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Inflammatory Bowel Disease Lamina Propria of Patients with Regulatory Defects in CD8+ Regulatory T Cells in the Lamina Propria of Patients with Inflammatory Bowel Disease This information is current as Jens Brimnes, Matthieu Allez, Iris Dotan, Ling Shao, of September 28, 2021. Atsushi Nakazawa and Lloyd Mayer J Immunol 2005; 174:5814-5822; ; doi: 10.4049/jimmunol.174.9.5814 http://www.jimmunol.org/content/174/9/5814 Downloaded from References This article cites 53 articles, 20 of which you can access for free at: http://www.jimmunol.org/content/174/9/5814.full#ref-list-1 http://www.jimmunol.org/ Why The JI? Submit online. • Rapid Reviews! 30 days* from submission to initial decision • No Triage! Every submission reviewed by practicing scientists • Fast Publication! 4 weeks from acceptance to publication by guest on September 28, 2021 *average Subscription Information about subscribing to The Journal of Immunology is online at: http://jimmunol.org/subscription Permissions Submit copyright permission requests at: http://www.aai.org/About/Publications/JI/copyright.html Email Alerts Receive free email-alerts when new articles cite this article. Sign up at: http://jimmunol.org/alerts The Journal of Immunology is published twice each month by The American Association of Immunologists, Inc., 1451 Rockville Pike, Suite 650, Rockville, MD 20852 Copyright © 2005 by The American Association of Immunologists All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. The Journal of Immunology Defects in CD8؉ Regulatory T Cells in the Lamina Propria of Patients with Inflammatory Bowel Disease1 Jens Brimnes, Matthieu Allez, Iris Dotan, Ling Shao, Atsushi Nakazawa, and Lloyd Mayer2 Mucosal tolerance is believed to be partly mediated by regulatory T cells. Intestinal epithelial cells (IECs) may play an important role in the generation of such regulatory cells, because they are able to process and present Ag to T cells. Furthermore, we have previously demonstrated that IECs are able to generate regulatory CD8؉ T cells in vitro. In the present study, we have analyzed lamina propria (LP) lymphocytes for the presence of such regulatory CD8؉ T cells in normal individuals as well as in patients with inflammatory bowel disease (IBD). The results of the present study show that LP CD8؉ T cells derived from normal controls possess regulatory activity, whereas both unfractionated LP lymphocytes and purified LP CD4؉ T cells do not. The LP CD8؉ T cells suppress Ig production by pokeweed mitogen-stimulated PBMCs by 31–80%, in a cell contact-dependent manner. No ؉ ؊ ؉ ؉ significant difference in suppression between CD28 and CD28 CD8 LP T cells was observed. In contrast to CD8 T cells from Downloaded from normal LP, CD8؉ T cells isolated from LP of IBD patients, did not suppress Ig production by pokeweed mitogen-stimulated PBMC (five of six ulcerative colitis specimens; six of six Crohn’s disease specimens). Furthermore, we demonstrate that the frequency of TCR V␤5.1-positive CD8؉ T cells, which we previously have demonstrated to be regulatory and to be expanded by IECs in vitro, is decreased in IBD LP compared with normal LP. In conclusion, this study demonstrates that CD8؉ T cells with regulatory activity are present in the LP of normal healthy individuals, but not in patients with IBD, suggesting that these cells might play an active role in mucosal tolerance. The Journal of Immunology, 2005, 174: 5814–5822. http://www.jimmunol.org/ he intestine harbors a complex microflora composed of a TGF-␤ might play a role (13, 14). Other subsets of murine CD4ϩ large variety of indigenous aerobic and anaerobic bacteria regulatory T cells, such as the Th3 cells generated during low-dose T (1). These bacteria are in close proximity to a vast number oral tolerance regimens and the in vitro-generated Tr1 cells, also of intestinal lymphocytes, yet it is unclear how the mucosal im- seem to act via secretion of regulatory cytokines (15, 16). Al- mune system is able to mount a rapid and effective response though the field of regulatory cells has been focused on CD4ϩ T against pathogenic bacteria, viruses, and parasites, while remain- cells, regulatory CD8ϩ T cells have been described in oral toler- ing tolerant to the resident enteric microflora and dietary Ags. The ance (17, 18), and recently a population of human regulatory cells, ϩ Ϫ importance of maintaining this tolerance is illustrated in inflam- characterized by their CD8 CD28 phenotype, has also been de- by guest on September 28, 2021 matory bowel diseases (IBD),3 because these diseases are believed scribed (19, 20). to be the result of a breakdown of tolerance to resident enteric In the context of the mucosal immune system, regulatory cells bacteria (2, 3). have primarily been demonstrated in rodents. Both the above-men- Accumulated data suggest that regulatory T cells play a central tioned Tr1 cells and the CD4ϩCD25ϩ T cells