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)

Susceptibility to experimental autoimmune thyroiditis (EAT) in the mouse is linked to the I-A subregion of the major histocompatibility complex. EAT can be induced in susceptible strains of mice by immunization with mouse thyroglobulin (MTg) and adjuvant. We have described a cell transfer system wherein spleen cells from EAT-susceptible CBA/J mice primed in vivo with MTg and lipopolysaccharide (LPS) can be activated in vitro with MTg to transfer EAT to naive syngeneic recipients. This cell transfer system was used to elucidate the cellular basis for the I-A restriction in EAT. While the cell active in transferring EAT was Thy 1+ I-A-, depletion of I-A+ cells from the in vitro culture prevented the activation of EAT effector T cells. MTg-pulsed mitomycin C-treated naive syngeneic spleen cells as antigen-presenting cells (APCs) could replace the I-A+ cells in vitro. Allogeneic (Balb/c) APCs were ineffective. Using APCs from several recombinant inbred strains of mice, it was shown that C3H/HEN and B10.A(4R) APCs were effective in activating MTg/LPS-primed CBA/J spleen cells to transfer EAT while B10.A(5R) APCs were ineffective. This maps the H-2 restriction to the K or I-A subregions. Addition of polyclonal anti-Iak or monoclonal anti-I-Ak or anti-L3T4 during in vitro activation inhibited both the generation of EAT effector cells and the proliferative response to MTg. Irrelevant anti-Ia reagents, monoclonal anti-I-Ek, and monoclonal anti-I-Jk were ineffective. Thus the I-A restriction in murine EAT appears to result from an I-A restricted interaction between Ia+ APCs and Ia- EAT effector T cells.
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PMID:The cellular basis for the Ia restriction in murine experimental autoimmune thyroiditis. 349 88

The effects of Ta-1, a peptide constituent of thymosin fraction 5, were studied on murine autoimmune thyroiditis using two congenic strains of mice, B10.Br (Br) and B10.D2 (D2), which are sensitive and resistant to experimental autoimmune thyroiditis (EAT) induction, respectively. EAT was induced by either 2 weekly iv injections of mouse thyroglobulin with adjuvant lipopolysaccharide (LPS) or intradermal injection of thyroglobulin mixed with complete Freund's adjuvant (CFA). The criteria for induction and intensity of thyroiditis were the level of lymphoid infiltration in the thyroid gland and the titer of anti-thyroglobulin antibodies. Ta-1 was given in 5 or 10 daily sc injections in doses ranging from 0.0001 to 0.1 microgram/injection. The injections were commenced at varying intervals from the 1st to the 4th week after immunization. T-Cell subsets in the spleens were determined 2 weeks after the first antigen injection and thyroid infiltration was determined 3 weeks later. Treatment with Ta-1 between the two antigen injections increased the level of thyroiditis in resistant mice, but had no effect in sensitive mice. Treatment for the first 2 weeks had similar effects in resistant mice, but also suppressed thyroiditis in the sensitive strain. Later treatments, during the 3rd and 4th weeks after immunization also revealed immunomodulating properties of Ta-1, with a suppressing effect on thyroiditis in sensitive mice and an enhancing effect in the resistant strain. Both effects of Ta-1 were dose dependent. The effects of Ta-1 on the individual phenotypes were also dose dependent. The dose of 0.01 microgram greatly lowered the percentages of Lyt-2+3+ cells in D2 mice and mildly increased the percentages in Br mice, but did not change the Lyt-1+ cell level in either strain. On the other hand, the dose of 0.001 microgram greatly increased the percentage of Lyt-1+ cells in D2 mice and mildly decreased it in the Br strain, but did not alter the Lyt-2+3+ cell subset in either strain. Thus, both doses of Ta-1 modulated Lyt-1+/2+3+ ratios, with each dose affecting a different T-cell subset. The changes in the response to thyroglobulin are apparently exerted through the regulation of the functional T-cell subset balance.
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PMID:Thymosin alpha 1-induced modulation of cellular responses and functional T-cell subsets in mice with experimental autoimmune thyroiditis. 387 93

Mice of the (C57BL/10 X B10.A)F1 combination were given a single i.v. inoculation of 3 to 4 X 10(7) B10.A spleen cells, which induces a graft-vs-host (GVH)-associated immune deficiency in F1 mice. Between 1 and 4 wk later, spleen cells from the F1 mice were tested for the expression of IL 2 receptors by flow microfluorometry, using the 7D4 rat monoclonal antibody directed against an epitope murine IL 2 receptor. A reduction in intensity of spleen cell staining with 7D4 was detected as early as 8 days after parental cell inoculation, and no IL 2 receptors were detected by 28 days after initiation of GVH. Furthermore, the loss of IL 2 receptors was correlated with abrogation of proliferative responses to concanavalin A and lipopolysaccharide, of IL 2 production, and of cytotoxic T lymphocyte responses. These observations may be relevant for our understanding of GVH reactions, of immune disorders associated with GVH, and possibly of primary and acquired immunodeficiencies in general.
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PMID:Interleukin 2 receptor dysfunction in mice undergoing a graft-vs-host reaction. 392 88

