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PubMed1996

[Activation of T-lymphocytes in Crohn disease and in ulcerative hemorrhagic rectocolitis. Therapeutic implications].

Inflammatory bowel disease (IBD) encompasses two forms of intestinal inflammation: ulcerative colitis and Crohn's disease. Besides abnormalities of immunoglobulins production and complement activation, T lymphocytes play an important role in pathogeny of these diseases. Although T-cells number is increased in intestinal mucosa of such patients, CD4/CD8 ratio of T lymphocytes subsets is normal in mucosa. Activated T-cells expressing interleukin-2 receptors (CD25) are increased in lamina propria from patients with IBD. Cytokines induce abnormal expression of class II antigens of major histocompatibility complex by epithelial cells which may act as antigen presenting cells to CD4 T-cells. Better understanding of pathogenic mechanisms in IBD might justify new immunosuppressive therapeutics to treat these patients.

Antibodies, Monoclonal↗
PubMed1984

Intestinal lymphocyte subpopulations in inflammatory bowel disease: an analysis by immunohistological and cell isolation techniques.

Lymphocyte subpopulations in the intestinal mucosa of patients with ulcerative colitis or Crohn's disease have been studied using a double marker immunofluorescence technique. Analysis of tissue sections revealed that the majority of intraepithelial lymphocytes (IEL) were T cells (Hle-1+ HuTLA+ UCHT1+). Of these, over 80% were of suppressor-cytotoxic phenotype (OKT8+:83 +/- 10.2%) with a small population of helper type IEL (OKT4+). Only one third of OKT8+ IEL reacted with the T cell antibody, anti-Leu-1. IEL were also Tac-, C3b-receptor- (C3RT05-), and Ig-. Within the lamina propria, OKT4+ T cells predominated (ulcerative colitis 64 +/- 6.0%; Crohn's disease 63 +/- 6.0%). Less than half of the smaller OKT8+ population in the lamina propria was Leu-1+. These finding did not differ from those seen in histologically normal tissues from controls, and are similar to those reported in the small intestine. Mononuclear cells were also isolated from the intestinal lamina propria using an enzymatic technique. The majority of lymphocytes obtained were T cells (OKT3+), with populations of OKT4+ and OKT8+ cells. Comparison of the ratio of OKT4+ to OKT8+ lymphocytes determined by immunohistological analysis with that obtained in mucosal isolates, however, suggested that the isolation procedure may deplete OKT8+ cells. These findings indicate that an imbalance of mucosal immunoregulatory T cells, as defined by monoclonal antibodies, does not occur in inflammatory bowel disease. They also emphasize that functional studies of isolated intestinal mucosal cells should be combined with morphological studies of cell populations in situ.

Adolescent↗
PubMed2001

T cells of the colonic mucosa in patients with infantile colitis.

BACKGROUND: Infantile colitis is a heterogeneous group of disorders, including enterocolitis complicating Hirschsprung disease, allergic colitis, inflammatory bowel disease, and Behçet syndrome. There are limited data concerning the immune responses induced by the inflammation of the intestine in young infants. METHODS: Twenty-four colonic biopsy specimens from 12 infantile colitis patients and 12 age-matched control patients were studied by immunohistologic methods. The authors compared the T cells, their subsets expressing the surface antigens CD8 and CD4, and T-cell receptors alphabeta and deltagamma, and densities of mononuclear and epithelial cells expressing human leukocyte antigen class II antigens. RESULTS: The density of CD3+ intraepithelial lymphocytes (IELs) in the large intestinal specimens was significantly higher (P = 0.036) in colitis patients than in the control group. The majority of the CD3+ IELs were CD8+-expressing cells, and only a minority were CD4+ cells in both groups. T-cell receptors alphabeta+ (P = 0.023) and deltagamma+ (P = 0.027) IELs were observed significantly more frequently in colitis patients than in the control group. In surface epithelium, delta non-disulphide-linked type T-cell receptor (deltaTCS1) IELs were found strikingly more frequently (P = 0.001) in the specimens taken from the colitis patients. Also, the density of the deltaTCS1+ cells in crypts of the large intestine was significantly higher in colitis patients than in the control patients (P = 0.047). CONCLUSIONS: A significant increase of CD3+ lymphocytes in the colonic epithelium of the patients with infantile colitis was noted. This increase involved both T-cell receptor alphabeta-positive and deltagamma-positive IELs. The finding of this study supports the proposal that intraluminal antigens, either microbial or food derived, are important in the pathogenesis of colitis in young infants.

