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At least 91 records · Page 5Linked to original sources
PubMed1984

Lymphotoxin detected in the blister fluid of bullous pemphigoid patients.

The role of lymphocytes in the pathogenesis of bullous pemphigoid was examined by assaying the blister fluid obtained from bullous pemphigoid patients for the presence of the lymphokine, lymphotoxin. Blister fluids from six bullous pemphigoid were assayed on L-929 target cells for the presence of cytolytic molecules in the standard lymphotoxin assay. Three of six blister fluids obtained from bullous pemphigoid patients and one linear IgA bullous dermatosis patient contained significant levels of cytolytic activity. Control blister fluids from suction blisters, herpes, pemphigus, and toxic epidermal necrolysis patients did not contain cytolytic activity. Serum from five bullous pemphigoid patients also had no cytolytic activity. Neutralization studies using rabbit anti-alpha-lymphotoxin demonstrated that 54 to 88% of the cytolytic activity found in bullous pemphigoid blister fluid was due to alpha-lymphotoxin. These results indicate that lymphotoxin is locally released in the skin of bullous pemphigoid lesions and is detectable in blister fluids.

Antibodies↗
PubMed1990

Lymphotoxin production by regional lymph node lymphocytes in patients with uterine cervical cancer.

The cytotoxin production by regional lymph node cells was examined in 25 patients with uterine cervical cancer and 10 patients with uterine myoma. The patients in stage I had significantly increased spontaneous release of cytotoxins compared with that in stages II, III, and IV. The spontaneous release in stages III and IV was markedly reduced. There was no difference in the release of cytotoxins from peripheral blood lymphocytes between cancer patients and patients with myoma or healthy controls. The cytotoxin production by lymph node cells was increased in stage III by stimulating with formalin-fixed QG-K cells derived from uterine cervical cancer, but not in stages I and II. Almost all of the cytotoxic activity of cytotoxin was abrogated by antilymphotoxin antibody. However, the cytotoxin activity was partially inhibited by anti-tumor necrosis factor antibody. These results suggest that cytotoxins released from the regional lymph node cells of uterine cancer patients are derived from, most of all, lymphotoxin.

Adult↗
PubMed1991

Defective T-lymphocyte signal transduction and function in leukocyte adhesion deficiency.

The lymphocyte function-associated antigen-1 (LFA-1) molecule is a cell surface heterodimeric protein that directly mediates cellular adhesion. However, it remains unclear whether LFA-1 molecules are also involved in transmembrane signaling and in the subsequent regulation of cellular functions. Previous attempts to evaluate this issue have been hampered by (1) the ubiquitous expression of LFA-1 on normal lymphoid cells, (2) the limited availability of assays for cellular activation that are not affected by cellular adhesion, and (3) the difficulties in interpreting studies where anti-LFA-1 mAbs are used to alternatively block or stimulate this antigen. In order to avoid these pitfalls, we first isolated and cloned T lymphocytes from a patient with leukocyte adhesion deficiency (LAD), an inherited disorder in which the defective expression of leukocyte integrins results in the production of LFA-1- T lymphocytes. Different T-cell lines from this patient and from normal individuals were then stimulated through their T-cell antigen receptor complex and were then tested for three aspects of cellular activation: (1) transmembrane signaling (i.e., phosphoinositide turnover), (2) lymphokine secretion (i.e., release of lymphotoxin), and (3) their capacity to mediate cellular cytotoxicity (using murine anti-CD3-producing hybridoma cells as targets). Using assay systems that did not involve LFA-1-mediated adhesion to antigen-presenting cells or target cells, the T-cell lines from the LAD patient were found to be intrinsically defective in all three of these parameters of T cell activation.(ABSTRACT TRUNCATED AT 250 WORDS)

Cell Adhesion↗
PubMed1992

Characterization of histamine-releasing activity: role of cytokines and IgE heterogeneity.

