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

The alloantigenic specificity Ly-4.2 can be detected on a proportion of lymphocytes by the antiserum (BALB/c times SWR)F1 anti-B10.D2. In the preceding study it was shown that these lymphocytes were not thymus-derived (T) cells, as they were Thy-1 (theta)(-), and were therefore presumably B (bone marrow-derived) cells. Evidence is now presented for the reaction of the Ly-4.2 antiserum with functional B cells. Thus, the LY-4.2 and Thy-1.2 specificities were detected on antigen-binding rosette-forming cells (RFC) in mice both immune and non-immune to sheep red cells (SRC). RFC formed to endotoxin lipopolysaccharide (LPS) were also Ly-4.2(+). Memory cells to both SRC andLPS could be detected with anti-Ly-4.2 and anti-Thy-1.2 antisera, thereby indicating that both T and B cells are involved in memory to these antigens. Both direct and indirect antibody-forming cells (the PFC) could be inhibited, in vitro, by anti-Ly-4.2 antiserum, although it is likely that not all PFC are Ly-4.2(+). Neither of the specificities Ly-4.2 nor Thy-1.2 were detected on the bone marrow precursor of the splenic colony forming unit (the CFU). In an assay for B cells, the treatment of lymph node or spleen cells with anti-Ly-4.2 before transfer to irradiated recipients could inhibit the ability of these cells to make PFC to SRC, and this capacity could only be restored by bone marrow cells and not by thymus cells. These studies provide clear evidence for the presence of the Ly-4.2 specificity on antibody-forming cells and their precursor (B cells).
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PMID:Ly-4.2: a cell membrane alloantigen of murine B lymphocytes. II. Functional studies. 108 20

Old (6 months) overtly autoimmune female NZB X NZW F1 (B/W) mice were markedly hyporesponsive to sheep erythrocytes (SRBC). The response to SRBC was restored by a) simultaneously injecting lipopolysaccharide (LPS) with SRBC or b) transferring bone marrow and thymocytes with SRBC into lethally x-irradiated (100 R) syngeneic old recipients. The in vitro PFC response of old B/W spleen cells to SRBC was restored by adding in culture a) theta-positive and radioresistant spleen cells from old B/W mice primed with homologous antigen or b) activated T cells from the spleens of lethally x-irradiated (1000 R) old B/W mice injected with old syngeneic thymocytes and SRBC but not horse erythrocytes. Various populations of unprimed lymphoid cells from young (4 to 6 weeks) female B/W mice, which respond normally to SRBC, were not capable of restoring the response of old syngeneic mice in vitro or in vivo. These results suggest the existence of a suppressor of T cell activation and/or B and T cell interaction in old autoimmune B/W mice.
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PMID:T cell activation and cellular cooperation in autoimmune NZB/NZW F hybrid mice. 109 16

TNP-lipopolysaccharide (TNP-LPS) is a potent T-independent antigen in vivo, inducing a TNP-PFC response in T-depleted animals. The structural integrity of the lipid A-KDO portion of the LPS carrier molecule appears to be required since the haptenated LPS from Salmonella minnesota Re595 is immunogenic whereas the haptenated derivative of base hydrolyzed LPS is not. The immune response is not associated with any of the common histocompatiblity types, but does depend on the ability of the host strain to respond to LPS. C3H/HeJ mice are not killed by low doses of LPS and give a poor PFC response to TNP-LPS. Lethality and immunogenicity are dominant responses in hybrids of C3H/HeJ and responder mice. The structural and genetic requirements for the response to TNP-LPS suggest an active role for the carrier in the immunogenicity of this T-independent antigen.
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PMID:Structural and genetic basis of the in vivo immune response to TNP-LPS. 110 Jul 25

