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)

In this study we investigated whether interleukin 2 (IL-2) acts on B cell proliferation and whether activated B cells express IL-2 receptors. First, the functional activity of immunoaffinity-purified or recombinant human IL-2 was studied in a B blast assay using positively selected murine surface Ig-positive cells that had been activated by lipopolysaccharide (LPS) plus anti-Ig antibodies (anti-Ig). In this assay, T cells were not detected by fluorescence-activated cell sorter analysis. It was found that both IL-2 preparations led to optimal B cell proliferation compared with supernatants obtained from murine or human spleen cells or murine cloned T helper cells. Second, we observed that the IL-2 requirement in this assay was about the same as in a proliferation assay using lectin-activated polyclonal murine Lyt-2-positive T cells. Third, analysis of the binding of radiolabeled immunoaffinity-purified IL-2 to B cells indicated that LPS plus anti-Ig-activated B cells expressed a mean of 3,500 IL-2 receptors per cell with an apparent dissociation constant of 150 pM. However, neither nonactivated B cells nor B cells activated by LPS alone exhibited significant specific IL-2 binding. The functional and the receptor data are consistent with the conclusion that IL-2 is a growth factor not only for T cells but also for B cells.
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PMID:Activated B cells express receptors for, and proliferate in response to, pure interleukin 2. 643 89

Lymph node and spleen cells of the autoimmune MRL/Mp-lpr/lpr mouse strain spontaneously produce (in the absence of mitogenic stimulation) a factor(s) that induces B cell differentiation. This factor is not produced by the congenic MRL/n mouse strain that lacks the lpr gene or by normal mouse strains. However, lymphoid cells of the B6-lpr/lpr (B6/1) strain also produce a B cell differentiation factor. Although the factor acts on resting B cells, its effect is greatly magnified by activating the B cells with anti-mu or lipopolysaccharide. MRL/l mice begin producing the factor as early as 1 mo of age but levels increase with age and appearance of lymphoproliferation. Cell depletion studies reveal that this factor is produced by T cells of the Lyt-1+2-phenotype. Because of its association with the lpr/lpr genotype, we term this B cell differentiation factor L-BCDF. Functional analysis of L-BCDF reveals that it acts regardless of cell density in culture and in the absence of interleukin 2 (IL-2). In fact, the increase in the production of L-BCDF by MRL/1 T cells with aging occurs concomitantly with a marked decrease in their ability to produce IL-2. No T cell replacing factor activity or B cell growth factor-like activity can be detected in MRL/l-derived supernatants. L-BCDF induces both IgM and IgG synthesis in lipopolysaccharide-activated B cells; however, it has a greater effect on IgG secretion. In particular, the production of IgG1, IgG2a, and IgG2b are markedly enhanced in the presence of L-BCDF. The spontaneous production of L-BCDF by T cells of SLE mice of lpr/lpr genotype suggests an association of this factor with autoimmunity.
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PMID:Identification of a B cell differentiation factor(s) spontaneously produced by proliferating T cells in murine lupus strains of the lpr/lpr genotype. 660 Apr 90

It has been previously reported that lipopolysaccharide-stimulated murine astrocytes produce a factor which enhances the proliferative response of thymocytes to lectins. The present report demonstrates that a rat astrocytoma cell (C6 cells)-derived factor appears to be similar to macrophage-derived interleukin 1 (IL 1) in its biological activities and biochemical characteristics. Upon injection into mice, supernatants of C6 cells induce the production of serum amyloid A. The C6 cell-derived factors enhance the response of thymocytes to phytohemagglutinin and the growth of fibroblasts whereas no effect on the growth of neuroblasts and of a strictly interleukin 2 (IL 2)-dependent T cell line was observed. On an AcA 54 column the C6-derived factors acting on thymocytes and fibroblasts coeluted as a single peak of Mr = 13 500 to 18 000; the semipurified factor was found to enhance the lymphocytes' production of IL 2. These observations demonstrate that cells not belonging to the mononuclear phagocyte lineage are able to produce factors identical or closely related to IL 1.
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PMID:Biological and biochemical characterization of an interleukin 1-like factor from rat C6 glioma cells. 660 83