Antibodies, Monoclonal↗
PubMed2004

Preventive effects of Escherichia coli strain Nissle 1917 on acute and chronic intestinal inflammation in two different murine models of colitis.

Escherichia coli strain Nissle 1917 (EcN) is as effective in maintaining remission in ulcerative colitis as is treatment with mesalazine. This study aims to evaluate murine models of acute and chronic intestinal inflammation to study the antiinflammatory effect of EcN in vivo. Acute colitis was induced in mice with 2% dextran-sodium sulfate (DSS) in drinking water. EcN was administered from day -2 to day +7. Chronic colitis was induced by transfer of CD4(+) CD62L(+) T lymphocytes from BALB/c mice in SCID mice. EcN was administered three times/week from week 1 to week 8 after cell transfer. Mesenteric lymph node (MLN) cytokine secretion (of gamma interferon [IFN-gamma], interleukin 5 [IL-5], IL-6, and IL-10) was measured by enzyme-linked immunosorbent assay. Histologic sections of the colon were analyzed by using a score system ranging from 0 to 4. Intestinal contents and homogenized MLN were cultured, and the number of E. coli-like colonies was determined. EcN was identified by repetitive extragenic palindromic (REP) PCR. EcN administration to DSS-treated mice reduced the secretion of proinflammatory cytokines (IFN-gamma, 32,477 +/- 6,377 versus 9,734 +/- 1,717 [P = 0.004]; IL-6, 231 +/- 35 versus 121 +/- 17 [P = 0.02]) but had no effect on the mucosal inflammation. In the chronic experimental colitis of the transfer model, EcN ameliorated the intestinal inflammation (histology score, 2.7 +/- 0.2 versus 1.9 +/- 0.3 [P = 0.02]) and reduced the secretion of proinflammatory cytokines. Translocation of EcN and resident E. coli into MLN was observed in the chronic colitis model but not in healthy controls. Administration of EcN ameliorated acute and chronic experimental colitis by modifying proinflammatory cytokine secretion but had no influence on the acute DSS-induced colitis. In this model, preexisting colitis was necessary for translocation of EcN and resident E. coli into MLN.

Acute Disease↗
PubMed2000

Cytotoxic T lymphocyte-associated antigen 4 plays an essential role in the function of CD25(+)CD4(+) regulatory cells that control intestinal inflammation.

It is now clear that functionally specialized regulatory T (Treg) cells exist as part of the normal immune repertoire, preventing the development of pathogenic responses to both self- and intestinal antigens. Here, we report that the Treg cells that control intestinal inflammation express the same phenotype (CD25(+)CD45RB(low)CD4(+)) as those that control autoimmunity. Previous studies have failed to identify how CD25(+) Treg cells function in vivo. Our studies reveal that the immune-suppressive function of these cells in vivo is dependent on signaling via the negative regulator of T cell activation cytotoxic T lymphocyte-associated antigen 4 (CTLA-4), as well as secretion of the immune-suppressive cytokine transforming growth factor beta. Strikingly, constitutive expression of CTLA-4 among CD4(+) cells was restricted primarily to Treg cells, suggesting that CTLA-4 expression by these cells is involved in their immune-suppressive function. These findings raise the possibility that Treg cell function contributes to the immune suppression characteristic of CTLA-4 signaling. Identification of costimulatory molecules involved in the function of Treg cells may facilitate further characterization of these cells and development of new therapeutic strategies for the treatment of inflammatory diseases.