Histamine-releasing factors (HRFs) are a group of cytokines that cause histamine release (HR) from basophils and mast cells. The concept of the priming effect of cytokines and the heterogeneity of IgE involved in the HRF-induced HR have been emphasized in recent years. In this study, we performed a series of experiments to elucidate the above-mentioned hypotheses. The stock HRF were obtained by stimulating mononuclear cells (MNC) with phytohemagglutinin (PHA). Maximal activity was observed 36 hr after culture. By gel filtration, HRF was eluted with a peak activity ranging from 12 to 18 KD. A large portion (75%) of HRF activity could be neutralized by a combination of antibodies against interleukin 1 (IL-1), IL-3, IL-8, granulocyte-macrophage colony-stimulating factor (GM-CSF), and tumor necrosis factor-alpha (TNF-alpha). The stimulation of basophils with 100 ng/ml each of IL-3, IL-6, IL-7, GM-CSF, or TNF-alpha alone caused 10% HR; however, when the cells were pretreated with 10 ng/ml of either IL-3, IL-6, IL-7, IL-8, TNF-alpha, or GM-CSF and then stimulated with anti-IgE, a marked increase in HR was regularly observed. The combination of 100 ng/ml each of IL-1, IL-3, IL-8, GM-CSF, and TNF-alpha could induce only about 20% HR; furthermore, such combinations did not have an additive or synergistic priming effect on anti-IgE-induced HR compared to the effect of single cytokines. Stripping of surface-bound IgE with lactic acid markedly reduced the capacity of basophils to release histamine in response to MNC-HRF and anti-IgE. Passive sensitization of IgE-stripped basophils with high-HRF responders' serum could restore their responsiveness to both MNC-HRF and anti-IgE, but passive sensitization with low-HRF responders' serum could restore responsiveness to anti-IgE only. Moreover, passage of MNC-HRF through high-, but not low-HRF, responders' IgE-Sepharose columns significantly reduced the HR activity of MNC-HRF. Finally, although the eluant could induce only 10% HR, the majority of its HR activity could be restored by the addition of effluent but not by the mixture of IL-1, IL-3, IL-8, GM-CSF, and TNF-alpha, suggesting the presence of a complex interaction among those cytokines. In summary, MNC-HRF contained at least two types of HRF activity; one was IgE dependent and the other was IgE independent.(ABSTRACT TRUNCATED AT 400 WORDS)

Basophils↗
PubMed1992

Altered cytokine production in black patients with keloids.

The treatment of keloids in black patients remains a medical dilemma. Previous studies have focused on primary alterations in the metabolism of fibroblasts as the key in the etiology of this condition. Yet alterations in the production of various cytokines which may alter fibroblast responses secondarily have received little attention. Twelve black patients with clinical and histological diagnosis of keloids and eight black control volunteers were studied. Peripheral blood mononuclear-cell (PBMC) fractions from both groups were assayed for production of interleukin-1 (IL-1), interleukin-2 (IL-2), interleukin-6 (IL-6), alpha-interferon (IFN-alpha), beta-interferon (IFN-beta), gamma-interferon (IFN-gamma), tumor necrosis factor-alpha (TNF-alpha), and tumor necrosis factor-beta (TNF-beta). The production of IFN-alpha, IFN-gamma, and TNF-beta were markedly depressed in keloid patients compared to normal controls. However, IL-1 and IL-2 production was not significantly different between the two groups. In contradistinction, keloid patients produce greater amounts of IL-6, TNF-alpha, and IFN-beta. Altered levels of immunoregulatory cytokines may play a significant role in the net increase in collagen which characterizes keloid formation.

Black People↗
PubMed1977

[Cold-lymphocytotoxic antibodies in the sera of cervix-carcinoma patients].

Sera of 120 patients with cervical cancer were screened for cold reacting, complement dependant autolympho-cytotoxins (CoCoCy). These antibodies occurred in 21,7% of the patients in comparison with 11,2% of 116 controls. The highest percentage of CoCoCy-antibodies was detected in the sera of patients with cervical cancer stage I (27,6%). Thus demonstration of CoCoCy-antibodies may be of pathogenetic rather than of diagnostic interest. CoCoCy-antibodies could be seen to reflect autoimmune reactions in cervical cancer.

