Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P43026 (lipopolysaccharide)
 62,215 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The cytokine interleukin 4 (IL-4) has been shown to induce lipopolysaccharide-activated murine B cells to differentiate into IgE-secreting cells and to stimulate IgE secretion by cultured human peripheral blood lymphoid cells. It is unclear, however, whether this effect of IL-4 on human peripheral blood lymphoid cells is a direct effect on the B cell because IL-4 can stimulate T cells and monocytes as well as B cells and does not induce purified human B cells to secrete immunoglobulin. To investigate this issue we studied the ability of IL-4 to induce IgE secretion by purified human B cells (93-96% CD20+, less than 1% CD3+) that were cultured with Epstein-Barr virus (EBV). Although B cells cultured with IL-4 alone did not secrete Ig and B cells cultured with EBV alone secreted IgM, IgG, and IgA but less than 150 pg of IgE per ml, the combination of EBV and IL-4 induced an IgE response that ranged from 11.4 to 40.3 ng/ml of culture supernatant after 26 days of culture. While IL-4 also enhanced IgM, IgG, and IgA secretion, as well as proliferation by EBV-infected B cells, these effects were less pronounced, occurred earlier during culture, and required a lower concentration of IL-4 than did the stimulation of IgE secretion. Furthermore, interferon gamma at 10 units per ml was found to inhibit IL-4/EBV-induced IgE secretion without inhibiting the other stimulatory effects of IL-4. We conclude that (i) IL-4 and interferon gamma can act directly on polyclonally activated human B cells to respectively stimulate and suppress IgE secretion and (ii) IL-4, in addition to its specific effect on IgE secretion, has a general stimulatory effect on the growth and differentiation of EBV-infected human B cells.
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PMID:IgE secretion by Epstein-Barr virus-infected purified human B lymphocytes is stimulated by interleukin 4 and suppressed by interferon gamma. 254 58

The results of cytogenetic studies are reported in 89 patients with B-cell CLL. LPS (E. coli lipopolysaccharide), PWM (pokeweed mitogen), PHA (phytohaemagglutinin), EBV (Epstein-Barr virus), TPA (phorbol 12-myristate 13-acetate), and LA (leucoagglutinin) were used as mitogens. Mitoses were obtained from 78 cases. Clonal aberrations could be demonstrated in 26 cases. Trisomy 12 was the most frequent finding (8 cases) and was sole abnormality in 4 cases. Chromosomes #14, #17, and #11 were involved in structural aberrations in 5, 7, and 7 cases respectively, but a t(11;14)(q13;q32) was the only structural aberration seen more than once. The median observation time was 47 months (range 1-87). The presence of clonal abnormalities did not influence survival significantly, either when calculated from diagnosis or from cytogenetic analysis. Patients with more than one aberration, however, had a significantly shorter survival than patients with normal mitoses only (p less than 0.05). The survival of 8 patients with trisomy 12 (in 4 as sole abnormality) was not different from that of patients with normal mitoses only.
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PMID:B-cell chronic lymphocytic leukaemia: clonal chromosome abnormalities and prognosis in 89 cases. 261 12

On stimulation with lipopolysaccharide (LPS), normal human macrophages (M phi) and endothelial cells (EC) produced factors which inhibited interleukin 2 (IL-2)-dependent lymphocyte proliferation and PHA plus interleukin 1 (IL-1)-dependent mouse thymocyte proliferation but not IL-1-dependent human fibroblast proliferation, suggesting that they were inhibitors of the IL-2 response. In addition, these factors inhibited the production of IL-2 by normal human peripheral blood mononuclear cells (PBMC). The factors also inhibited PBMC proliferation in response to PHA and concanavalin (Con A) but did not inhibit the proliferation of EC, U937 cells, or Epstein-Barr virus-transformed B cells. On Sephadex G200 gel filtration, the inhibitory factors from both M phi and EC were detected almost entirely in a 130- to 150-kDa fraction, but active material was also detected in a 15- to 20-kDa fraction. On isoelectric chromatofocusing of the 130- to 150-kDa fraction, inhibitory activity was associated with fractions eluted at three isoelectric points, pH 7.0, 5.4, and 4.8. The isoelectric fractions isolated from M phi and EC showed similar patterns of inhibition. When 130- to 150-kDa fractions from Sephadex G200 of the M phi and EC supernatants were treated with an antibody against a macrophage-derived suppressor factor produced by the human monocytic leukemia cell line THP-1, the activity of both fractions was neutralized. The above findings suggest that normal M phi and EC secrete an identical or closely related inhibitor of IL-2 synthesis and IL-2 response, and this inhibitor regulates these IL-2-related functions by a suppressive action on the T lymphocyte.
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PMID:T cell inhibitor secreted by macrophages and endothelial cells. 267 71