Monocrotaline (MCT) is a member of a class of naturally occurring phytotoxins known as pyrrolizidine alkaloids, and is a toxicological concern to both man and his livestock. The purpose of these studies was to evaluate the effect of a 14-day oral MCT (0-100 mg/kg per day) exposure on the functional integrity of various immunocyte effector systems in C57BL/6 mice, as well as to investigate potential mechanisms for its immunotoxicity. Decreases in lymphoid organ weights and cellularity, and resident peritoneal exudate cell (PEC) number were only observed after exposure to the highest dose of 100 mg/kg MCT. This dose also inhibited NK cell cytotoxicity, while the total number of NK lytic units per spleen was decreased (-53%) after exposure to 50 mg/kg MCT. Following i.p. injection of SRBC, the percentage of PEC macrophages containing engulfed SRBC was significantly increased in MCT-exposed mice, while the percentage of large vacuolated (activated) macrophages was decreased in a dose-dependent manner. Exposure to MCT significantly decreased the total number of Ig+ cells without altering the number of CD4+ and CD8+ cells. The antibody responses (PFC/10(6) spleen cells) to two T cell-independent antigens, TNP-LPS and DNP-Ficoll, were significantly decreased at all MCT doses, and the degree of suppression of both responses was identical at coincident doses. MCT exposure (25 mg/kg) significantly suppressed the blastogenic response to the T cell mitogen concanavalin A (-38%), and to the B cell mitogen lipopolysaccharide (-58%). These results indicate that exposure to MCT can alter the functional integrity of various immune effector responses in a dose-dependent manner, and suggest that the B cell may be a relatively more sensitive target of MCT immunotoxicity compared to T cells, macrophages and NK cells.
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PMID:Tier-2 studies on monocrotaline immunotoxicity in C57BL/6 mice. 177 39

B lymphocytes from the pulmonary lymphoid tissues were stimulated with a variety of thymus-independent (TI) antigens by intratracheal (i.t.) immunization. Immune responses in the lungs and hilar lymph nodes (HLN), which are part of the localized lymphoid tissue, as well as in the spleen, the systemic lymphoid organ, were studied. Thus, primary i.t. immunization of mice with the TI-1 antigen trinitrophenyl-lipopolysaccharide (TNP-LPS) elicited both antigen-specific and polyclonal plaque-forming cell responses from HLN, lung, and splenic B lymphocytes. These responses appeared as early as 3 days after immunization and declined by day 7. Similar immunization with another TI-1 antigen, TNP-Brucella abortus, resulted in anti-TNP responses in both pulmonary and systemic lymphoid tissues, although the kinetics of the antibody response were different than those to TNP-LPS. Interestingly an i.t. immunization with a TI-2 antigen, TNP-Ficoll, failed to induce an anti-TNP PFC response from HLN and lung B cells, although there was good antibody formation from splenic B cells. Antibody response to TNP-Ficoll was restored in pulmonary tissues when mice were immunized with TNP-Ficoll mixed with unconjugated B. abortus. In conclusion, our results indicate that TI-1 and TI-2 antigens differ in their ability to induce antibody responses in the pulmonary lymphoid tissues. The inability of TNP-Ficoll to elicit an antibody response in pulmonary lymphoid tissues has significance in the development of vaccines containing bacterial polysaccharides.
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PMID:Primary antibody responses to thymus-independent antigens in the lungs and hilar lymph nodes of mice. 211 56

The present study has examined a functional role of Ia molecules expressed on murine B cells in polyclonal B cell differentiation induced by lipopolysaccharide (LPS). Reverse, IgM PFC responses of unprimed B cells induced by LPS in the apparent absence of T cells and adherent accessory cells were markedly inhibited in a haplotype-specific manner by Fab monomer fragment of anti-class II (Ia) but not anti-class I MHC monoclonal antibody (mAb). However, the degree of inhibition of LPS responses of H-2-heterozygous F1 B cells expressing both parental I-A products by either one of anti-I-A mAb was at best half that of the parental B cells. Interestingly, when (B10 x B10.-BR)F1 (H-2b/k) B cells were fractionated into adherent and nonadherent populations by their ability to bind to parental B10 B cell monolayers, LPS responses of F1 B cells adherent to and nonadherent to the B10 B cell monolayers were selectively inhibited by anti-I-Ab and anti-I-Ak mAb, respectively. These results suggest that LPS-responsive F1 B cells comprise at least two separate populations with restriction specificity for only one of the parental I-A products expressed on B cells. In addition, it was demonstrated that the I-A-restriction specificity of LPS-responsive B cells is "plastic" and determined by H-2-genotype of bone marrow cells present during B cell ontogeny but not by that of radiation-resistant host elements. Namely, the LPS responses of B10-derived B cells from (B10 + B10.BR) (H-2b x H - 2k)F1 radiation bone marrow chimeras but not from B10 (H-2b x H-2k)F1 chimeras became sensitive to the inhibition of anti-I-Ak mAb in the presence of mitomycin C-treated I-Ak-positive B cells, supporting a notion of receptor-Ia molecules interactions rather than like-like interactions. Thus, the present results provide evidence indicating that B-B cell interaction via recognition of self-I-A products is a crucial event in the polyclonal B cell differentiation induced by LPS.
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PMID:Involvement of I-A-restricted B-B cell interaction in the polyclonal B cell differentiation induced by lipopolysaccharide. 232 98