from normal mice role in maintaining tolerance in the mucosal immune system (4). have been shown to be capable of preventing the development of Several subsets of both CD4ϩ and CD8ϩ T cells have been shown experimental colitis in SCID mice (14, 16, 21). Recently, it has to act as regulatory cells. In both humans and rodents, it has been also been demonstrated that CD4ϩ T cells with regulatory activity demonstrated that naive CD4ϩCD25ϩ T cells possess regulatory can be isolated from the intestinal lamina propria (LP) of normal activity (5–7). The CD4ϩCD25ϩ cells are anergic, but after TCR mice (22, 23). The induction of low-dose oral tolerance mediated triggering, these cells are able to inhibit immune responses both in by the above-mentioned Th3 cells is another example of the gen- vitro and in vivo (5, 8, 9). In vitro, the suppression seems to be eration of regulatory cells in the intestinal mucosa. mediated via cell contact-dependent mechanisms (5, 10–12), Little is known about the mechanisms by which regulatory cells whereas in vivo studies suggest that cytokines such as IL-10 and are generated in vivo in the mucosa. It has been suggested that immature dendritic cells located in the subepithelial dome region of the Peyer’s patch are able to induce regulatory T cells (24, 25). Immunobiology Center, Mount Sinai Medical Center, New York, NY 10029 However, intestinal epithelial cells (IECs) may also play an im- Received for publication February 20, 2004. Accepted for publication February 18, 2005. portant role in the generation of regulatory cells, because these The costs of publication of this article were defrayed in part by the payment of page cells are able to process and present luminal Ags to T cells in the charges. This article must therefore be hereby marked advertisement in accordance LP (26–28). Using an allogeneic in vitro coculture system, we with 18 U.S.C. Section 1734 solely to indicate this fact. have previously demonstrated that interactions between IECs and 1 J.B. was supported by the Danish Medical Research Agency. L.M. was supported by peripheral blood T cells (PBTs) leads to the preferential expansion National Institutes of Health Grants AI23504, AI24671, and AI44236. M.A. and I.D. ϩ Ϫ were supported by a Crohn’s and Colitis Foundation fellowship award. of CD8 CD28 T cells with regulatory activity (27, 29). We have recently shown that a subset of the expanding CD8ϩ T cells is 2 Address correspondence and reprint requests to Dr. Lloyd Mayer, Immunobiology 4 Center, Mount Sinai Medical Center, 1425 Madison Avenue, New York, NY 10029. characterized by the biased usage of the TCR V␤5.1 chain. The E-mail address: [email protected] 3 Abbreviations used in this paper: IBD, inflammatory bowel disease; LP, lamina propria; IEC, intestinal epithelial cell; UC, ulcerative colitis; CD, Crohn’s disease; 4 M. Allez., J. Brimnes, L. Shao, L. Dotan, A. Nakazawa, and L. Mayer. Mucosal LPMC, LP mononuclear cell; PWM, pokeweed mitogen; PBT, peripheral blood T expression of CD8ϩ T regulatory cells by CD1d and a CEA family member. Sub- cell. mitted for publication. Copyright © 2005 by The American Association of Immunologists, Inc. 0022-1767/05/$02.00 The Journal of Immunology 5815 expansion of these regulatory cells is dependent on the expression coll (Amersham Biosciences) density gradient and the LPMCs were har- vested from the 40–60% interface. Viability was Ͼ90%. of the nonclassical MHC class I molecule, CD1d, and the carci- ϩ ϩ noembryonic Ag subfamily member, gp180, on the surface of the LP CD4 and CD8 T cells were purified after culturing the isolated LPMC with 20 ng/ml IL-15 overnight followed by staining with allophy- IEC (29–32). We have termed these cells TrE cells. In contrast to cocyanin-conjugated anti-CD3, PE-conjugated anti-CD4, and FITC-conju- normal IECs, IECs from patients with IBD have an aberrant ex- gated anti-CD8 mAbs (all BD Pharmingen). The cells were then isolated by pression of gp180 and cannot expand these regulatory CD8ϩ T sorting using a MoFlo Sorter (DakoCytomation). Purity of the sorted cells cells in vitro (33) (I. Dotan, manuscript in preparation). Taken was Ͼ98%. together, these data suggest that defects, which interfere with the IEC:LPL coculture and cytokine stimulation of LPLs normal IEC-mediated generation or expansion of regulatory CD8ϩ TrE cells, may play a role in the pathogenesis of IBD. LPMCs were labeled with CFSE and cocultured with gamma-irradiated IECs (3000 rad). Both LPMC and IEC were adjusted to 1 ϫ 106 cells/ml In the present work, we have investigated whether such regula- and cocultured in serum-free AIM-V medium containing 50 U/ml penicil- ϩ tory CD8 TrE cells are present in vivo in the LP. Our results lin, 50 ␮g/ml streptomycin, and 2 mM L-glutamine (Invitrogen Life Tech- ϩ show that CD8 T cells with regulatory activity are present in the nologies) for 5–8 days at 37°C, 5% CO2.
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