Biomedical subjects

E C Ebert

Publications and source records attributed to E C Ebert.

At least 37 records · Page 2Linked to original sources

PubMed1998

Migration of intestinal intraepithelial lymphocytes into a polarized epithelial monolayer.

Intraepithelial lymphocytes (IEL) are a phenotypically distinct population of lymphocytes that reside in mucosal epithelia, below the intercellular tight junctions. Although adhesive functions of this population have been previously studied, relatively little is known about IEL migration from the microvasculature into the epithelium. We demonstrated that cultured human IEL were capable of migration into polarized epithelial cells in vitro, where they assumed a subjunctional position, identical to that observed in vivo. The migration was rapid and efficient and was directionally polarized, such that IEL migrated into epithelial monolayers from the basolateral, but not the apical, aspect. After a 4-h period of residence, up to one-half of the IEL then exited the monolayer basolaterally. Migration was partially inhibited by pertussis toxin, suggesting a potential mechanism for IEL migration by chemokine receptor-mediated signaling. The conditions and ligand pairs used in IEL migration were different from those for neutrophils, another cell type known to migrate through epithelia. This system may serve as a model for microenvironmental homing of IEL into the epithelium.

CD8-Positive T-Lymphocytes↗

PubMed1997

Mesenchymal cells stimulate human intestinal intraepithelial lymphocytes.

BACKGROUND & AIMS: Intraepithelial lymphocytes (IELs) from human intestinal mucosa proliferate minimally to T-cell stimuli. Optimal growth may depend on factors that are missing in vitro, such as accessory cells. The aim of this study was to determine whether mesenchymal cells costimulate IELs. METHODS: IELs were isolated from human jejunum and cultured with fibroblasts or smooth muscle cells (mesenchymal cell models for mucosal myofibroblasts) and various T-cell stimuli. Proliferation was determined by [3H]thymidine incorporation, and interleukin 2 (IL-2) production was measured by enzyme-linked immunosorbent assay. Surface molecules were detected by immunofluorescence and flow cytometry. RESULTS: The proliferative responses of IELs to mitogen (phytohemagglutinin), superantigen (staphylococcal enterotoxin B), or anti-CD3 antibody were increased greatly by coculture with mesenchymal cells, while only slightly by peripheral-blood monocytes, the classical antigen-presenting cells. IL-2 production and receptor expression also increased. Mesenchymal cell costimulation of IEL growth required direct contact between the two cell types and was partly dependent on the integrin alpha4beta1 (very late activation 4[VLA-4]) and major histocompatibility complex (MHC) class I, as their respective antibodies blocked the effect. The surface molecules B7 (CD80), CD2, and MHC class II were not involved. CONCLUSIONS: Optimal IEL growth depends on their contact with mesenchymal cells, an interaction that is mediated by VLA-4 and MHC class I. In mucosal immunity, basement membrane myofibroblasts likely serve this role.

CD8-Positive T-Lymphocytes↗

PubMed1997

Intestinal perforation. A common complication of scleroderma.

The known intestinal complications of systemic sclerosis (SSc) stem mainly from motor disturbances. Autopsy findings were studied to identify anatomic abnormalities that may be associated with this disease. Descriptions of intestinal organs at autopsy were compared in 16 patients with SSc and 18 patients with systemic lupus erythematosus (SLE), a related disease control. There was a high incidence of perforation in SSc (7 of 16 patients) compared to SLE (1 of 18 patients) (P < 0.05). In SSc, perforations involved all parts of the bowel: transmural esophageal fibrosis (after heater probe cautery), dehiscence of suture line after gastric resection, perforated duodenal ulcers (N = 2), terminal ileal ischemia, and diverticulitis (N = 2). Two of the perforations in SSc were silent and were discovered at autopsy. The one perforation in SLE was due to full-thickness necrosis from vasculitis. This study suggests that the intestinal walls of patients with SSc are inherently weak; the gastroenterologist should keep this in mind when performing invasive procedures.

Adult↗

PubMed1997

Intestinal intraepithelial lymphocytes have a promiscuous interleukin-8 receptor.

