892183.
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J Clin Cell Immunol. 2016 Apr;7(2). doi: 10.4172/2155-9899.1000411. Epub 2016 Apr 29.

Adoptive Transfer of Dendritic Cells Expressing Fas Ligand Modulates Intestinal Inflammation in a Model of Inflammatory Bowel Disease.

Journal of clinical & cellular immunology

Edelmarie Rivera de Jesus, Raymond A Isidro, Myrella L Cruz, Harry Marty, Caroline B Appleyard

Affiliations

  1. Ponce Health Sciences University-Medical School and Ponce Research Institute, Ponce, PR 00732, USA; Department of Biology, University of Puerto Rico - Ponce Campus, Ponce, PR 00732, USA.
  2. Ponce Health Sciences University-Medical School and Ponce Research Institute, Ponce, PR 00732, USA.

PMID: 27274906 PMCID: PMC4892183 DOI: 10.4172/2155-9899.1000411

Abstract

BACKGROUND: Inflammatory bowel diseases (IBD) are chronic relapsing inflammatory conditions of unknown cause and likely result from the loss of immunological tolerance, which leads to over-activation of the gut immune system. Gut macrophages and dendritic cells (DCs) are essential for maintaining tolerance, but can also contribute to the inflammatory response in conditions such as IBD. Current therapies for IBD are limited by high costs and unwanted toxicities and side effects. The possibility of reducing intestinal inflammation with DCs genetically engineered to over-express the apoptosis-inducing FasL (FasL-DCs) has not yet been explored.

OBJECTIVE: Investigate the immunomodulatory effect of administering FasL-DCs in the rat trinitrobenzene sulfonic acid (TNBS) model of acute colitis.

METHODS: Expression of FasL on DCs isolated from the mesenteric lymph nodes (MLNs) of normal and TNBS-colitis rats was determined by flow cytometry. Primary rat bone marrow DCs were transfected with rat FasL plasmid (FasL-DCs) or empty vector (EV-DCs). The effect of these DCs on T cell IFNγ secretion and apoptosis was determined by ELISPOT and flow cytometry for Annexin V, respectively. Rats received FasL-DCs or EV-DCs intraperitoneally 96 and 48 hours prior to colitis induction with TNBS. Colonic T cell and neutrophil infiltration was determined by immunohistochemistry for CD3 and myeloperoxidase activity assay, respectively. Macrophage number and phenotype was measured by double immunofluorescence for CD68 and inducible Nitric Oxide Synthase.

RESULTS: MLN dendritic cells from normal rats expressed more FasL than those from colitic rats. Compared to EV-DCs, FasL-DCs reduced T cell IFNγ secretion and increased T cell apoptosis

CONCLUSION: FasL-DCs are effective at treating colonic inflammation in this model of IBD and represent a possible new treatment for patients with IBD.

Keywords: Adoptive transfer; Dendritic cells; FasL (CD95L); Inflammatory bowel disease; Macrophages

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