Mouse thymocytes and spleen cells from unprimed C57BL/6 donors generate broadly reactive cytotoxic cells during 5 days of culture in vitro with polyinosinic acid (5') (poly(I] and/or supernatant from PMA-treated EL4 leukemia cells which contains interleukin 2 (IL-2) activity. We refer here to such cytotoxic cells as "supplement-induced cytotoxic cells" or SICC. Thymocytes are dependent on the supernatant factor(s), whereas spleen cells are usually stimulated by poly(I) alone. Polyinosinic acid acts synergistically with supernatant factor(s) to stimulate generation of SICC by both thymocytes (SICC-T) and spleen cells (SICC-S) when the IL-2 activity of the supernatant is inadequate alone. SICC can be generated by both splenocytes and thymocytes in medium supplemented with fetal calf serum or syngeneic plasma. SICC are active in 4 hr 51Cr-release tests against syngeneic, allogeneic, and xenogeneic tumors but not against lipopolysaccharide-induced lymphoblasts. Embryonic fibroblasts, too, are sensitive to SICC generated by thymocytes. In complement-dependent depletion tests, cytotoxic activity is partially sensitive (SICC-T) or fully sensitive (SICC-S) to anti-Thy-1 and -H-2 but not to anti-Lyt-1, -Lyt-2, or -asialo GM1.
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PMID:Supplement-induced cytotoxic cells (SICC) generated from mouse thymus or spleen cells cultured in the presence of interleukin 2 and/or polyinosinic acid. 660 5

Spleen cells of diabetes-prone BB Wistar rats were found to generate excessively low proliferative responses, and interleukin 2 (IL-2) levels in response to T-dependent mitogens. This abnormality was not due solely to abnormal T cell numbers since: (a) addition of BB spleen cells of BB splenic macrophages to normal major histocompatibility complex (MHC)-matched Wistar Furth (WF) spleen cells resulted in severe suppression of concanavalin A (Con A)-, phytohemagglutinin (PHA)-, and pokeweed mitogen (PWM)-mediated proliferation, and IL-2 production; (b) macrophage depletion from BB spleen cells, but not B cell or T cell depletion, removed completely the suppressive effects of BB cells on WF cells; (c) macrophage depletion greatly enhanced the response of BB lymphocytes to T-dependent mitogens. Although suppressor macrophages could also be found in the spleen of WF control rats they were present in much smaller numbers than in the spleen of BB rats. The suppressive effect of BB macrophages was partially reduced by addition of the prostaglandin synthetase inhibitor indomethacin to cultures. Furthermore, indomethacin (but not catalase or PMA) considerably augmented IL-2 secretion of Con A-stimulated BB spleen cells, but had little effect on WF spleen cells. In contrast, prostaglandins E1 and E2 (PGE1 and PGE2) suppressed IL-2 production. While IL-2 secretion was severely depressed in BB rats unstimulated and lipopolysaccharide (LPS)-stimulated IL-1 secretion by splenic macrophages was normal. BB macrophages did not inactivate IL-2. Low IL-2 production and macrophage-mediated suppression were features of all BB rats tested.
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PMID:Immune dysfunction in diabetes-prone BB rats. Interleukin 2 production and other mitogen-induced responses are suppressed by activated macrophages. 660 15

A procedure is described for the preparation of long-term lines of normal mouse B lymphocytes. Surface immunoglobulin-bearing splenic B lymphocytes were purified with the fluorescence-activated cell sorter and then cultured with lipopolysaccharide for 1-4 wk. The cells were then transferred into medium supplemented with a T-hybridoma-derived supernatant containing interleukin 2 (IL2). Continuous feeding with this supernatant led to the establishment of cell lines that also could be propagated to IL 2-free medium containing interleukin 1 but not in culture medium alone. Cell lines have been propagated in this manner for as long as 10 mo. The cells in these lines have the appearance for small, dense lymphocytes, which all bear surface IgM detectable by immunofluorescence, rosetting, and surface radiolabeling and immunoprecipitation. The cells express Ia and lack Thy 1. These cultured B lymphocytes are unresponsive to lipopolysaccharide but can be activated to become more rapidly dividing, immunoglobulin-secreting cells by exposure to culture supernatants containing both T-cell-replacing factor and IL 2.
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PMID:Long-term culture of normal mouse B lymphocytes. 679 35

We have previously described an epidermal cell-derived thymocyte-activating factor (ETAF), which is produced by the murine PAM 212 keratinocyte cell line. ETAF appeared to be similar to macrophage-derived interleukin 1 (IL 1) in its biologic activities and biochemical characteristics. Both IL 1 and ETAF augment thymocyte proliferation, enhance lymphocyte production of interleukin 2 (IL 2), and are 15,000 m.w. polypeptides that are stable at pH 4 to 11 and from -70 degrees C to 60 degrees C. In this study we describe a quantitative microassay to obtain standardized assessment of ETAF activity, which enabled us to further define the characteristics of ETAF and its relationship to IL 1. Just as stimulated macrophages produce more IL 1 activity, Pam 212 keratinocyte production of ETAF activity was increased by stimulation with lipopolysaccharide (LPS) or silica. Increased levels were also obtained by mechanical disruption of confluent monolayers of keratinocytes and by blocking proliferation of the Pam 212 cells with hydroxyurea at the G1/S interphase. These observations in conjunction with a concomitant decrease in keratinocyte viability suggest that "injurious" stimuli that prolong the G1 phase of the cell cycle factor ETAF production. ETAF, like murine IL 1, has an isoelectric point of 5.2. The same subpopulations of PNA-thymocytes that respond to PHA and IL 1 are responsible for the enhanced proliferative response to ETAF. Furthermore, as in the case of IL 1, PNA- Lyt-2- thymocytes were most responsive to ETAF, but not PNA+ LYt-2+ thymocytes. Finally, ETAF activity, like IL 1, appears to be a mitogenic signal for fibroblasts. Although produced by different cell types, these observations continue to support the view that ETAF may be identical or closely related to IL 1.
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PMID:Murine epidermal cell-derived thymocyte-activating factor resembles murine interleukin 1. 680 Nov 32

