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C Fiocchi

Publications and source records attributed to C Fiocchi.

At least 73 records · Page 4Linked to original sources
PubMed1988

Expression of HLA-DR antigens in inflammatory bowel disease mucosa: role of intestinal lamina propria mononuclear cell-derived interferon gamma.

The expression of HLA-DR antigens on the surface of immune cells is crucial for appropriate antigen presentation and a normal immune response. In the intestinal mucosa involved by Crohn's disease and ulcerative colitis the expression of HLA-DR antigens is increased in both immune and nonimmune cells, a phenomenon probably mediated by soluble factors, such as interferon gamma, produced by locally activated mononuclear cells. This study investigated the production of interferon gamma by inflammatory bowel disease and control intestinal lamina propria mononuclear cells, and the ability of this endogenously produced lymphokine to induce expression of HLA-DR antigens on the monocytic cell lines U937 and ML3. After in vitro stimulation with interleukin 2 or phytohemagglutinin, but not spontaneously, lamina propria mononuclear cells produced variable amounts of interferon gamma, and their culture supernatants could induce de novo expression of HLA-DR antigens on the monocytic indicator cells. When the mononuclear cells were derived from inflammatory bowel disease mucosa, both the amount of interferon gamma present in the supernatants and the number of HLA-DR-positive cells induced by these supernatants were decreased as compared to controls. These results suggest that, in inflammatory bowel disease, interferon gamma may not be the only mediator of HLA-DR induction in the gut and that other soluble factors or agents, alone or interacting with interferon gamma, may also be responsible for this event, resulting in the enhanced HLA-DR antigen expression observed in the inflamed intestinal mucosa.

Adult↗
PubMed1988

Interferon gamma production by human intestinal mucosal mononuclear cells. Decreased levels in inflammatory bowel disease.

Immune (gamma) interferon is a substance produced by immunologically activated mononuclear cells. Besides its antiviral activity, interferon gamma has a crucial role in immunoregulation, by acting directly upon lymphocytes and monocytes, and interacting with other soluble mediators of the immune response. Studies of the interferons system in inflammatory bowel disease have been limited, and little information is available on the generation of interferon during immunological events occurring in the human gut. To investigate the capacity of intestinal mucosal mononuclear cells to produce interferon gamma, lamina proprial mononuclear cells, isolated from Crohn's disease, ulcerative colitis, and control patients, were incubated with interleukin 2 or phytohemagglutinin, and the amounts of interferon gamma present in the culture supernatants were measured by a virus cytopathic effect inhibition assay. Under identical stimulatory conditions, culture supernatants of cells derived from actively involved mucosa of inflammatory bowel disease specimens contained two- to fivefold less interferon gamma than those of cells from control tissue. However, the amount of interferon gamma present in supernatants of cells from uninvolved inflammatory bowel disease mucosa was similar to that found in control supernatants. These results indicate that, in patients with active Crohn's disease and ulcerative colitis, mononuclear cells produce decreased amounts of interferon gamma in the intestinal mucosa. The exact significance of these findings is unclear, but because of the importance of interferon gamma in a variety of cell-mediated immune phenomena, its impaired availability might be relevant to the pathogenesis of inflammatory bowel disease.

Adolescent↗
PubMed1988

Modulation of intestinal immune reactivity by interleukin 2. Phenotypic and functional analysis of lymphokine-activated killer cells from human intestinal mucosa.

There is evidence indicating that interleukin 2 may be important in the regulation of intestinal immunity, as suggested by its capacity to induce nonspecific cytotoxic (lymphokine-activated killer) activity from human intestinal mucosal mononuclear cells. The present study was designed to further explore the phenotypic and functional changes induced by interleukin 2 on intestinal lymphocytes derived from inflammatory bowel disease and control tissues. Immunohistology of intestinal mucosa demonstrated few cells bearing the activation antigen recognized by anti-Tac (anti-interleukin 2 receptor) monoclonal antibody. However, when isolated lamina proprial mononuclear cells were exposed to interleukin 2 in culture, the number of Tac-positive cells increased dramatically, a phenomenon paralleled by the generation of lymphokine-activated killer cell activity. This cytotoxic function was critically dependent on the continuous availability of interleukin 2, but not on the expression of the Tac antigen, since Tac-negative cells were also cytotoxic. Depletion of natural killer cells, fractionation into T cell-enriched and -depleted cells before and after culturing with interleukin 2, and separation into Tac-positive and -negative cells after interleukin 2 activation failed to eliminate lymphokine-activated killer cell activity, suggesting that this phenomenon is mediated by phenotypically and functionally heterogeneous cell subsets. During the induction of lymphokine-activated killer cells variable amounts of interferon-gamma were produced, but these did not correlate with the degree of cytotoxicity. No differences were observed between the response to interleukin 2 by inflammatory bowel disease and control cells. Therefore, in view of its capacity to induce significant phenotypic and functional changes in different subpopulations of intestinal mucosal mononuclear cells, interleukin 2 should be regarded as an important modulator of intestinal immune reactivity.