Rabbit antibodies obtained after immunization of mouse immunoglobulin (MIg)-tolerant rabbits with B6 anti-CBA IgG and having specificity for B6 anti-CBA IgG and T-cell receptors (antiserum 5936) were used to isolate 5936-reactive molecules from B6 anti-CBA mixed lymphocyte culture supernatants. Such 5936-reactive molecules were produced by the B6 T cells, and they did not react with rabbit anti-MIg antisera. They had a mol. wt of 50,000-75,000, and were single-chain polypeptides that did not react with concanavalin A (Con A)--Sepharose. These molecules were in turn injected into rabbits, and the antisera thus obtained had the following characteristics: (1) they reacted against B6 anti-CBA T-cell receptor material but not against B6 anti-CBA IgG; (2) they reacted with about 35% of B6 (H-2b, Ig-1b) anti-CBA T cells, 25% of B6 Con A blasts and 0-10% of normal B6 T cells but not with B6 lipopolysaccharide (LPS) blasts, C3H.B10 (H-2b, Ig-1j) anti-CBA or CBA anti-B6 T cells, CBA Con A blasts or normal CBA T cells; and (3) they reacted with the same 50,000-75,000 mol. wt, T-cell-derived molecules as did antiserum 5936. The implications of these findings are discussed in relation to the nature of T-cell receptors.
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PMID:Rabbit antisera with specificity for isolated mouse T-lymphocyte receptors. 617 77

By using monoclonal antibodies, a tumor-specific antigen (TSA 41.5) was detected on the cell surface of a B lymphoma CH-1 tumor variant, CH-1.1. This antigen is not expressed by normal lymphocytes (spleen cells, lymph node cells, thymocytes, bone marrow cells, or blast cells) of B10.A mice, the host strain of CH-1.1, or by the CH-1 lymphoma. Immunoprecipitation and biochemical characterization of TSA 41.5 with the use of two-dimensional gel electrophoresis showed this antigen to be a surface protein of CH-1.1 cells with an Mr of 80k and pI of 4.6. TSA 41.5 is not related to the murine transferrin receptor, and not to gp70, a viral envelope protein expressed by CH-1.1 cells, shown by comparative peptide map analysis of these three proteins. TSA 41.5 is a surface antigen unique to the CH-1.1 tumor, which is not expressed by the 19 different murine tumor lines that were tested nor by spleen cells of 15 independent mouse strains. In addition, treatment of spleen cells with bacterial lipopolysaccharide did not induce the expression of TSA 41.5. These characteristics of TSA 41.5 make it unlikely to be a product of viruses. Additional evidence against TSA 41.5 being a viral protein was obtained by the observation that antisera against viral proteins could not block the binding of the anti-TSA monoclonal antibody to its antigen. In vitro treatment of CH-1.1 cells with anti-TSA monoclonal antibody specifically inhibited the in vitro growth of the tumor cells in a dose-dependent fashion. The CH-1.1 tumor and monoclonal antibodies could be a useful murine model system for the exploration of the use of monoclonal antibodies for the in vivo treatment of cancer.
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PMID:Description of a murine B lymphoma tumor-specific antigen. 620 65

A hen egg-white lysozyme-lipopolysaccharide complex (HEL-LPS) can stimulate an in vitro IgG response, but only from HEL-primed B lymphocytes; unprimed cells only produce an IgM response. These conditions were used to determine whether IgG memory B cells are cryptically induced in B10 nonresponder (H-2b) mice after an HEL injection protocol. The usual i.p. immunization that triggers IgG memory production in congenic responder strain mice fails to yield IgG in vitro from HEL-primed B10 spleen cells after stimulation with HEL-LPS. However, injection protocols immunogenic for B10 mice do engender IgG-memory cells. These results imply that the T helper cell population necessary for triggering B cells to the IgG memory stage cannot develop in the nonresponder mouse, presumably due to HEL-specific T suppressor cells.
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PMID:The failure of nonresponder mice to develop IgG memory assessed by in vitro culture with an antigen-LPS conjugate. 697

The quantitative expression of surface I-A determinants has been used to define functional B cell heterogeneity based on responsiveness to the trinitrophenyl (TNP) hapten on various classes of carrier molecules. Unprimed, anti-Thy 1 and complement-treated B10.A (I-Ak) B cells were stained with a monoclonal anti-I-Ak reagent that had been fluorescein (FL) conjugated. By using a fluorescence-activated cell sorter these cells were then sorted into 2 populations of cells staining heavily or lightly with this reagent. These populations of cells were then assayed for anti-TNP precursor frequency, in responses to 3 TNP-antigens, by limiting dilution analysis. B cells responsive to TNP-lipopolysaccharide (LPS) and TNP-sheep red blood cells (SRBC) were found in both the B cells that expressed a low amount of surface I-A and the B cells that expressed a high amount of I-A. However, B cells with the ability to respond to TNP-Ficoll were found only in the B cells that expressed a low amount of surface I-A. These experiments suggest that the quantitative expression of surface I-A can be used to define B cell populations with different abilities to respond to hapten coupled to Ficoll.
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PMID:Functional subsets of B cells defined by quantitative differences in surface I-A. 697 99