BACKGROUND: Human intraepithelial lymphocytes (IELs), predominantly T cells of the CD8+CD45RO+ phenotype that are situated between epithelial cells, have a chemotactic response to the alpha-chemokines, IL-8 and GRO, and the beta-chemokine, and the protein termed regulated on activation, normal T cell expressed and secreted (RANTES). AIM: To evaluate the specificity of the IL-8 receptor on IELs. METHODS: Specificity was determined by the degree of desensitisation of the IL-8 response caused by each chemokine and the degree of inhibition of IL-8 binding to the cell. RESULTS: IELs migrated towards two additional beta chemokines, macrophage inflammatory protein-1 and monocyte chemotactic protein (MCP). All chemokines inhibited IL-8 induced chemotaxis and calcium ion mobilisation by IELs, with IL-8 having the greatest effect and MCP the least. In addition, specific binding of radiolabelled IL-8 to IELs was reduced by each of the five chemokines in cold competition experiments, whereas only GRO and IL-8 itself displaced 125I-IL-8 from receptors on peripheral blood mononuclear cells. CONCLUSIONS: The IL-8 responsiveness of IELs is desensitised by chemokines of both the alpha and beta families, and this is likely to occur by the binding of the chemokines to common receptors.

Antigens, CD↗

PubMed1997

Intraepithelial lymphocytes in normal human intestine do not express proteins associated with cytolytic function.

Human small intestine contains a very large population of intraepithelial T lymphocytes (IELs) that are oligoclonal, appear functionally to be cytolytic T cells, and may contribute to the normal and pathological turnover of intestinal epithelial cells. This report addresses the cytolytic function of IELs in normal small intestine by examining their expression of molecules that carry out cell-mediated cytolysis. Immunohistochemical analyses of granzyme B, perforin, Fas ligand, and tumor necrosis factor-alpha demonstrated these proteins were not expressed by small intestinal IELs in situ. These proteins also were not expressed by colonic IELs or by lamina propria lymphocytes in the small or large intestine. Granzyme A, however, was expressed by a large fraction of IELs. In contrast to these in situ results, isolated and in vitro activated IELs were shown to express effector proteins consistent with cytolytic T cells, including granzyme B, Fas ligand, tumor necrosis factor-alpha, and interferon-gamma. These results are most consistent with the vast majority of IELs in normal human small intestine being resting cytolytic T cells and suggest that these cells do not contribute to the apoptotic cell death of epithelial cells in normal intestine.

Fas Ligand Protein↗

PubMed1996

p126 (CDw101), a costimulatory molecule preferentially expressed on mucosal T lymphocytes.

Intestinal mucosal lymphocytes are defined by their anatomic location within the epithelium (intraepithelial lymphocytes), the interstitium between the epithelial basement membrane and the underlying muscularis mucosa (lamina propria lymphocytes), or in organized lymphoid tissues (Peyer's patches). Although intestinal intraepithelial lymphocytes have a distinct localization, their function has not been determined. To define cell surface proteins that are involved in intestinal intraepithelial lymphocyte localization or function, cultured human mucosal lymphocytes were used as immunogens to develop mAbs that react predominantly with this cell population in an immunohistochemical screening assay. Three mAbs were selected that subsequently were found by biochemical analysis to identify a 200-kDa homodimeric polypeptide on 88 to 98% of CD3+ mucosal lymphocytes but only 18 +/- 13% of PBLs. Expression on granulocytes and monocytes was also observed. This polypeptide has been termed p126 based on its SDS-PAGE-determined M(r) under reducing conditions. Cleveland digest maps demonstrated similarity between the p126 and CDw101 polypeptides. Determined amino acid sequence analysis of the purified p126 polypeptide revealed that it is the protein product of the recently identified V7 gene, which has structural similarities to members of the Ig gene superfamily. Two of the anti-p126 mAbs were costimulatory with suboptimal concentrations of anti-CD3 mAb inducing proliferation of cultured intestinal intraepithelial lymphocytes. Thus, we conclude that p126 is CDw101 encoded by a gene that predicts a seven-Ig domain chain-like structure. It has restricted expression predominantly on mucosal T lymphocytes and appears to have a costimulatory function of special relevance for CD28- T cells and for mucosal lymphocytes.

Animals↗

PubMed1996

Costimulation of the CD3 pathway by CD28 ligation in human intestinal lymphocytes.