Adjuvants, Immunologic↗
PubMed1988

Polyclonal nature of the intestinal mucosal lymphocyte populations in inflammatory bowel disease. A molecular genetic evaluation of the immunoglobulin and T-cell antigen receptors.

To define the clonality of the intestinal lymphocytes involved in the immune response of inflammatory bowel disease, we performed a molecular genetic analysis of the arrangement of the immunoglobulin and antigen-specific T-cell receptor genes of isolated lamina propria lymphocytes derived from resected intestinal specimens of 12 patients with Crohn's disease, 5 patients with chronic ulcerative colitis, and 7 patients with other gastrointestinal diseases. The sensitivity of this technique is sufficient to detect a monoclonal population when there is as little as 1% clonal expansion in a mixed cell population. In all these groups of patients, deoxyribonucleic acid from the non-T cells demonstrated only a germ-line gene pattern, and no non-germ-line rearrangements of immunoglobulin genes as assessed by an immunoglobulin-joining heavy-chain gene probe. Deoxyribonucleic acid from the lamina propria T cells showed a rearrangement pattern of the antigen-specific T-cell receptor beta- and gamma-chain genes that is characteristic of polyclonal T cells as assessed by T-constant beta- and T-joining gamma-gene probes. These results indicate that the lamina propria non-T and T-lymphocyte populations in inflammatory bowel disease and controls are polyclonal.

Adult↗
PubMed1988

Lymphokine-activated killer (LAK) cells from human intestinal mucosa: cytotoxic activity against tumor cell lines and modified self but not autologous and allogeneic colon cancer cells.

Patients with colorectal cancer respond poorly to in vivo immunotherapy with lymphokine-activated killer (LAK) cells generated from peripheral blood mononuclear cells (PBMC). We postulated that gut-derived immune cells could be a more relevant source of LAK cells directed against colorectal cancer. Intestinal lamina propria mononuclear cells (LPMC) and colonic adenocarcinoma cells were isolated from operative specimens by combination of mechanical and enzymatic dissociation methods. LAK cells were generated by culturing PBMC and LPMC with recombinant interleukin 2 (IL2), with and without OKT3 monoclonal antibody, in short- (4 days) and long-term (21 days) cultures. Other cultured tumor cells, normal intestinal fibroblasts, and hapten-modified autologous LPMC were used as control targets. Cytotoxicity was measured by a 4-hr 51Cr release assay. Short-term cultured LAK cells exhibited a strong to moderate degree of killing against normal intestinal fibroblasts, hapten-modified self cells, and four different tumor cell lines. Instead, fresh colon cancer cells were resistant to cytotoxicity, regardless of their degree of histologic differentiation and the autologous or allogeneic nature of the LAK cells. Long-term culture with IL2 remarkably increased LAK cell activity against all tumor targets, but not against colonic adenocarcinoma cells. The results of this study, showing that freshly isolated colon cancer cells are intrinsically resistant in vitro to highly activated cytotoxic effector cells, may explain the poor clinical results observed in human trials with in vivo administration of IL2 or LAK cells.

Adenocarcinoma↗
PubMed1988

(2'-5')Oligoadenylate synthetase activity in intestinal mononuclear and epithelial cells of inflammatory bowel disease patients.

The activity of (2'-5')oligoadenylate synthetase, an enzyme induced by and mediating the antiviral action of interferon, was measured in extracts of intestinal mononuclear and epithelial cells isolated from patients with Crohn's disease, ulcerative colitis, and a control group. No significant differences were detected among (2'-5')oligoadenylate synthetase activities of lamina propria mononuclear cells derived from inflammatory bowel disease-involved and histologically normal control mucosa. Similarly, epithelial cells from inflammatory bowel disease and control patients expressed comparable levels of the enzyme, but these were significantly higher (p less than 0.01) than those found in autologous mononuclear cells. These results indicate that interferon is locally produced along the human intestinal mucosa under normal and inflammatory conditions. While this study supports the contention that induction of an antiviral state does not play a significant role in the pathogenesis of inflammatory bowel disease, it does not exclude the activation of the interferon system for other immunologic functions.