Abatacept↗
PubMed1990

Malignant lymphoma in ulcerative colitis. Report of a case.

The authors present the case of a 40-year-old woman with primary malignant lymphoma complicating chronic ulcerative colitis. Twenty-one cases reported in the literature are reviewed and the various available data analyzed. Variations in the distribution of lymphoma in both the normal and colitic bowel supports a relationship between both conditions. Any lymphocytic infiltrate seen in biopsies obtained from ulcerative colitis should be assessed to exclude associated lymphoma. The prognosis is poor.

Adult↗
PubMed2005

Defining the role of T cell-derived leptin in the modulation of hepatic or intestinal inflammation in mice.

The role of leptin in the immune system has been well established. While adipocytes represent the major source, leptin production by lymphocytes, infiltrating at the site of inflammation, was recently demonstrated. However, the significance of this locally released leptin remains unresolved. In the present study, two models in which absence of leptin-signalling is associated with protection were employed: the model of ConA-induced hepatitis and the CD4(+)CD45Rb(high) transfer model of colitis. For the ConA model, scid mice were reconstituted with either WT or leptin-deficient (ob/ob) CD4(+) T cells. Eight weeks post transfer, ConA was injected and serum ALT, TNFalpha, leptin as well as liver mononuclear cell activation and histological signs of inflammation were evaluated. No difference between recipients of WT or ob/ob cells was observed for any of the parameters evaluated. In the second model, either WT or ob/ob CD4(+)CD45Rb(high) cells were transferred into scid mice. No histological differences were detected, although recipients of ob/ob cells showed higher weight loss compared to recipients of WT cells. Spontaneous production of IL-6 from colon cultures obtained from recipients of ob/ob cells was reduced compared to recipients of WT cells, whereas stimulation of lamina propria lymphocytes with leptin resulted in a higher IFNgamma release in recipients of ob/ob cells compared to recipients of WT cells. In conclusion, the present study provides evidence that T cell-derived leptin does not play a major role in the regulation of the inflammatory process, indicating that the adipose tissue is the critical player in the immune-modulating effects of leptin.

Animals↗
PubMed1988

Natural, lectin- and phorbol ester-induced cellular cytotoxicity in Crohn's disease and ulcerative colitis.

Cellular cytotoxicity of peripheral blood cells was studied in patients with Crohn's disease or ulcerative colitis and healthy controls. The spontaneous cytotoxicity or natural killer (NK) cell activity, evaluated against the erythroleukemia K-562 and the colon cancer CaCo-2 and HT-29 cell lines, of total mononuclear cells and enriched lymphocytes was depressed in Crohn's disease and ulcerative colitis patients compared to the controls. Phytohaemagglutinin (PHA) increased the cytotoxicity in the patients, to a similar maximal level as the stimulated controls. In contrast, the phorbol ester, phorbol-myristate-acetate (PMA), enhanced the cytotoxicity in patients and in controls, but in the patients not to the levels of the controls. No cytotoxicity was observed in the monocyte-enriched fraction both in patients and controls using the same assay system. A similar small but significant stimulation of monocyte cytotoxicity was obtained by PHA and PMA in patients and in controls. In conclusion, inflammatory bowel disease is associated with a depressed NK cell activity in peripheral blood which is not target specific. PHA but not PMA could restore the deficient NK cell activity. Monocytes seem not to be involved in the decreased NK cell activity in patients with inflammatory bowel disease.

Adolescent↗
PubMed1982

Cold-reactive lymphocytotoxins in Crohn's disease and ulcerative colitis. I. Incidence and characterization.

