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)

T cell dependency of antibody response to polyvinylpyrrolidone (PVP), sheep red blood cells (SRBC), bovine gamma globulin (BGG), and bovine serum albumin (BSA) was examined. PVP and the other three are known as a T cell-independent antigen and T cell-dependent antigens respectively. Adult mice were thymectomized, X-irradiated, reconstituted with syngeneic bone marrow cells (TxXB mice), with bone marrow cells plus thymus cells (TxXBT mice), or with bone marrow cells treated with anti-Thy-1.2 serum and complement (TxXB-theta mice) and used as experimental animals. The anti-PVP response of TxXBT mice was significantly lower than that of TxXB mice, suggesting that T cells exerted a suppressive effect on the response to PVP. Both IgM and IgG responses to SRBC and BGG occurred even in TxXB-theta mice with the aid of bacterial lipopolysaccharide (LPS). However, a significant response to BSA was not observed in TxXB mice even in the presence of LPS or several other adjuvants. These results indicate that the T cell dependency of antigens is different among so called thymus-dependent antigens, that antibody response less dependent on the helper action of T cells can be supported by LPS in the absence of T cells, and that anti-BSA response seems to be extremely T cell dependent.
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PMID:Hierarchy of T cell dependency in antibody response among different antigens. 9 45

CBA/N mice have an X-linked immune defect in B lymphocyte function which leads to their inability to respond to several thymus-independent antigens. We report here that these mice and immunologically defective F1 male (CBA/N X DBA/2N) mice can respond to Brucella abortus and to 2,4,6-trinitrophenyl derivatives of Brucella abortus (TNP-BA). These responses can be obtained in vivo and in vitro and are thymus-independent by the criteria that (a) they can be transferred to irradiated recipients by bone marrow cells and anti-Thy-1.2 and complement-treated spleen cells; (b) that nu/nu BALB/c spleen cells respond to TNP-BA in vitro; and (c) that anti-Thy-1.2 and complement-treated (CBA/N X DBA/2N)F1 male spleen cells respond to TNP-BA in vitro. B. abortus and TNP-BA are poor polyclonal B cell activators (PBA) and poor B cell mitogens, unlike lipopolysaccharide which is both a powerful PBA and B cell mitogen. These results therefore indicate that mice with the CBA/N B cell defect can respond to some thymus-independent antigens, namely TNP-BA, and as shown previously, TNP-LPS, although not to other thymus-independent antigens. This, in turn, suggests that thymus-independent antigens may be subdivided on the basis of their ability or inability to stimulate responses by CBA/N B lymphocytes.
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PMID:T-independent responses in B cell-defective CBA/N mice to Brucella abortus and to trinitrophenyl (TNP) conjugates of Brucella abortus. 9 20

Old (15-20 month) male (NZB x NZW)F1 (B/W) mice have severely impaired spleen cell reactivity to phytohemagglutinin (PHA), a mitogen which stimulates mainly T lymphocytes. Spleen cells from old mice markedly suppressed the PHA response of splenocytes from young (3-4 month) B/W males. Similar suppressor activity was not present in the spleens of old mice of four nonautoimmune strains. The suppressor activity of old B/W spleen cells was mediated by a nonphagocytic, radioresistant, mononuclear leukocyte. Although this cell was eluted in the "T lymphocyte" fraction of nylon wool colums, it was not sensitive to treatment with anti-Thy-1 antiserum and complement. Suppressor activity was lost after 18 h incubation at 37 degrees C in tissue culture medium. Supernatants of these overnight cultures had no suppressive effect on fresh young B/W spleen cells. Old B/W spleen cells suppressed PHA reactivity more than concanavalin A or lipopolysaccharide reactivity. Kinetic studies demonstrated an increasing suppression with time over 72 h of culture. This study demonstrate that the severely impaired PHA reactivity of old B/W mice is mediated, at least in part, by active suppression.
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PMID:Suppressor cells and immunodeficiency in (NZB x NZW)F1 hybrid mice. 15 83