2',5'-Oligoadenylate Synthetase↗
PubMed1986

Intestinal immunity and inflammation: recent progress.

The previous sections illustrate that we are still defining (a) which sets of lymphoid cells are present in the intestine and which are not, (b) which sets are peculiar to the intestine, and (c) how the sets that are there function in the intestinal microenvironment. An understanding of the latter point is going to require knowledge of how these sets communicate with and regulate one another via cell surface molecules such as MHC class I and class II molecules, and via soluble mediators or lymphokines. The recent advances in various technologies make this a particularly exciting time in this field because the tools are now available to address and answer some of these basic and important questions in mucosal immunology. At the same time these advances hold great promise for our eventual understanding of chronic inflammatory diseases of the intestine. As was mentioned at the outset, the immune system has considerable power for both protection and destruction. It remains a puzzle how this latter potential is contained and controlled in the intestine of most individuals, such that they do not have inflammatory disease even in the setting of intense stimulation by substances, such as endotoxin, that are phlogistic elsewhere in the body. An answer to the question of why everyone does not have intestinal inflammation could provide new insights into the mechanisms involved in chronic intestinal inflammatory diseases. The recent advances just detailed, as well as others sure to come, suggest that it is only a matter of time before such questions are answered.

Animals↗
PubMed1986

Phenotypic analysis of lamina propria lymphocytes. Predominance of helper-inducer and cytolytic T-cell phenotypes and deficiency of suppressor-inducer phenotypes in Crohn's disease and control patients.

To better define the nature of intestinal T cells, the phenotypes of isolated lamina propria lymphocytes (LPL) were determined in both Crohn's disease patients and control patients using combinations of monoclonal antibodies that have been found to correlate with particular immunoregulatory functions. Isolated LPL and autologous peripheral blood lymphocytes (PBL) were stained with multiple combinations of monoclonal antibodies and studied by dual immunofluorescence flow cytometry. In LPL, compared with PBL, there was a significant increase in the proportion of T cells having the Leu-3+, Leu-8- and Leu-3+, 2H4- phenotypes (associated with helper-inducer function) and a corresponding decrease in the proportion of T cells having the Leu-3+, Leu-8+ and Leu-3+, 2H4+ phenotypes (associated with suppressor-inducer function). It was also found that in LPL, compared with PBL, the percentage of cells with the Leu-2+, Leu-15+ phenotype (associated with suppressor-effector function) was significantly lower. However, the percentage of T cells with the Leu-2+, 9.3+ phenotype (associated with cytolytic function) was similar in PBL and LPL in control patients. There were no major differences comparing Crohn's disease patients with control patients, except that the proportion of Leu-2+, 9.3+ lymphocytes was higher in PBL in Crohn's disease patients. These results show that the lymphocyte subpopulations in the lamina propria differ from those in peripheral blood in having predominantly the phenotypes of helper-inducer and cytolytic T cells, whereas the phenotypes of suppressor-inducer cells and activated suppressor cells are less frequently observed.

Adult↗
PubMed1985

Human intestinal mucosal mononuclear cells exhibit lymphokine-activated killer cell activity.

Previous investigations have shown that mononuclear cells present in human intestinal mucosa possess cytotoxic properties that are unique and different from those of cells circulating in the peripheral blood. We have further explored the cytolytic capacity of human intestinal mucosal mononuclear cells using both phenotypic and functional criteria. Using an immunoperoxidase technique on gut frozen sections, we failed to identify cells bearing surface markers displayed by natural killer cells and recognized by the monoclonal antibodies Leu7, Leu11, and Leu15. Freshly isolated human lamina proprial mononuclear cells (LPMC) were unable to lyse K562 target cells, even after using a variety of experimental conditions which included depletion of adherent cells, fractionation by Percoll gradients or panning with monoclonal antibodies, and treatment with a prostaglandin synthetase inhibitor or interferon-gamma. In contrast, when LPMC were cultured in the presence of the lymphokine interleukin 2 (IL 2), they displayed high levels of cytotoxicity against both K562 and Daudi target cells. Such cytolytic activity appeared after 1 or 2 days of culture, was dependent on the amount of IL 2 added to the cultures, was independent of plastic adherent cells, and could be inhibited by agents that block proliferation. Interferon-gamma, when used under experimental conditions identical to those adopted for IL 2, was unable to induce any significant cytotoxicity by LPMC or enhance the level of killing obtained by stimulation with IL 2 alone. This IL 2-induced, nonspecific cytotoxicity of LPMC probably represents a form of lymphokine-activated killer cell function similar to that recently described for human peripheral blood lymphocytes. In view of the absence of morphologic and functional evidence for natural killer cells in human intestinal mucosa, the phenomenon of lymphokine-activated killer cell activity displayed by LPMC may represent an alternate cytotoxic function potentially relevant to intestinal mucosa immunity.