The incidence of cold-reactive lymphocytotoxins in the serum of patients with Crohn's disease or ulcerative colitis has been investigated. Twenty-seven percent of patients with Crohn's disease and twenty-two percent of those with ulcerative colitis had circulating lymphocytotoxins. This is significantly higher than the 4% found in a normal control population. The presence of lymphocytotoxins did not correlate with age or sex of the subjects studied nor with clinical parameters. As in previous studies, the lymphocytotoxin is an antibody of IgM class, is optimally effective at 15 degrees C in the presence of complement and reacts with both T and B lymphocytes. The lymphocytes from patients with active Crohn's disease or ulcerative colitis are poorly susceptible to lysis by lymphocytotoxins but lymphocytes from patients in remission are as susceptible as normal lymphocytes. This implies that the lymphocyte surface is altered during active disease although the pathogenetic significance of this is unclear.

Adolescent↗
PubMed2003

Depletion and decreased function of antigen-presenting dendritic cells caused by lymphocytapheresis in ulcerative colitis.

PURPOSE: The therapeutic efficacy of lymphocytapheresis in autoimmune diseases is presumed to be caused by depletion of activated lymphocytes. However, nothing is known about the inducer of activated lymphocytes, the antigen-presenting dendritic cells, during lymphocytapheresis. BASIC PROCEDURES: Six sessions of lymphocytapheresis were done in five patients with ulcerative colitis. Dendritic cells were enriched from the buffy coat of depleted lymphocytes and also from the peripheral blood. The phenotype and function of dendritic cells were studied by dual-color flow cytometry and in allogenic mixed leukocyte reaction, respectively. The serum levels of inflammatory cytokines (interleukin-1alpha 6, 8, 10, and 12 and tumor necrosis factor-alpha and beta) were measured before and after lymphocytapheresis in all cases. MAIN FINDINGS: Lymphocytapheresis was safe and caused clinical, endoscopic or histologic improvements in all patients with ulcerative colitis. Many CD83-positive mature dendritic cells were found in the buffy coats after each session of lymphocytapheresis. The function of dendritic cells, the frequencies of CD83-positive dendritic cells and the levels of interleukin-6 and interleukin-8 were down regulated in all patients with ulcerative colitis after lymphocytapheresis compared with their levels before lymphocytapheresis. CONCLUSIONS: Depletion and down regulation of the function of dendritic cells and diminished levels of inflammatory cytokines caused by lymphocytapheresis may contribute to the therapeutic efficacy of lymphocytapheresis.

Adolescent↗
PubMed1974

The immune competence of patients with inflammatory bowel disease.

Previous investigations of immune function in patients with Crohn's disease have yielded conflicting results. A comprehensive study of immune competence-peripheral lymphocyte count, serum immunoglobulin levels (IgG, IgA and IgM), lymphocyte response to PHA, Mantoux test, and DNCB response-has been performed in a large number of patients with inflammatory bowel disease. A total of 52 patients with Crohn's disease, 20 patients with ulcerative colitis, and 46 control patients with benign gastrointestinal disease were investigated. The patient groups were subdivided into ;well' and ;ill' in view of the differing clinical states of patients with inflammatory bowel disease. Some of the Crohn's and colitis patients were receiving steroid therapy. The peripheral blood lymphocyte count and lymphocyte response to PHA were similar in all patient groups. Serum IgA levels were elevated in Crohn's disease but fell significantly in ;ill' Crohn's patients following excisional surgery. Serum IgM levels rose significantly in ;ill' Crohn's patients after surgery. Steroid therapy was associated with diminution of both Mantoux and DNCB responses in the ;ill' Crohn's patients. There was no evidence of impairment of immune competence in either Crohn's disease or ulcerative colitis.

Adolescent↗
PubMed2005

CD4+CD25+ T cells regulate colonic localization of CD4 T cells reactive to a microbial antigen.