The effects of eicosapentaenoic acid (EPA) on the humoral immune response in fat free diet-fed (FF) mice were studied. The lowered anti-SRBC PFC activity of ICR male FF mice was restored in a dose-dependent manner when EPA was administered orally at doses of 60-360 mg/kg/day for 20 days. In in vitro experiments, EPA similarly enhanced anti-SRBC PFC activity but did not affect the response against lipopolysaccharide. Furthermore, EPA did not cause any substantial effect on T suppressor cell activity induced by Concanavalin A in vitro. On the other hand, T helper cell activity induced by keyhole limpet hemocyanin was augmented. From these results, it is suggestive that EPA caused immunopotentiation to FF mice at least partially by an enhancement of T helper cell activities.
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PMID:Ethyl eicosapentaenoate restored the immunosuppression in mice fed fat-free diet. 284 87

Previous studies have shown that male mice of strains with high target organ responsiveness to androgen, the C57L/J and RF/J, have lower plasma immunoglobulin levels and weaker antibody responses to protein and polysaccharide antigens than mice of low androgen responder (LAR) strains, the A/J and 129/J. In the current report, the relationship between high androgen responsiveness and low immune performance has been investigated in another strain, the C57BR/cdj. Compared to LAR A/J males, C57BR/cdj males had significantly higher target organ responses to androgen as measured by both seminal vesicle bioassay and haematocrit. High androgen responder (HAR C57BR/cdj males were lower than A/J's in PFC responses to sheep red blood cells (SRBC), lipopolysaccharide (LPS) induced spleen cell proliferation and polyclonal B cell activation. HAR C57BR/cdj males were not significantly different from C57BR/cdj females or A/J mice in proliferative responses to concanavalin A (Con A) or phytohaemagglutinin (PHA). These results are compatible with our previous findings in other HAR strains and suggest that the consistently low in vivo immune responses of HAR males may be due to B cell weakness or T suppressor dysregulation.
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PMID:Low immune responses in high androgen responder C57BR/cdj males. 293 80

Acute Trypanosoma cruzi infection of mice results in a very marked polyclonal activation of B and T lymphocytes, accompanied by high numbers of Ig-secreting PFC and lectin-dependent effector CTL. Treatment of mice with monoclonal anti-L3T4 antibodies from the time of infection (days 0, 4, and 8) completely suppresses the polyclonal PFC response and CTL generation. Treatment of nude mice with antibody does not alter the lipopolysaccharide-induced polyclonal PFC response, and it only modulates the isotypic profile of the PFC response to T. cruzi infection, without reducing its magnitude. Furthermore, antibody-treated, T. cruzi-infected euthymic mice do not develop the typical B cell blastogenic response, but show high numbers of activated Lyt-2+ lymphoblasts in the spleen. These results indicate that effector cell generation in T. cruzi-infected mice is predominantly helper T cell-dependent.
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PMID:Suppression of polyclonal antibody production in Trypanosoma cruzi-infected mice by treatment with anti-L3T4 antibodies. 295 44

Peritoneal macrophages from normal mice which do not secrete interleukin 1 (IL 1) spontaneously release a factor with an approximate m.w. of 30,000-35,000. In contrast, in the presence of silica only IL 1 is produced. IL 1 as well as this macrophage-replacing factor (MRF) can restore the antibody response of macrophage-depleted spleen cells. IL 1, however, is the only one that has the capacity to increase the proliferation of thymocytes. In every strain of mice studied, including nude mice, we observed a spontaneous release of MRF and a silica-induced shift to the secretion of IL 1, except in lipopolysaccharide (LPS)-hyporesponsive C3H/HeJ mice. Macrophages from these mice are unable to secrete MRF spontaneously, or IL 1 when stimulated with silica. The kinetics of the secretion of MRF and IL 1 appear to be similar. Macrophages, regardless of whether they have been stimulated to secrete IL 1, produce an intracellular IL 1-like activity with an approximate m.w. of 15,000. In contrast, the intracellular PFC-restoring activity is widely distributed in the 15,000-60,000 m.w. range; one of these compounds could be related to IL 1 precursor and/or to MRF itself. Chromatofocusing and chromatography on Blue Trisacryl have led to a partial purification and resolution from a possible contamination by IL 1. Purified MRF induces, in conjunction with lymphokines, the differentiation of B cells into antibody-forming cells.
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PMID:Characterization of a 30,000-35,000 m.w. monokine involved in the specific immune response: intracellular production, secretion and partial purification. 296 41


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