When treated with lipopolysaccharide (LPS), cultured murine astrocytes released significant amounts of prostaglandin E, which caused an inhibition of the in vitro proliferative response of C3H/HeJ thymocytes to mitogen. In addition, an interleukin 1 (IL 1)-like factor secreted by LPS-treated glia cell cultures and by C6 glioma cells was detected. The characterization of the factor as an IL 1-like mediator is based on the findings that the factor 1) enhances the mitogen-induced thymocyte proliferation, 2) exhibits no interleukin 2 (IL 2) activity, but 3) augments IL 2 production by mitogen-stimulated thymocytes, and 4) has a m.w. between 13,500 and 18,000 when generated in serum-free conditions. These observations suggest that astrocytes may interact with the immune system by elaborating nonspecific factors that modulate lymphocyte proliferation. This property of astrocytes may be important in the generation of specific immune responses in the brain, which is considered to be an immunologically privileged organ as it is anatomically sequestered from the immune system.
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PMID:Production of prostaglandin E and an interleukin-1 like factor by cultured astrocytes and C6 glioma cells. 698 21

Previous studies suggested that trinitrophenyl (TNP)-modified syngeneic red cells induced humoral autoimmune response in mice with defective T cell function but not in normal mice. The ability of modified self antigen to induce autoimmune response in immunodeficient mice was further explored using the delayed-type hypersensitivity (DTH) as an assay system. Mice were immunized with syngeneic TNP-modified spleen cells (TNP-SC) and challenged by syngeneic nonmodified concanavalin A (Con A) or lipopolysaccharide (LPS)-stimulated spleen cells injected into their footpads. The DTH response was assessed 24, 48 and 72 h later by measuring the footpad swelling and was transferred to naive recipients with enriched T cells from TNP-SC-immunized irradiated A mice but not with serum or non-T cells. Adult thymectomized, X-irradiated (250 rds) and cyclophosphamide-treated mice injected with syngeneic TNP-SC generated a DTH response when subsequently challenged with syngeneic lymphoblasts (induced with Con A or LPS) but not when challenged with allogeneic blast cells. In contrast, normal mice treated in a similar manner exhibited a much less significant DTH response. SC incubated 1 to 3 h with Con A failed to elicit the DTH response of immunodeficient mice previously injected with TNP-SC. Both lymphoblasts that were induced in vitro with Con A diluted in fetal calf serum or in normal mouse serum-containing media, and lymphoblasts that were induced in vivo by interleukin 2 elicited DTH responses in X-irradiated, TNP-SC immunized mice. The syngeneic DTH response of the immunodeficient mice injected with TNP-SC was abrogated when they were simultaneously transplanted with syngeneic SC or nylon wool-passed syngeneic SC. If the transplanted splenocytes had been treated with anti-Thy-1 antiserum and complement they failed to abrogate the syngeneic-DTH response of the above mentioned mice. This result suggests that suppressor cells are programmed to control the autoimmune response induced with modified self antigens.
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PMID:Delayed-type hypersensitivity induced in immunodeficient mice with syngeneic modified self antigens: a suggestive model of autoimmune response. 698 70

The role of fever in host defense, if indeed it has one, is poorly understood. Fever in response to exogenous agents is mediated by a host macrophage product called endogenous pyrogen (EP). Recently it has been shown that EP is probably identical to interleukin 1 (IL1), an immunostimulatory macrophage product that induces T-cell proliferation. We postulated that the pyrogenic and immunostimulatory actions of this host mediator might be interrelated and tested T-cell proliferation induced by IL1 at a temperature characteristic of fever. The T-cell proliferative response to IL1 (and to the lymphokine, interleukin 2) was greatly increased at 39 degrees C compared to 37 degrees C, while B-cell mitogenesis in response to lipopolysaccharide was not. These findings suggest that, if similar events occur in vivo, fever may have important immunoregulatory significance and call into question the current indiscriminate use of antipyretic agents.
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PMID:Fever and immunoregulation: hyperthermia, interleukins 1 and 2, and T-cell proliferation. 698 7


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