Autoantibodies↗
PubMed1991

Gene expression of cytokines suppressing hematopoietic progenitor cells in lymphoid malignancies.

The expression of cytokine genes for tumor necrosis factor alpha (TNF alpha), lymphotoxin and transforming growth factor beta (TGF beta), all of which are known to suppress normal hematopoiesis, was investigated in 32 patients with lymphoid malignancies using Northern blot analysis. Messenger RNA (mRNA) for TNF alpha, lymphotoxin and TGF beta was detected in 9 cases, 2 cases and 7 cases, respectively. When the relationship between cytokine gene expression and surface phenotype was analyzed, the expression of CD19 correlated significantly with expression of the TNF alpha gene (P less than 0.05). This suggests that B cell malignancies are likely to produce TNF alpha. When the hematological parameters of patients expressing and not expressing the gene were compared, the expression of TNF alpha mRNA was found to correlate with more profound anemia in acute lymphoblastic leukemia (P less than 0.05). Both granulocyte and platelet counts were lower in patients expressing TNF alpha mRNA; however, the decreases were not significant. Neither lymphotoxin nor TGF beta gene expression correlated significantly with any hematological parameter.

Adolescent↗
PubMed1984

[Lymphocyte function in children with iron deficiency].

In 23 children with mild iron-deficiency anemia, 22 children with latent iron-deficiency, and in 46 healthy controls the 3H-thymidine incorporation in blood lymphocytes after stimulation with phytohemagglutinin, concanavalin A, pokeweed mitogen, and serum against thymocyte cells was measured. In 11 of the children with iron-deficiency anemia, in 13 of the children with latent iron-deficiency, and in 20 controls the lymphotoxin secretion after phytohemagglutinin stimulation was also performed. All patients studied were without intercurrent infections and were well nourished. No alteration of the lymphocyte function in the patients was found. The concentrations of immunoglobulins and the components C3 and C4 of complement system were also found to be normal. It is suggested that lymphocyte functions are eventually only altered in more severe states of iron-deficiency anemia.

Anemia, Hypochromic↗
PubMed1990

Lymphokine mRNA profile and functional analysis of a human CD4+ clone with unique antitumor specificity isolated from renal cell carcinoma ascitic fluid.

We here describe the isolation, characterization, profile of lymphokine expression and T-cell-receptor gene rearrangement pattern of 444P.3, a CD3+ CD4+ CD8- 4B4+ interleukin-2 (IL-2)-dependent clone derived from the malignant ascites of a patient with renal cell cancer. The 444P.3 clone exhibited unique antitumor specificity between days 45 and 84 in culture and then lost its lytic, but not its proliferative, capacity. To our knowledge this is the first description of a specific antitumor reaction in a patient with renal cell cancer against autologous tumor. IL-2-expanded 444P.3 cells, tested on day 104 in culture, expressed mRNA for tumor necrosis factor (TNF), IL-2 and tumor growth factor beta (TGF-beta) but not for IL-1, lymphotoxin or granulocyte/macrophage-colony stimulating factor (GM-CSF). The parental noncloned population expressed mRNA for TNF, lymphotoxin, GM-CSF and TGF-beta but not for IL-1 beta or IL-2. Analysis of established human T cell clones should include profiles of lymphokine secretion in addition to growth and proliferation patterns, antitumor activity and surface phenotype. Such characterization of clones may provide a better understanding of the immunoregulatory role and functional potential of various T cell subsets involved in human antitumor reactivity.

Ascites↗
PubMed1990

Lysing of fresh human tumor by a cytotoxic factor derived from autologous large granular lymphocytes independently of other known cytokines.