A method for infection of lymphocytes with Moloney(Abelson) murine leukemia virus [M(A)-MuLV] is described. Only lymphoblasts obtained after stimulation of normal spleen cells by the B cell mitogen lipopolysaccharide (LPS) were satisfactory targets for virus-specific, secondary cytotoxic T lymphocytes (CTL), whereas spleen cells stimulated by the T cell mitogen concanavalin A were not. The secondary CTL response against M(A)-MuLV could be efficiently measured using M(A)-MulV-infected LPS blasts as stimulating cells for secondary in vitro restimulation and as target cells for virus-specific destruction. Cold target inhibition demonstrated virus specificity of CTL. The T cell character of the cytotoxic cells was demonstrated by their sensitivity to anti-Thy-1.2 treatment. Using syngeneic virus-infected LPS blasts as target and stimulator, CTL responses were measured with effector cells from C57BL mice of the H-2b haplotype and of recombinant haplotypes sharing either K or D alleles with H-2b. In analogy with previous studies on Moloney virus-specific CTL, it was observed that C57BL/6 (H-2b) effector cells predominantly lysed Db-compatible, virus-infected target cells; B10.A(5R), (KbDd) effector cells showed a poor CTL response against syngeneic, virus-infected target cells. The combined findings indicate the existence of an Ir gene in the H-2D region regulating the CTL response against Moloney leukemia virus.
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PMID:Cytotoxic T cell response against lymphoblasts infected with Moloney (Abelson) murine leukemia virus. Methodological aspects and H-2 requirements. 697 10

Different strains of mice were examined for the capacity to produce an Ig subclass-specific antibody response to purified Pseudomonas aeruginosa lipopolysaccharide (PALPS). With the exception of the AKR strain, the predominant isotype for most of the strains tested was IgG3 whereas the least frequent isotype expressed was either IgG2b or IgG1. AKR mice were unique in that the predominant isotype produced was IgG2a, rather than IgG3; however, the administration of anti-interferon gamma antibody, at the time of immunization with PALPS caused a substantial decrease in the IgG2a antibody response. Selected B10 congenic strains were used to assess the relationship between the antibody responses and the major histocompatibility complex (MHC) genes. Here, the isotype-patterns for the antibody responses were essentially the same regardless of the MHC haplotype. Interestingly, an increase in IgG2a, with a concomitant decrease in IgM and IgG1 antibody was noted when C3H mice were given interferon gamma at the time of immunization. These studies indicate that, in general, the antibody response to PALPS consists of IgG3 antibody as the predominant isotype, and that the antibody response can be modified by interferon gamma.
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PMID:Effects of interferon gamma on the antibody response to Pseudomonas aeruginosa lipopolysaccharide in mice. 775 Sep 85

Leishmania major are intramacrophage parasites whose eradication requires the induction of T helper 1 (Th1) effector cells capable of activating macrophages to a microbicidal state. Interleukin 12 (IL-12) has been recently identified as a macrophage-derived cytokine capable of mediating Th1 effector cell development, and of markedly enhancing interferon gamma (IFN-gamma) production by T cells and natural killer cells. Infection of macrophages in vitro by promastigotes of L. major caused no induction of IL-12 p40 transcripts, whereas stimulation using heat-killed Listeria or bacterial lipopolysaccharide induced readily detectable IL-12 mRNA. Using a competitor construct to quantitate a number of transcripts, a kinetic analysis of cytokine induction during the first few days of infection by L. major was performed. All strains of mice examined, including susceptible BALB/c and resistant C57BL/6, B10.D2, and C3H/HeN, had the appearance of a CD4+ population in the draining lymph nodes that contained transcripts for IL-2, IL-4, and IFN-gamma (and in some cases, IL-10) that peaked 4 d after infection. In resistant mice, the transcripts for IL-2, IL-4, and IL-10 were subsequently downregulated, whereas in susceptible BALB/c mice, these transcripts were only slightly decreased, and IL-4 continued to be reexpressed at high levels. IL-12 transcripts were first detected in vivo by 7 d after infection, consistent with induction by intracellular amastigotes. Challenge of macrophages in vitro confirmed that amastigotes, in contrast to promastigotes, induced IL-12 p40 mRNA. Reexamination of the cytokine mRNA at 4 d revealed expression of IL-13 in all strains analyzed, suggesting that IL-2 and IL-13 may mediate the IL-12-independent production of IFN-gamma during the first days after infection. Leishmania have evolved to avoid inducing IL-12 from host macrophages during transmission from the insect vector, and cause a striking induction of mRNAs for IL-2, IL-4, IL-10, and IL-13 in CD4+ T cells. Each of these activities may favor survival of the organism.
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PMID:Leishmania promastigotes evade interleukin 12 (IL-12) induction by macrophages and stimulate a broad range of cytokines from CD4+ T cells during initiation of infection. 790 17


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