A distinctive characteristic of human intestinal lymphocytes is their low responsiveness to stimuli of the CD3 pathway in vitro. This may be due to anergy resulting from CD3 stimulation without costimulation. Costimulatory molecules, such as HML-1, VLA-4, CD44, and CD28, may be lacking or unresponsive to ligation. Expression of these costimulatory markers was examined by immunofluorescent staining and flow cytometry. Their ability to costimulate intestinal lymphocytes was tested by measuring changes in proliferation, IL-2 production, and calcium ion mobilization. HML-1 was found on 87 +/- 8% of intraepithelial lymphocytes but only 52 +/- 10% of lamina propria lymphocytes; the density of expression was three times higher on the former. VLA-4 and CD44 were expressed on more than 80% of both lymphocyte types. CD28 was found on 31 +/- 26% of intraepithelial lymphocytes and 55 +/- 15% of lamina propria lymphocytes; virtually all CD4+ T cells and 15 to 26% of CD8+ T cells were CD28+. Of the four costimulatory molecules, ligation of only CD28 increased proliferation and IL-2 production; none affected calcium ion mobilization with stimulation through the CD3 pathway. The marker B7/BB1, a binding partner to CD28, was not present on lymphocytes or epithelial cells by flow cytometry. CD28 is the only one of these costimulatory molecules that enhanced CD3-induced functions of both intestinal lymphocyte types, but little ligand is available in vivo. Without coligation, CD3 activation may lead to anergy.

CD28 Antigens↗

PubMed1996

Human intestinal intraepithelial lymphocytes bind to mucosal mesenchymal cells through VLA4 and CD11A.

Human intestinal intraepithelial lymphocytes (IEL), predominantly CD8+ T lymphocytes, are uniquely situated at the basolateral surfaces of epithelial cells in contact with the myofibroblasts that comprise the basement membrane. Since mesenchymal cells may anchor IEL in this location and may also serve as antigen-presenting cells, the mechanism of binding to IEL was investigated. Lymphocytes were radiolabeled with [51Cr] sodium chromate, cocultured with mesenchymal cell monolayers, and the nonadherent lymphocytes removed by washes. Those adherent to the monolayers were counted by measuring the amount of radiolabel retained in the well. A large fraction of IL-2-activated IEL bound to KD (lip fibroblast), HISM (jejunal smooth muscle), and JF (jejunal fibroblast) cell lines after a 2-hr incubation: 33 +/- 11, 37 +/-14, and 48 +/- 15%, respectively. When monoclonal antibodies directed at the alpha chains of the very late activation antigens (CD49) were added alone or combined with anti CD11a to assays measuring IEL binding to KD or JF monolayers, the greatest inhibition (33 to 38%) occurred with anti-alpha 4 combined with anti-CD11a. The majority of IEL expressed alpha 1 and alpha 4 before and after a 3-day culture with IL-2, with no change in surface density. VCAM-1, a binding partner to alpha 4, was not expressed on KD or JF cells, and anti-VCAM antibody had no effect on binding. In summary, alpha 4 and CD11a on IEL mediate binding to mesenchymal cells.

Cell Adhesion↗

PubMed1996

Mechanisms of colon cancer binding to substratum and cells.

Binding of colon cancer to extracellular matrix (ECM) proteins and mesenchymal cells that comprise the basement membrane is important in migration and metastasis. This study defines the conditions and surface structures necessary for adhesion of HT-29 cells to ECM proteins and cell monolayers. Binding began within minutes and peaked by 1 hr, with 80-95% of HT-29 cells binding to the ECM proteins, collagen IV, laminin, fibronectin, and vitronectin and 40-75% binding to monolayers of fibroblasts, smooth muscle cells, and HT-29 cells. Treating mesenchymal cells with the fibrogenic cytokines, IL-1, IL-4, or TNF-alpha, which increase production of ECM proteins, did not alter binding of HT-29 cells to these monolayers. Attachment of HT-29 cells to cell monolayers was inhibited by cytochalasin D and sodium azide, but not cycloheximide or neuraminidase. Attachment to ECM proteins, in contrast, was unaffected by any of these metabolic inhibitors but required certain divalent cations (Mg2+ and Mn2+ but not Ca2+). Antibody to the integrin beta 1, chain (CD29) eliminated binding to collagen and laminin but not to fibronectin, fibroblasts, and HT-29 monolayers. Antibody to the vitronectin receptor inhibited binding to fibronectin. Antibodies to integrin alpha 1-alpha 6 chains had no effect on any adhesion event. Three colon cancer cell lines were tested for expression of VLA antigens: alpha 2 and alpha 3 were detected on all three, alpha 1 and alpha 6 were variably expressed, while alpha 4 and alpha 5 were absent. This study demonstrates that several mechanisms account for tumor cell attachment to substratum and cells.

