Functional Expression of Fas and Fas Ligand on Human Colonic Intraepithelial T Lymphocytes

Hongo, T.; Morimoto, Yoshihiro; Ishibashi, Hiromi; Kobashi, Kazufumi; Yoshii, Masataka; Urushihara, Naoto; Hizuta, Akio; Tanaka, Noriaki

doi:10.1177/147323000002800304

Cited by 10 publications

(4 citation statements)

References 27 publications

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“…Because of the persistent exposure to a diverse number of antigens encountered in the gastrointestinal tract, gut lamina propria T lymphocyte (T-LPL) numbers are controlled by induction of Fas-mediated apoptosis (12). T-LPL often express high levels of Fas (12,19); however, in cases of inflammatory bowel disease, Fas expression levels in T-LPL as well as T-LPL sensitivity to Fas-mediated apoptosis are often decreased (3,5,41,42). In the functional level, it was reported that mice with Fas deficiency in the colon tissues are hypersensitive to DSSinduced colitis (34), whereas mice lacking FasL exhibited more severe and persistent colitis than control WT mice (36).…”

Section: Discussionmentioning

confidence: 99%

Butyrate suppresses colonic inflammation through HDAC1-dependent Fas upregulation and Fas-mediated apoptosis of T cells

Zimmerman¹,

Singh²,

Martin³

et al. 2012

American Journal of Physiology-Gastrointestinal and Liver Physi

238

147

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Section: Discussionmentioning

confidence: 99%

Butyrate suppresses colonic inflammation through HDAC1-dependent Fas upregulation and Fas-mediated apoptosis of T cells

Zimmerman¹,

Singh²,

Martin³

et al. 2012

American Journal of Physiology-Gastrointestinal and Liver Physi

238

147

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show abstract

“…Expression of both molecules has been demonstrated within other cell types, including the testicular Leydig cell, 22 natural killer cells, 23 and colonic intraepithelial T lymphocytes. 24 Fas/Fas ligand binding usually induces apoptosis within the Fas expressing cells. 25 This suggests that pancreatic islet cells must possess an additional mechanism for inhibiting "self-induced" Fas/ Fas ligand triggered apoptosis.…”

Section: Discussionmentioning

confidence: 99%

Apoptosis and proliferation of acinar and islet cells in chronic pancreatitis: evidence for differential cell loss mediating preservation of islet function

Bateman

Turner²,

Thomas³

et al. 2002

Gut

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Background: Chronic pancreatitis is characterised clinically by early exocrine insufficiency, with diabetes mellitus occurring as a late phenomenon. This is mirrored pathologically by extensive acinar cell destruction and islet preservation. The mechanisms underlying this differential rate of cellular destruction are unknown. Aims: To test the hypothesis that acinar loss and islet preservation in chronic pancreatitis occurs due to differential epithelial kinetics and investigate the role of inflammatory cells and cell cycle associated molecules. Methods: Archival tissue from six chronic pancreatitis cases was compared with six normal controls using TUNEL and immunohistochemistry for CD3, CD20, CD68, MIB-1, Bcl-2, Bax, Fas, Fas ligand, retinoblastoma protein (Rb), and tissue inhibitor of metalloproteinases 1 (TIMP-1) and 2 (TIMP-2).Results: The acinar cell apoptotic index (AI) and proliferation index were higher in chronic pancreatitis than controls. T lymphocytes diffusely infiltrated fibrous bands and acini but rarely islets. Acinar Bcl-2 expression exceeded islet expression in chronic pancreatitis and controls while Bax was strongly expressed by a subset of islet cells and weakly by centroacinar cells. Islet Fas and Fas ligand expression exceeded acinar expression in chronic pancreatitis and controls. Acinar Rb expression was higher in chronic pancreatitis than in controls. Islets in chronic pancreatitis and controls showed intense TIMP-1 and TIMP-2 expression. Conclusion: Apoptosis plays a significant role in acinar loss in chronic pancreatitis. Acinar Bcl-2 and islet Bax expression indicates complex AI control. Increased acinar Rb expression in chronic pancreatitis may differentially promote acinar loss. Fas ligand expression may be restricted to islet cell membranes through TIMP-1 expression and inhibit islet damage by promoting apoptosis of cytotoxic T lymphocytes.

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“…These lymphocyte populations are important for immunologic development, immunoglobulins, cytokines and growth factors production, epithelial cells proliferation and differentiation, and intestinal tolerance [16][17][18]. Thus, mucosal lymphocytes have a series of patterns recognition receptors that interact with bacterial molecular patterns, helping to modulate intestinal innate immunity and an appropriate adaptive immune response [19], also providing the most effective immune protection in a strictly regulated fashion, to preserve the integrity and the vital functions of the intestinal mucosal epithelium [20].…”

Section: Discussionmentioning

confidence: 99%

Colonic Lymphoid Aggregates in Slow Transit Constipation

et al. 2007

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Information available on colonic lymphoid aggregates, apart from data of patients with inflammatory conditions, is scarce in other pathologic conditions. We investigated colonic lymphoid aggregates in patients with severe slow transit constipation, unresponsive to conventional therapeutic measures, and undergoing surgery for relief of their symptoms. Tissues from 27 patients with intractable slow transit constipation were obtained and compared with 10 controls. The number, diameter, lymphocyte distribution, and proliferative index were calculated and compared in both groups. Constipated patients displayed a significantly increased number of colonic lymphoid aggregates compared with controls. No differences were found concerning the other variables. The increase of colonic lymphoid aggregates found in severely constipated patients may represent a protective mucosal mechanism toward the chronic fecal stasis.

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Functional Expression of Fas and Fas Ligand on Human Colonic Intraepithelial T Lymphocytes

Abstract: The expression of Fas, a cell surface receptor directly responsible for triggering cell death by apoptosis, and its ligand (FasL) was investigated on both human colonic intraepithelial T lymphocytes (IELs) and peripheral blood mononuclear lymphocytes (PBMLs).

Cited by 10 publications

References 27 publications

Butyrate suppresses colonic inflammation through HDAC1-dependent Fas upregulation and Fas-mediated apoptosis of T cells

Butyrate suppresses colonic inflammation through HDAC1-dependent Fas upregulation and Fas-mediated apoptosis of T cells

Apoptosis and proliferation of acinar and islet cells in chronic pancreatitis: evidence for differential cell loss mediating preservation of islet function

Colonic Lymphoid Aggregates in Slow Transit Constipation

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