The effects of ultraviolet-B radiation (UV-B) on accessory function of human blood adherent mononuclear cells (ADH) for antigen and mitogen-induced responses, and production by ADH of the amplifying cytokine interleukin 1 (IL-1) were examined. Responder lymphocytes were rendered accessory cell dependent by treatment of nonadherent cells with OKIal+complement. UV-B depressed accessory function of ADH in a dose-dependent manner. UV-B at 5 mJ/cm2 decreased accessory function of 2 x 10(4) ADH for tetanus toxoid-induced responses (measured as incorporation of 3H-thymidine) by 84% (P less than 0.001, n = 6) and phytohaemagglutinin-induced responses 91% (P less than 0.001, n = 4). UV-B also decreased accessory activity of peripheral blood mononuclear cells but not Epstein-Barr virus-transformed B cells for a PPD-reactive T cell line. Viability was approximately 90% 0-72 h after exposure of ADH to 5 mJ/cm2 of UV-B. Interleukin 1 (IL-1) activity of supernatants of ADH was assayed on C3H/HeJ mouse thymocytes. Pretreatment of ADH with 5 mJ/cm2 UV-B decreased lipopolysaccharide-stimulated IL-1 activity from 169 +/- 34 (mean U/ml +/- s.e.) to 4 +/- 1 (P less than 0.01, n = 4). Lysates of UV-B irradiated. LPS-stimulated ADH had no discernible IL-1 activity. Addition of IL-1 partially restored accessory activity of UV-B irradiated ADH for lymphocyte responses to TT. Exposure of ADH to TT or PHA for 30 min before irradiation blocked the inhibitory effect of UV-B on accessory activity. Thus, low doses of UV-B are deleterious to accessory function and to production of IL-1 by ADH. Interference with production of cytokines and with initial interactions of accessory cells with antigen and mitogen may be critical to the effects of UV-B on immunoregulatory function of ADH.
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PMID:Deleterious effect of ultraviolet-B radiation on accessory function of human blood adherent mononuclear cells. 296 88

The activities of two glycolipid synthetases, globoside synthase or UDP-N-acetylgalactosamine-trihexosylceramide beta-N-acetylgalactosaminyltransferase (beta-GalNAc transferase; EC 2.4.1.79) and Forssman synthase or UDP-N-acetylgalactosamine-globoside-alpha-N-acetylgalactosaminyltransfer ase (alpha-GalNAc transferase; EC 2.4.1.88), were assayed in various human lymphoblastic cell lines. The activity of beta-GalNAc transferase was much higher than that of alpha-GalNAc transferase except in Molt 3 and Molt 4 lines, which were derived from T-cells. In cultivated human peripheral lymphocytes concanavalin A (Con A), lipopolysaccharide (LPS), and Epstein-Barr virus (EBV) stimulated the activities of alpha- and beta-GalNAc transferases in addition to having their known stimulative effect on thymidine incorporation. Characteristic differences between alpha- and beta-GalNAc transferases were noted in the responses to the above mitogens, but activities of both enzymes were greatly increased by exposure of the lymphocytes to EBV. Treatment of lymphocytes with either dactinomycin (actinomycin D) or cycloheximide 24 hours after the addition of Con A, LPS, or EBV decreased the activities of the transferases. This observation suggests that stimulation of alpha- and beta-GalNAc transferases requires transcriptional and translational processes.
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PMID:Globoside and Forssman synthases in human lymphocytes exposed to Epstein-Barr virus and mitogens. 298 38

Infection with Epstein-Barr virus (EBV) is initiated by virus binding to the C3dg-C3d receptor CR2. Several workers have implicated this receptor in the control of B-cell activation by examining the effects of antibodies to CR2 and isolated C3d on B-cell proliferation and differentiation. We report here on the activating effects of irradiated EBV, which retains its capacity to bind to CR2 but loses its ability to function as a T-independent B-cell activator. EBV synergized with B-cell growth factor in the induction of uptake of tritiated thymidine by T cell-depleted leukocytes from seronegative donors but did not induce secretion of immunoglobulin. Synergism could be inhibited with an anti-viral antibody that inhibited binding of EBV to CR2. No similar synergism was found between EBV and recombinant interleukin 2, interleukin 1 alpha, or gamma interferon or with the lipid A fraction of bacterial lipopolysaccharide. EBV may thus initiate B-cell activation as it binds to CR2. Infectious virus may, under normal circumstances, induce the cell to make those growth factors necessary to support B-cell proliferation; the difficulty of transforming cells with transfected EBV DNA may in part reflect the absence of an activation event provided by intact virus as it attaches to CR2. The synergism of EBV and B-cell growth factor more clearly distinguishes the effects of B-cell growth factor from those of interleukin 1 and interleukin 2 in other models of B-cell activation. Thus, this may be a useful model for further delineation of unique effects of B-cell growth factor on B-cell function.
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PMID:Synergistic activation of cells by Epstein-Barr virus and B-cell growth factor. 302 4