Basement Membrane↗

PubMed1996

IL-4 down-regulates the responsiveness of human intraepithelial lymphocytes.

IL-4 is an important regulator of intestinal inflammation, yet little is known regarding its action on intestinal lymphocytes. Intestinal lymphocytes were isolated from jejunal mucosa of patients undergoing gastric bypass operations for morbid obesity. The impact of IL-4 was measured by its effects on proliferation using 3H-thymidine incorporation, IL-2 production using the CTLL assay, and IL-2 receptor generation using immunofluorescence. The production of IL-4 was measured by ELISA. IL-4 significantly inhibited the proliferation of intraepithelial lymphocytes (IEL) to a variety of stimuli as well as the development of lymphokine-activated killer (LAK) cells. In contrast, it had no effect on the proliferation of CD8+ T cells from peripheral blood. The inhibitory effect of IL-4 on IEL did not occur during activation, since IL-2 production and receptor expression were not altered. Rather, it occurred during cell cycling, since over 50% inhibition resulted whether IL-4 was added at the initiation of an IL-2-stimulated culture or after 24 or 48 h incubation. IL-4 was secreted by activated lamina propria lymphocytes (LPL) but not by IEL. IL-4, produced by activated LPL, may enter the epithelial compartment and down-regulate responsiveness of IEL.

Down-Regulation↗

PubMed1995

Pitfalls in the characterization of small intestinal lymphocytes.

The morphological characteristics of human intestinal lymphocytes may vary depending upon whether they are examined in tissue sections or after isolation. This study uncovered some causes of these discrepancies. The majority of intraepithelial lymphocytes (IEL) and lamina propria lymphocytes (LPL) are of the same size and granularity as peripheral blood mononuclear cells (PBMC), negating the idea that most IEL are large granular lymphocytes. LPL were previously shown to express markers of early activation by flow cytometry but not by immunohistochemistry. This study shows that it is the low density of surface antigen expression that explains this discrepancy: only the highly sensitive flow cytometric analysis can detect such low-density expression. Previous reports of intestinal macrophage and B cell numbers and functions vary markedly. This may be due to variable amounts of contamination with epithelial cells (EC) that lose their characteristic columnar appearance and cytoplasmic mucin upon isolation. They share many features of macrophages (such as morphology and binding to plastic and latex beads) but lack phagocytic ability and superoxide generation, explaining, perhaps, the wide variation in the reported functions of presumed intestinal macrophages. In addition, a large fraction of EC non-specifically strain with anti-immunoglobulin antibodies. Their contamination of intestinal lymphocyte preparations accounts for the discrepancy in B cell numbers identified by surface immunoglobulin expression versus B cell markers. Intestinal lymphocytes do indeed differ in many ways from circulating lymphocytes, but investigators must be attentive to factors that may artifactually alter their results.

Antibodies, Monoclonal↗

PubMed1995

Interleukin-7 activates intestinal lymphocytes.

Human intestinal lymphocytes, particularly intraepithelial lymphocytes, proliferate minimally to some agents, like mitogens and stimuli of the CD3 pathway. This in vitro finding may be due, in part, to a loss of factors found in vivo. Three T-cell growth factors, IL-7, IL-9, and IL-12, were tested for their ability to stimulate the proliferation of intestinal lymphocytes. Both intraepithelial lymphocytes and lamina propria lymphocytes proliferated more vigorously to IL-7 than to IL-9 or IL-12, and only IL-7 increased stimulation through the CD3 pathway. The IL-7-induced response was IL-2-dependent: IL-2 receptors appeared on both intestinal lymphocyte types, and antibody to the IL-2 receptor blocked IL-7-induced proliferation. Both CD4+ and CD8+ T-cell subsets responded to this cytokine as shown by phenotype-depletion experiments and constancy in the CD4/CD8 ratios after culture with IL-7. In addition, the T-cell receptor alpha beta and gamma delta subsets responded equally well to IL-7. This newly described selective proliferative response of intestinal lymphocytes to IL-7, but not to IL-9 or IL-12, requires no preactivation and may enhance growth in vivo.

Antibodies↗

PubMed1995

Human intestinal intraepithelial lymphocytes have potent chemotactic activity.