When thymus cells which are unresponsive to LPS are combined with numbers of peripheral lymphoid cells giving minimal responses to LPS, synergistic incorporation of [3H]thymidine occurs. Synergy requires that both components proliferate, but most of the augmented response is the result of peripheral cell proliferation. The thymus cell is a T cell of variable density, low in thy-1.2 antigen, not concanavalin A responsive, present in the major thymus subpopulation, and may be from lipopolysaccharide (LPS)-unresponsive strains. The peripheral cell is sensitive to anti-IgG or IgM plus complement (C'), resistant to anti-Thy-1.2 and C', exhibits adherence properties of B lymphocytes, and must be from LPS-responsive strains. Synergistic responses depend on critical thymus/peripheral cell ratios, inhibition occurring at high peripheral cell numbers. The data provide evidence that B-cell proliferative responses to LPS may be regulated by a subclass of thymus T cells.
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PMID:Regulation of B-cell proliferative responses to lipopolysaccharide by a subclass of thymus T cells. 30 Jul 82

Mice depleted of T cells by adult thymectomy, X-irradiation and reconstitution with syngeneic bone marrow cells, either untreated or treated with anti-Thy-1 serum and complement, were immunized intensively with alum-precipitated bovine serum albumin (AP-BSA) along with or without bacterial lipopolysaccharide (LPS), but no significant anti-BSA antibody response was detected. Priming of the T-cell depleted mice, however, either by a single injection of AP-BSA plus LPS or by multiple injections of AP-BSA without LPS, resulted in the generation of immunological memory. A single injection of AP-BSA without LPS was ineffective. The memory required the aid of syngeneic T cells to be recalled by the challenge with AP-BSA plus LPS. On the other hand, multiple injections of AP-BSA plus LPS did not cause the generation of memory and the response of these mice to the challenge was lower than that of unprimed control mice. These results suggest that (1) the anti-BSA response is highly dependent on the helper function of T cells, (2) the degree of T-cell requirement for the memory generation is very low, and (3) priming with too much strong stimulation in the absence of functional T cells leads to the suppression or abortion of previously generated immunological memory.
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PMID:Studies on B-cell memory. I. Generation and exhaustion of B-cell memory by thymus-dependent antigen in T-cell depleted mice. 31 22

Rabbit antiserum against mouse brain tissue (anti-brain-associated T cell antigen, anti-BAT) was capable of killing splenic natural killer (NK) cells of CBA/J, BALB/c, C 57 Bl/6J, C 3 H/He and nude mice, which were detected with Molony virus-induced lymphoma (YAC-1) and radiation-induced leukemia (RL male 1) cells as targets. The same antiserum abolished T cell functions, e.g. carrier-specific helper function and the responsiveness to concanavalin A, but not B cell functions, e.g. immunological memory for the secondary antibody response and the responsiveness to lipopolysaccharide. After absorption of the anti-BAT with thymocytes, the ability to kill T cells was completely abrogated, leaving the activity to kill NK cells intact. No other heterologous and isologous antisera, i.e. rabbit anti-mouse thymocyte antiserum, goat antiserum against antigens shared by thymus and B cells, anti-Thy-1.2 and anti-Ia antisera, could eliminate NK function regardless of their definite reactivity against T or B cells. The results indicate that the absorbed anti-BAT can distinguish NK cells from other known subsets of T and B cells.
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PMID:Surface markers on natural killer cells of the mouse. 31 6