Lymphocytes from healthy volunteers and from cystic fibrosis patients were transformed with Epstein-Barr virus and cultured at a limiting dilution to generate lymphoblastoid cell lines that secreted human monoclonal antibodies specific for lipopolysaccharide (LPS) from Pseudomonas aeruginosa. Three cell lines (RM5, FDD7, and 11F9) produced immunoglobulin M (IgM) antibody species that reacted specifically with P. aeruginosa Fisher immunotypes 2, 4, and 5, respectively, and with LPS extracted from these immunotypes. A fourth cell line (9H10) produced a single IgM antibody species that recognized P. aeruginosa immunotypes 3, 6, and 7 and LPS extracted from them. Monoclonal antibodies secreted by cell lines RM5, FDD7, and 11F9 protected neutropenic mice prophylactically against challenge with P. aeruginosa immunotypes 2, 4, and 5, and those secreted by 9H10 protected against P. aeruginosa immunotypes 3 and 6 but did not protect against immunotype 7. In vivo experiments indicated that antibodies protected mice against infection by increasing the rate of bacterial clearance.
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PMID:Human monoclonal antibodies that protect mice against challenge with Pseudomonas aeruginosa. 313 64

Chromosomal aberrations occur in both B-CLL and T-CLL. The polyclonal B-cell mitogens, in particular Epstein-Barr virus and lipopolysaccharide from E. coli, have been used successfully to reveal chromosomal abnormalities in 40-60% of patients with B-CLL, while T-cell mitogens have shown chromosomal aberrations in T-CLL. The most common clonal chromosomal aberration in B-CLL is an extra chromosome 12, alone or together with other abnormalities. Other common aberrations are 14q+, structural aberrations on 6, 11, 12 and 13. Proto-oncogenes are frequently located close to breakpoints. The proto-oncogene c-K-ras is located on chromosome 12 and an abnormal transcript has recently been implicated in a subset of B-CLL-patients. An extra chromosome 12 as well as multiple chromosomal abnormalities in B-CLL appear to predict a less favourable prognosis. T-CLL is in most patients characterized by an inv(14), an extra 8q and structural abnormalities in chromosome 7. The genes for the specific T-cell receptor as well as the immunoglobulin heavy chain are located on these chromosomes. Chromosomal aberrations appear to have pathogenetic importance in both B-CLL and T-CLL.
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PMID:Role of chromosomal abnormalities in chronic lymphocytic leukemia. 333 2

The chromosomal constitution of stimulated lymphocytes in 13 patients with B cell chronic lymphocytic leukemia (B-CLL) were sequentially examined using polyclonal B cell activators (PBA), i.e., Epstein-Barr virus (EBV), lipopolysaccharide W from E. coli (LPS), pokeweed mitogen (PWM), and protein A from Staphylococcus aureus (PA). Of the 11 patients (44 samplings) with abnormal clones, 2 patients had only trisomy 12, 6 patients had trisomy 12 plus other clonal abnormalities, such as +8, +9, +16, +18, 6q-, 15q+, and t(4;15), and the remaining 3 cases had various clonal abnormalities other than trisomy 12, such as trisomy 3, 8, 20, 21, and insertion of #7 and #12. These findings suggest that even though trisomy 12 may be a common abnormality in B-CLL, various other abnormal clones may also be present in vivo for relatively long periods of time. It appears that stimulated lymphocytes in patients with previous therapy tend to show chromosome abnormalities more frequently than those in untreated patients.
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PMID:Sequential chromosome abnormalities in B cell chronic lymphocytic leukemia: a study of 13 cases. 348 71

We describe clonal chromosome abnormalities in 13 new cases of B-cell type prolymphocytic leukemia (B-PLL) investigated using pokeweed, lipopolysaccharide B, TPA (phorbol ester), and Epstein-Barr virus (EBV) as mitogens. B-PLL showed a much better response to all four mitogens when compared with B-cell chronic lymphocytic leukemia (B-CLL). A 14q+ was the most frequent abnormality and was observed in 7 of the 13 cases. A t(11;14)(q13;q32) was observed in 2 patients in this series and in 2 cases from a previous series of 9 patients studied in this laboratory, giving an incidence in B-PLL of 18% for this abnormality. The more frequent rearrangement of both IgH genes in B-PLL when compared to B-CLL may predispose to a higher incidence of 14q+ in B-PLL. Trisomy 12 which is a feature of B-CLL was observed in one case in the present series. Other abnormalities of chromosome 12 included 12p-(p12-13) in 2 cases and t(12;14)(q22;q32) in 1 case. The t(6;12) previously described as a specific abnormality in B-PLL was not observed in the 22 cases (13 present series, 9 previous series) studied in our laboratory.
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PMID:Cytogenetic studies on prolymphocytic leukemia. 1. B-cell prolymphocytic leukemia. 350 70


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