BACKGROUND & AIMS: Inflammation is created by the movement of leukocytes toward soluble attractants (chemokines). The aim of this study was to identify the chemokines that attract intestinal lymphocytes. METHODS: Intraepithelial and lamina propria lymphocytes were isolated from human jejunal mucosa of healthy individuals and cultured in interleukin (IL) 2 for 3 days. Migration was assessed using the Boyden transwell assay. Increases in cytoplasmic calcium ion concentration ([Ca2+]i) were measured from changes in fluorescence in Fura-2-loaded lymphocytes on exposure to the cytokines. RESULTS: A large number of intraepithelial lymphocytes migrated toward IL-8 and RANTES (regulated on activation, normal T cell expressed and secreted), and a small number migrated toward IL-10. In contrast, only a few lamina propria lymphocytes migrated toward IL-8, and none responded to the other chemokines tested. The chemokines IL-8 and IL-10, but not RANTES, increased [Ca2+]i in intraepithelial lymphocytes; this calcium mobilization was not affected by ethylene glycol-bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid, indicating that calcium is released from intracellular sources. None of the factors caused calcium mobilization by lamina propria lymphocytes. CONCLUSIONS: This study shows that intraepithelial lymphocytes have greater migratory and calcium-mobilizing activity than lamina propria lymphocytes and that these two activities do not correlate with each other.

Calcium↗

PubMed1994

Distribution of dominant T cell receptor beta chains in human intestinal mucosa.

The majority of human intestinal intraepithelial lymphocytes (iIELs) are CD8+ T cells that use the T cell receptor (TCR)-alpha/beta. Previous studies have shown that iIELs isolated from segments of small intestine or colon contain one or several dominant alpha/beta T cell clones. It is not known whether these clones expand only locally in response to a particular antigen or whether they are widely distributed throughout the intestine. To address this question, iIELs were purified from near the proximal and distal margins in a series of intestinal resections for noninflammatory diseases. TCR-beta expression was then assessed by semiquantitative polymerase chain reaction amplification, analysis of N-region length, and DNA sequencing. The previously described oligoclonal expansion of iIELs was confirmed in each sample. Identical dominant clones were identified in the proximal and distal samples from most cases, including samples taken from sites as distant as the transverse and sigmoid colon or rectum. Distinct clones were found in only one case with samples from the terminal ileum and transverse colon. These results demonstrate that a relatively small number of widely dispersed T cell clones comprise the majority of cells in the human intestinal mucosa.

Adult↗

PubMed1994

Distinct structural and functional epitopes of the alpha E beta 7 integrin.

Intestinal intraepithelial lymphocytes (iIEL) are predominantly CD3+, CD8+ T lymphocytes located above or adjacent to the mucosal basement membrane. Although they are positioned to interact with intercellular luminal antigen or with enterocytes, the function of iIEL remains unknown. Most (> 85%) of the iIEL express the alpha E beta 7 integrin which appears to be involved in the adhesion of lymphocytes to epithelial cells. We report the characterization of three monoclonal antibodies (mAb) termed alpha E7-1, alpha E7-2, and alpha E7-3, that react with the alpha E beta 7 integrin recognized by the previously described mAb HML-1 as demonstrated by identical sodium dodecyl sulfate-polyacrylamide gel electrophoresis mobility and charge. Flow cytometric analysis of antibody cross-blocking indicated that these mAb recognize distinct epitopes of alpha E beta 7. While all of the mAb were capable of blocking the adhesion of cultured iIEL to a breast epithelial cell line, only HML-1 and alpha E7-1 (which recognize an identical or closely related epitope) were co-stimulatory with suboptimal concentrations of anti-CD3 mAb in inducing proliferation of cultured iIEL. Thus, these mAb appear to recognize functionally distinct epitopes of alpha E beta 7 and will be useful to study relationships between the structure and function of this integrin.

Animals↗

PubMed1994

Intestinal mucosal lymphocytes have H1 receptors: H1 antagonists reduce their proliferation and cytotoxicity.