During interaction with autologous tumor cells large granular lymphocytes (LGL) of cancer patients released a soluble cytotoxic factor, termed LGL-derived cytotoxic factor, which mediated lysing of autologous fresh tumor cells. The cytotoxic factor was compared with purified human recombinant cytotoxic cytokines, including tumor necrosis factor (TNF), lymphotoxin (LT), interferon (IFN) alpha, IFN gamma, interleukin-1 alpha (IL-1 alpha) and IL-2. The LGL cytotoxic factor exhibited cytotoxicity against autologous and allogeneic fresh human tumor cells in an 18-h 51Cr-release assay, while these target cells were resistant to lysing by any of the recombinant cytokines. Mixtures of recombinant(r) TNF, rLT, rIFN alpha, rIFN gamma, rIL-1 alpha and rIL-2 were still unable to produce cytotoxic effects on fresh human tumor cells. Treatment with monoclonal and polyclonal antibodies directed against rTNF, rLT, rIFN alpha, rIFN gamma, or rIL-1 alpha did not inhibit the cytotoxic activity of LGL-derived cytotoxic factor against fresh human tumor cells. Even a mixture of all the antibodies was incapable of blocking the cytolytic activity of the factor to fresh human tumor cells. Furthermore, intact LGL-mediated lysing of autologous tumor cells was not inhibited by any of the antibodies. These results may indicate that a cytotoxic factor produced by LGL in response to autologous tumor cells mediates lysing of fresh human tumor cells independently of TNF, LT, IFN, IL-1 and IL-2.

Adenocarcinoma↗
PubMed1977

[Suppression of the cell-mediated immunity in minor histoincompatible rat kidney allograft recipients (author's transl)].

To study the immunological status of recipients of major compatible and minor incompatible kidney allografts, we transplanted FiS and FLF1 kidneys into LEW rats. Most of the FiS kidneys were rejected within 55 days. Of 24 recipients, only 4 survived longer than 4 months. However, two-thirds of the FLF1 recipients survived longer than 4 months. The other third died with 64 days. During the first postoperation week a high level of lymphocytotoxin was detected in the serum of the FiS kidney recipients. Thereafter hardly any alternation of its titer was found, and no variation among the recipients of major histocompatible kidney allografts was shown. The FLF1 kidney recipients showed a low titer of antibody. The hemagglutinin titer showed the same trend as the lymphocytotoxin titer. A blocking serum factor could not be found in the serum of the kidney recipients with the microcytotoxity assay method or with the allorosette-formation inhibition test. Cellular immunity, which was studied with the GvH-reaction and microcytotoxity assay, was detected in the first postoperative week. However, this immunity was gradually supressed, and after 6 weeks was no longer to be found. This immunological status remained unchanged in the indefinitive surviving kidney-recipients in spite of antigen inoculation with two skin allografts of donor origin. This immunological status could be defined as "graft acceptance".

Animals↗
PubMed1990

Cytokine-induced release of histamine from basophil leukocytes from AIDS patients.

Cytokine-induced histamine release from basophil leukocytes was examined in cell suspension from AIDS patients and compared with healthy controls. Cells from approximately half of the AIDS patients, in contrast to none from the control group, showed histamine release after stimulation with interleukin-4 (IL-4), tumor necrosis factor alpha (TNF alpha), lymphotoxin (LT) and interferon gamma (IFN gamma). These cytokines seem to induce histamine release from cells from AIDS patients by interaction with the cell surface immunoglobulins, since removal of the immunoglobulins prior to the exposure of the cytokines completely abolished the response to the cytokines. IL-1 alpha, IL-1 beta, IL-3, colony stimulating factor (CSF) and granulocyte-macrophage-CSF (GM-CSF) caused significant histamine release from cells from a similar number of AIDS patients and controls.

Acquired Immunodeficiency Syndrome↗
PubMed1985

Enhanced thromboxane synthesis and vacuolization in human polymorphonuclear leucocytes induced by human lymphokine containing supernatants.

PMN's were cultivated in vitro and treated with supernatants obtained from mitogenic-induced lymphocytes of human tonsil. Cytoplasmic vacuolization increased with time and there was a lower number of neutrophilic clumps in the culture treated with a supernatant containing lymphotoxin. In addition, the PMN's released more thromboxane B2 which was inhibited by indomethacin. We conclude that the action of lymphotoxin on the target PMN's is not mediated by the production of thromboxane B2.

Adult↗