Adolescent↗
PubMed1985

Immunoregulatory function of lamina propria T cells in Crohn's disease.

The pathogenesis of Crohn's disease may involve altered function of immunoregulatory T cells in the intestine. To investigate this hypothesis, lamina propria lymphocytes were isolated from intestinal specimens resected from patients with active Crohn's disease and control subjects (colon carcinoma and diverticular disease) using an enzymatic technique. The T-cell phenotypes and function of these lymphocytes were compared with that of peripheral blood lymphocytes. The proportion of Leu-2-positive (suppressor/cytotoxic) cells was similar in peripheral blood and isolated lamina propria lymphocytes, both in Crohn's disease and control patients. Although the proportion of Leu-3-positive (helper/inducer) lymphocytes was lower in lamina propria lymphocytes than peripheral blood lymphocytes, there was no difference comparing Crohn's disease and control patients. Helper T-cell function, as determined by measuring the ability of T cells to increase immunoglobulin synthesis by pokeweed mitogen-stimulated normal peripheral blood B cells, was similar in peripheral blood lymphocytes and lamina propria lymphocytes, and comparing Crohn's disease with control patients. Suppressor T-cell function, as determined by measuring the ability of T cells to inhibit immunoglobulin production by cultures containing pokeweed mitogen-stimulated normal peripheral blood T and B cells, was also similar comparing peripheral blood lymphocytes and lamina propria lymphocytes, and comparing Crohn's disease with control patients: neither peripheral blood lymphocytes nor lamina propria lymphocytes significantly suppressed immunoglobulin synthesis. OKT8 (suppressor/cytotoxic)-enriched lamina propria lymphocytes mediated only marginal suppression, whereas concanavalin A-activated intestinal T cells did mediate significant suppression, in both Crohn's disease and control patients. Thus, patients with active Crohn's disease have no alteration of immunoregulatory T-cell function for polyclonal mitogen-induced immunoglobulin synthesis at the gut mucosal level, despite the presence of an inflammatory process in the intestine.

Adolescent↗
PubMed1985

(2'-5') oligo adenylate synthetase activity in leucocytes of patients with inflammatory bowel disease.

The activity of an interferon induced enzyme, (2',5') oligo adenylate synthetase, was determined in peripheral blood mononuclear cells and granulocytes of patients with inflammatory bowel disease and compared with its activity in cells isolated from normal subjects. In spite of the fact that circulating interferon is detected in patients with inflammatory bowel disease, we failed to see any increase in (2',5') oligo adenylate synthetase activity in these patients. The mean +/- SE enzyme activity given in nmol ATP incorporated into (2',5') isoadenylate oligomers by extracts of 10(5) peripheral blood mononuclear cells/21 hours was in normal subjects 1.84 +/- 0.30 (n = 27), in patients with active Crohn's disease 1.38 +/- 0.15 (n = 20) and in patients with active ulcerative colitis 1.14 +/- 0.23 (n = 21). (2',5') oligo adenylate synthetase activity in granulocytes was also similar in normal subjects and in patients with active ulcerative colitis or Crohn's disease. The enzyme activity in patients with active disease was similar both prior to and during steroid therapy. The low (2',5') oligo adenylate synthetase activity in peripheral blood mononuclear cells and granulocytes of patients with active inflammatory bowel disease may reflect decreased cellular response to interferon or a difference in the type of interferon elevated in viral diseases and in inflammatory bowel disease.

2',5'-Oligoadenylate Synthetase↗
PubMed1985

Sensitization to epithelial antigens in chronic mucosal inflammatory disease. Characterization of human intestinal mucosa-derived mononuclear cells reactive with purified epithelial cell-associated components in vitro.

