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Adoptive Transfer of Dendritic Cells Expressing Fas Ligand Modulates Intestinal Inflammation in a Model of Inflammatory Bowel Disease | OMICS International | Abstract
ISSN: 2155-9899

Journal of Clinical & Cellular Immunology
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Short Communication

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

Edelmarie Rivera de Jesus1,2#, Raymond A Isidro1#, Myrella L Cruz1, Harry Marty1 and Caroline B Appleyard1*
1Ponce Health Sciences University-Medical School and Ponce Research Institute, Ponce, PR 00732, USA
2Department of Biology, University of Puerto Rico – Ponce Campus, Ponce, PR 00732, USA
#These authors contributed equally to this manuscript
*Corresponding Author : Caroline B Appleyard, PhD
Department of Basic Sciences
Ponce Health Sciences University-Medical School
and Ponce Research Institute
PO Box 7004, Ponce, PR 00732-7004, USA
Tel: 787-840-2575 ext 2165
Fax: 787-841-1040
E-mail: [email protected]
Received date: March 02, 2016; Accepted date: April 20, 2016; Published date: April 29, 2016
Citation: Rivera de Jesus E, Isidro RA, Cruz ML, Marty H, Appleyard CB (2016) Adoptive Transfer of Dendritic Cells Expressing Fas Ligand Modulates Intestinal Inflammation in a Model of Inflammatory Bowel Disease. J Clin Cell Immunol 7:411. doi: 10.4172/2155-9899.1000411
Copyright: © 2016 Rivera de Jesus E, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.


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 in vitro. Adoptive transfer of FasL-DCs decreased macroscopic and microscopic damage scores and reduced colonic T cells, neutrophils, and proinflammatory macrophages when compared to EV-DC adoptive transfer.
Conclusion: FasL-DCs are effective at treating colonic inflammation in this model of IBD and represent a possible new treatment for patients with IBD.