BACKGROUND: In patients with inflammatory bowel diseases, T-cell activation driven by microflora has been implicated as a mechanism causing clonal expansion and infiltration of CD4+ T cells in colonic lamina propria (LP). We explored a regulatory mechanism preventing infiltration of CD4+ T cells specific to a microbe-associated antigen in the gut. METHODS: SCID mice were reconstituted with CD4+ T cells specific to ovalbumin (OVA) and were orally administered with Escherichia coli engineered to produce OVA. RESULTS: OVA-specific CD4+ T cells (KJ1-26+) were recruited to colonic LP in an Ag-dependent manner, which was inhibited by adoptive transfer of naturally occurring CD4+CD25+ T (Treg) cells. KJ1-26+ T cells and Treg cells are localized preferentially to the colonic follicles that contain dendritic cells. In mice given Treg cells, LP CD4+ T cells showed a decrease in proliferative and interferon gamma response and an increase in transforming growth factor beta1 response to OVA stimulation. Treg cells inhibited both antigenic activation of effector CD4+ T cells and class II/CD80/CD86 up-regulation of dendritic cells. CONCLUSION: : Treg cells suppress recruitment of CD4+ T cells specific to a microbe-associated antigen to LP, which was associated with colocalization of effector CD4+ T cells and Treg cells in colonic follicles.

Animals↗
PubMed1976

Analysis of the lympho-plasmacytic infiltrate in Crohn's disease with special reference to identification of lymphocyte-subpopulations.

Lympho-plasmacytic infiltrates in cryostat sections (resected small intestine or colon specimens and rectal biopsies) from 29 patients with Crohn's disease (CD) were studied with the immunoperoxidase and immunofluorescence technique, by means of specific anti-human lymphocyte globulin (ALG) and specific anti-human T-lymphocyte globulin (ATG). Control specimens were obtained from 16 patients with ulcerative colitis (UC) and 12 subjects without inflammatory bowel disease. Characteristic transmural inflammatory infiltrates in CD consisted mainly of lymphocytes. A wide variation of the relative T-cell proportion was observed. However, in contrast with UC, abundant numbers of T-lymphocytes in CD were often detected, particularly in the deeper layers of the bowel wall. Furthermore, in serial sections immunoglobulin-containing plasma cells were counted, using specific anti-IgA, -IgM, and -IgG antisera. A significant reduction of the IgA/IgM plasma cell-ratio was found in CD in comparison with UC and controls. Our results indicate that in CD a chronic cellular immune reaction is going on within the diseases gut, involving increased numbers of lymphocytes and particularly T-cells. It remains to be established whether a deficient IgA barrier has to be considered of primary pathogenetic importance.

Adolescent↗
PubMed2002

Preferential Th1 immune response in invariant chain-deficient mice.

MHC class II molecules associate with the invariant chain (Ii) molecule during biosynthesis. Ii facilitates the folding of class II molecules, interferes with their peptide association, and is involved in MHC class II transport. In this study, we have investigated the in vitro and in vivo immune response of Ii-deficient mice (Ii(-/-)). Our results have demonstrated that CD4(+) T cells from Ii(-/-) mice proliferate normally in vitro after in vivo immunization with protein Ags. However, cytokine secretion profiles of Ag-primed CD4(+) T cells from Ii(-/-) mice differ from CD4(+) T cells from wild-type mice. Whereas cells from wild-type mice secrete IFN-gamma and IL-4, cells from Ii(-/-) mice secrete mostly IFN-gamma. Moreover, Ii(-/-) mice exhibit a normal Th1 response in the delayed-type hypersensitivity and trinitrobenzene sulfonic acid colitis models; however, these mice lack an in vivo Th2 response, as demonstrated in the asthma model. Therefore, we suggest that defective Ag presentation in Ii(-/-) mice leads selectively to a Th1 effector response.

Animals↗
PubMedDate not supplied

Gut-associated lymphoid tissues in ulcerative colitis.