To explore the auto-reactive potential of cells infiltrating the gut mucosa in idiopathic chronic inflammatory bowel disease, intestinal lamina propria mononuclear cells (LPMC) were isolated, characterized morphologically and phenotypically, and evaluated for antigen-specific reactivity. The last was assessed by quantitating LPMC cytotoxic capabilities against purified, aqueous-soluble, organ-specific epithelial cell-associated components (ECAC) characterized previously. Enzyme-isolated inflammatory bowel disease LPMC were constituted primarily by T lymphocytes (57 +/- 12% OKT 3-positive), B lymphocytes (18 +/- 9% surface immunoglobulin-positive), and macrophages (11 +/- 6% esterase-positive), and were responsive to phytohemagglutinin (mean uptake 86,933 cpm/5 X 10(5) cells). LPMC present in abnormal segments from 71% of patients with chronic inflammatory bowel disease were cytotoxic for ECAC isolated from colon (12.5 +/- 8.9% specific lysis) and small bowel (7.1 +/- 6.5%), but not for kidney control antigen (0.8 +/- 1.1%) isolated in a manner analogous to that used for ECAC (P less than 0.02). In contrast, despite comparable responses to phytohemagglutinin (mean uptake 59,200 cpm/5 X 10(5) cells), LPMC from histologically normal mucosa of patients with benign (adult megacolon, Hirshsprung's disease, diverticulosis) or malignant disease failed to lyse indicator cells labeled with colon-derived ECAC (0.3 +/- 0.08%), small bowel-derived ECAC (0.4 +/- 1.11%), or kidney antigen (0.29 +/- 0.79%). LPMC reactivity for individual gel-purified macromolecules of small bowel-derived ECAC (designated as the "P" series of components) was greatest against component P1 (by 2-3-fold), but was detectable against three other purified components as well. The addition of patient's serum did not enhance cytotoxicity to ECAC. Characterization of the cytotoxic cell showed that it was nonadherent to plastic surfaces, bore T lymphocyte-specific markers detectable by OKT 11 and OKT 3 monoclonal antibodies, and could be depleted by removal of cells with receptors for sheep erythrocytes. ECAC-specific reactivity was markedly reduced (greater than 93%) in most experiments when LPMC were preincubated for 1 h with ECAC. These data support the concept that autosensitization to several epithelial cell-associated components has occurred in patients with chronic inflammatory bowel disease, and provide initial evidence that antigen-specific, cell-mediated mechanisms may play a role in the pathogenesis of these disorders.

Adult↗
PubMed1984

Interleukin 2 activity of human intestinal mucosa mononuclear cells. Decreased levels in inflammatory bowel disease.

Interleukin 2, a soluble product of activated T lymphocytes, is of central importance in the development of an appropriate T-cell immune response. Defects in the production of or response to this lymphokine have been described in a variety of immune deficiency and autoimmune states, thus suggesting a role in the pathogenesis of such disorders. To investigate potential abnormalities of interleukin 2 in inflammatory bowel disease, we measured its activity in cultures of intestinal mucosa mononuclear cells derived from Crohn's disease and ulcerative colitis patients. Lamina propria mononuclear cells from inflamed and control tissues were incubated with phorbol myristate acetate, and the amount of the lymphokine in the supernatants was quantitated in a biological assay using cloned, interleukin 2-dependent, cytotoxic mouse T-cell lines. We found that, in culture supernatants of cells from both forms of inflammatory bowel disease, interleukin 2 levels were significantly lower than those detected in cultures containing cells from histologically normal mucosa. Low levels were not correlated to duration, clinical activity, and anatomical location of the disease process or corticosteriod therapy. Deficient activity of this essential growth factor could contribute to abnormal T-cell proliferation and clonal expansion at the gut mucosal level, perhaps inducing a defective immune response leading to a chronic inflammatory reaction in Crohn's disease and ulcerative colitis.

Adolescent↗
PubMed1983

Immunoregulatory function of human intestinal mucosa lymphoid cells: evidence for enhanced suppressor cell activity in inflammatory bowel disease.