Histamine and H1 antagonists inhibit the proliferation and natural killer activity of peripheral blood mononuclear cells, which express large numbers of H1 receptors. This study examined the presence of H1 receptors and the effects of histamine, H1 antagonists (pyrilamine and diphenhydramine), and H2 antagonists (cimetidine and ranitidine) on human intestinal lymphocyte proliferation and cytotoxicity. Intestinal lymphocytes were obtained by chemical and enzymatic treatment of surgical specimens and purified by Percoll density gradient centrifugation. Proliferation was measured by [3H]thymidine incorporation of mitogen-stimulated lymphocytes; cytotoxicity was measured by the standard 51Cr-release assay using HT-29 adenocarcinoma target cells. Scatchard analysis of radioligand binding using [3H]pyrilamine demonstrated H1 receptors. The mitogen-induced proliferative responses of intraepithelial lymphocytes and lamina propria lymphocytes were inhibited by histamine and the H1 antagonists but not the H2 antagonists. Cytotoxic activities of fresh or IL-2-stimulated mucosal lymphocytes (spontaneous and lymphokine-activated killing, respectively) were also reduced by the H1 antagonists. A large number of H1 receptors were found on intraepithelial lymphocytes and peripheral blood mononuclear cells and still more on lamina propria lymphocytes. Intestinal lymphocytes bear H1 receptors; histamine and H1 antagonists have immunomodulatory effects on these cells.

Cell Division↗

PubMed1993

Human intestinal intraepithelial lymphocytes are derived from a limited number of T cell clones that utilize multiple V beta T cell receptor genes.

Intestinal intraepithelial lymphocytes (IEL) are a phenotypically distinct T cell population of unknown function. The majority of human intestinal IEL express the TCR-alpha beta, the CD8 accessory molecule, and the CD45RO Ag, suggesting that they are MHC class I-restricted memory T cells. Recent analyses of the TCR alpha- and beta-chains expressed by these cells have shown marked skewing toward one or several V region genes in individual donors and revealed the presence of clonally expanded cells. In addition, functional data has suggested that the MHC class I-like CD1 molecules may be the target ligands for some human intestinal IEL clones. This report examines in detail the TCR-beta repertoire of human jejunal IEL to determine what fraction of these cells are clonally expanded and to determine whether a particular subset of V beta genes are utilized by the clonally expanded cells. The results demonstrate that the majority of IEL are derived from the expansion of a relatively few T cell clones and that these clones can utilize a large number of different V beta genes. Oligoclonal expansion is also demonstrated among lamina propria lymphocytes (LPL), with overlapping but distinct clones detected in the LPL vs the IEL populations. These results indicate that most intestinal IEL-alpha beta, and a subpopulation of LPL, are specific for a limited number of Ag and place constraints on the possible roles played by IEL in the defense against diverse environmental pathogens or in the generation of oral tolerance.

Amino Acid Sequence↗

PubMed1993

Do the CD45RO+CD8+ intestinal intraepithelial T lymphocytes have the characteristics of memory cells?

Human intraepithelial lymphocytes (IEL) are predominantly CD45RO+ (memory) CD8+ T lymphocytes located between intestinal epithelial cells. This study determines whether IEL share other characteristics with circulating CD45RO+ lymphocytes. Memory cells are large and have an upregulated expression of adhesion molecules. In contrast, the majority of IEL are the same size as peripheral blood (PB) T cells. In addition, IEL do not have an increased density of adhesion molecules, although a larger percentage express CD54 and CD58 compared to PBL. Allo-CTL activity, demonstrated by CD45RO+ PBL, could not be shown using either IEL or lamina propria lymphocytes (LPL) after a 5-day culture with alloantigen. However, after a 2.5-week culture with allogeneic PBL and interleukin-2 (IL-2), both IEL and LPL were capable of this cytotoxic function. The addition of IL-4 or IL-6 did not alter CTL activity by mucosal lymphocytes. Alloantigen-stimulated IEL, LPL, and PB CD8+ T cell lines were propagated for up to 16 weeks. All lines demonstrated alloantigen-specific proliferation. The PB CD8+ T lymphocytes maintained their phenotype and allo-CTL activity. In contrast, the CD4+ subset in the IEL and LPL became the predominant lymphocyte type and demonstrated potent lytic activity that was not alloantigen specific. This study shows that (1) IEL do not have increased density of adhesion molecules, (2) mucosal lymphocytes demonstrate allo-CTL activity, (3) CD8+ T cells in the mucosa cannot be perpetuated long-term by alloantigen and IL-2, and (4) mucosal CD4+ T cell lines demonstrate marked alloantigen-nonspecific cytotoxicity. The only characteristic shared by IEL and circulating memory cells is allo-CTL activity.

CD8 Antigens↗