BACKGROUND: The main feature of ulcerative colitis (UC) is numerous infiltration of not only lymphocytes and plasma cells but also neutrophils and macrophages, indicating acute on chronic inflammation. Recent studies show that apoptosis may play an important role in the regulation of gut-associated lymphoid tissues (GALT). Therefore, this study was performed to clarify apoptosis of lymphocytes in the peripheral blood and colonic mucosa of UC. METHODS: Three-color flow cytometry was used to clarify apoptosis of lymphocytes in the peripheral blood and colonic mucosa of patients with active and inactive UC compared with controls using fluorescence-labeled monoclonal and polyclonal antibodies such as Fas (CD95), Fas ligand, CD4, CD8, CD45RO, etc. RESULTS: The ratio of Fas and CD45RO double-positive cells in the peripheral blood of UC patients was significantly increased in CD8 but not CD4 T cells when compared with controls. The ratio of Fas-positive and CD45RO-negative cells was significantly increased in CD4 and CD8 T cells of UC when compared with controls. There was unbalanced immunoregulation between CD4 and CD8 T cells in the colonic mucosa of UC probably due to apoptosis through Fas-Fas ligand system. CONCLUSIONS: Abnormal GALT system was found in UC probably due to dysregulation of T cells through Fas-Fas ligand system.

Antigens, CD↗
PubMed2006

Flow cytometric analysis of expression of transforming growth factor-beta and glucocorticoid-induced tumor necrosis factor receptor on CD4(+) CD25(+) T cells of patients with inflammatory bowel disease.

To determine whether human CD4(+)CD25(+) cells express glucocorticoid-induced tumor necrosis factor receptor (GITR) and transforming growth factor-beta (TGF-beta) and the difference in CD4(+)CD25(+) cells between patients with inflammatory bowel diseases and healthy subjects, peripheral blood lymphocytes were obtained from patients with ulcerative colitis (UC; n = 50), Crohn's disease (CD; n = 49), and healthy volunteers (control; n = 50) and flow cytometric analysis was performed. In control subjects, the expression of GITR on CD4(+)CD25(+) cells (41.8 +/- 10.5%) was significantly higher than on CD4(+)CD25(-) cells (11.1 +/- 7.4%). Similarly, TGF-beta expression on CD4(+)CD25(+) cells (5.3 +/- 4.6%) was higher than on CD4(+)CD25(-) cells (1.2 +/- 1.4%). There were no significant differences among UC, CD, and control in CD4(+)CD25(+)/CD4(+) ratio. However, there was a significant difference in the CD4(+)CD25(+) TGF-beta+/CD4(+)CD25(+) ratio between active UC and inactive UC (2.7 +/- 2.6 and 7.2 +/- 3.9%, respectively). The results suggest that TGF-beta is involved in the induction or sustained remission of UC.

Adolescent↗
PubMed1990

Lack of induction of suppressor T cells by intestinal epithelial cells from patients with inflammatory bowel disease.

The mechanisms underlying the chronic unrelenting inflammatory response seen in inflammatory bowel disease (IBD) are poorly understood. We have recently proposed a novel role for the normal intestinal enterocyte, that of antigen presenting cell. However, in contrast to conventional antigen presenting cells, normal enterocytes appear to selectively activate CD8+ antigen nonspecific suppressor T cells. To determine whether failure of this process may be occurring in inflammatory bowel disease, freshly isolated enterocytes from small and large bowel from normal patients, patients with Crohn's disease, ulcerative colitis, and inflammatory (diverticulitis, ischemic colitis, and gold induced colitis) controls were co-cultured with allogeneic T cells in a modified mixed lymphocyte reaction. In contrast to normal enterocytes, 42/42 Crohn's and 35/38 ulcerative colitis-derived epithelial cells stimulated CD4+ T cells, whereas 65/66 and 9/9 normal and inflammatory control enterocytes, respectively, stimulated CD8+ T cells (as previously described), suggesting that the results seen were not just a reflection of underlying inflammation. Furthermore, IBD enterocytes from both histologically involved and uninvolved tissue were similar in their ability to selectively activate CD4+ T cells, speaking for a more global defect in epithelial cells in IBD. Finally, activated T cells from IBD epithelial cell-stimulated mixed lymphocyte cultures displayed potent T helper activity in an antigen nonspecific fashion. Taken together, these data suggest that there may be an intrinsic defect in epithelial cells from patients with IBD, resulting in the inability to normally stimulate suppressor T cells in an antigen overloaded environment.

Antigens, Differentiation, T-Lymphocyte↗