Abnormalities in immune regulation at the gut level may be relevant to the pathogenesis of inflammatory bowel disease, but little is known about the immunoregulatory properties of intestinal mononuclear cells. Therefore, we wished to see if lymphoid cells derived from the lamina propria of surgically resected bowel specimens have any modulatory effect upon the immune response of peripheral blood mononuclear cells from patients with ulcerative colitis or Crohn's disease. When autologous peripheral blood and intestinal lamina propria lymphoid cells were mixed at different ratios and cultured in the presence of phytohaemagglutinin, we were able to show that intestinal mononuclear cells had the capacity to modify the mitogenic response of the cultured cells. These intestinal immunoregulatory cells, when obtained from mucosa affected by inflammatory bowel disease, express a significantly enhanced suppressor cell activity as compared with those from non-inflamed control mucosa. Such suppressor cell activity varies with cell concentration and requires cell proliferation, but it is independent of anatomical origin (small vs large bowel), type of inflammatory bowel disease (ulcerative colitis vs Crohn's disease) or immunosuppressive therapy. These findings point to an important functional difference between inflammatory bowel disease and control intestinal mucosa mononuclear cells. The enhanced suppressor activity of lamina propria mononuclear cells may be associated with impairment of cell-mediated immunity at the gut level. This may be related to the pathogenesis of inflammatory bowel disease by leading to defective intestinal immune regulatory events, which may not be detectable at the peripheral level.

Adolescent↗
PubMed1981

Studies on isolated gut mucosal lymphocytes in inflammatory bowel disease. Detection of activated T cells and enhanced proliferation to Staphylococcus aureus and lipopolysaccharides.

To determine whether a defective proliferation of gut mucosal lymphocytes is a contributory factor to the pathogenesis of inflammatory bowel disease, we assessed their reactivity toward mitogens and bacterial antigens. Spontaneous replication of intestinal lymphoid cells was higher than that of patient-matched peripheral blood lymphocytes. That gut mucosal lymphocytes appear to be activated in loco was confirmed by a striking, time-dependent increase in the number of stable E rosettes generated by culturing unstimulated Crohn's disease intestinal lymphoid cells. The responses of lymphocytes from inflamed and normal mucosa to polyclonal mitogens were not only comparable to each other, but to those of corresponding peripheral lymphocytes, as well. Peripheral blood lymphocytes from patients with Crohn's disease showed less proliferation to Bacteroides and lipopolysaccharide antigens than did those from control individuals, but replicated similarly in response to Staphylococcus aureus and the enterobacterial common antigen: In contrast, when cultured with Staphylococcus aureus or with lipopolysaccharides, but mucosal lymphocytes from Crohn's disease proliferated 3-5 times more than did those from normal mucosa, while lymphoid cells from both sources were equally stimulated by Kunin antigen. Overall, this study found no evidence for a defective proliferative capacity of immune competent cells at the gut mucosal level in inflammatory bowel disease.

Colitis↗
PubMed1979

Gut mucosal lymphocytes in inflammatory bowel disease: isolation and preliminary functional characterization.

We have developed an enzymatic technique for isolating human intestinal mucosal lymphoid cells. This method was found to be superior to mechanical methods in regard to cell yield and survival. It is based on treating mucosa with serum-free solutions containing collagenase and deoxyribonuclease, followed by isolating the lymphoid cells through centrifugation steps involving fetal calf serum and ficoll-hypaque. Exposure of peripheral blood lymphocytes to the components of the enzymatic solution did not appreciably alter their uptake of tritiated thymidine in the presence or absence of mitogens. Application of the method to derive lymphoid cells from Crohn's disease, ulcerative colitis, and normal intestinal mucosa has shown that gut mucosal lymphocytes from inflammatory bowel disease (1) exceed the number of those from normal mucosa by a factor of 3 to 5; (2) show different degrees of tritiated thymidine uptake, spontaneously and in response to mitogens, depending upon the time they are harvested during the dissociation process; (3) are better stimulators than responders in the allogeneic mixed lymphocyte reaction; (4) generate suppressor cell activity comparable to that of peripheral blood lymphocytes; (5) cannot, in contrast to peripheral blood lymphocytes, generate antibody-dependent cell mediated cytotoxicity; and (6) produce an average of 5 times more IgM than equal numbers of peripheral blood lymphocytes.

Antibody-Dependent Cell Cytotoxicity↗
PubMed1976

Pseudoobstruction in ceroidosis.

Diffuse deposition of ceroid pigment in the muscularis propria of the gastrointestinal tract in a patient with a long history of malabsorption of unknown origin is reported. The depostion of this waste pigment is not reversible and is related to prolonged depletion of vitamin E. Progressive dilatation and hypomotility of the entire gastrointestinal tract are demonstrated by radiographic studies and possibly related to infiltrate of ceroid pigment in the smooth muscle cell with resulting functional impairment. In the differential diagnosis of ceroidosis with other disease, scleroderma has the closest roentgenographic similarity. Pseudoobstruction of the small bowel which can develop must be treated conservatively to avoid unnecessary bowel resection.

Adult↗