The antiserum (B6 X A-Tlab) anti-A (Tlaa) defines several TL antigens expressed exclusively on thymocytes. When reacted with peripheral lymphocytes, the same antiserum defines another antigenic system, provisionally termed Qa-1. The genotypic disparity distinguishing the recipients and donors in this immunization comprises a section of chromosome 17 extending from a crossover point between H-2D and Tla to a presently unmarked point beyond Tla. Therefore although Qa-1 may constitute a single cell surface component, it is equally probable that the Qa-1 system defines two or more cell surface components determined by genes in this region, each of which may be expressed on a different cell set. Cytotoxicity assays indicate that Qa-1 antigen is expressed on Lyt-1 cells and Lyt-123 cells, and may serve to subclassify these two cell sets; it is not known whether Qa-1+ cells may occur within the small Lyt-23 set. There may be also be a cell set with the phenotype Thy-1--:Qa-1+. Another distinctive feature of the Qa-1 system is the characteristic profile of responses to mitogens exhibited by spleen cell populations from which Qa-1+ cells have been eliminated; in conventional assay of [3H]thymidine incorporation the response to lipopolysaccharide was essentially unchanged, the response to phytohemagglutinin M (PHA-M) was virtually abolished, and the response to concanavalin A (Con A) was reduced by 40%. The third distinctive feature of the Qa-1 system is the characteristic profile of changes which elimination of Qa-1+ cells produces in tests of immune function in vitro: (a) proliferation, measured by [3H]thymidine incorporation, in mixed lymphocyte culture (MLC) with major histocompatibility complex (MHC)-incompatible stimulator cells, was not affected. (b) in tests of cell-mediated cytotoxicity (CMC) of MHC-incompatible target cells, neither the generation nor the effector functions of cytotoxic lymphocytes was affected, implying that Lyt-23 prekiller and killer cells are Qa-1--. (c) primary and secondary responses to SRBC were considerably augmented, suggesting that Qa-1+ cells may be responsible for suppression in this test system. (d) accordingly the suppression of the anti-sheep erythrocyte (SRBC) response normally engendered in spleen cells by culture with SRBC was profoundly reduced by elimination of Qa-1+ cells, either before or after culture. (e) the suppression of the anti-SRBC response normally engendered in spleen cells cultured with Con A was reduced by removal of Qa-1+ cells before but not after culture with Con A. Although analysis is as yet far from complete, the Qa-1 system should already be of considerable value because it distinguishes a population of lymphocytes that is not defined by any other antigenic system, according to three criteria: (a) representation of Qa-1 cells among T-cell sets defined by Lyt phenotypes, (b) the profile of responses to mitogens exhibited by lymphocyte populations depleted of Qa-1+ cells, and (c) the profile of immune responses of lymphocyte populations depleted of Qa-1+ cells.
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PMID:The Qa-1 antigenic system. Relation of Qa-1 phenotypes to lymphocyte sets, mitogen responses, and immune functions. 70 65

Among bone-marrow-derived (B) lymphocytes exist subpopulations of cells that can be induced to express the markers: surface immunoglobulin (Ig), the antigen associated with the immune response gene (Ia), and the receptor for the third complement component (CR). Inducible cells for the first two markers are found in bone marrow, and inducible cells for all three are in spleen. Experiments were designed to determine whether induction involves a single precursor cell population that on triggering with lipopolysaccharide expresses all three surface markers, or three separate precursor cell populations each of which expresses a single marker. Specific B cell subpopulations were eliminated by treatment with anti-Ig or anti-Ia and complement, or by rosette formation with erythrocytes-antibody-complement followed by differential centrifugation, and surviving cells were subsequently tested for inducibility of the three B cell markers. After anti-Ig cytolysis only Ig, but not Ia and CR, could be induced, implying that the Ia- and the CR-inducible cells are Ig+. Similarly, after anti-Ia cytolysis Ig and Ia but not CR could be induced. Thus, CR-inducible cells must have the Ig+Ia+ phenotype. Elimination of CR+ cells did not affect the induction of Ig, Ia, or CR from their precursors. None of the three elimination experiments affected the conversion of prothymocytes (Thy-1-) to thymocytes (Thy-1+). From these results we propose the hypothesis that the differentiation of B lymphocytes proceeds through at least four distinct stages characterized by the following phenotypes: Ig-Ia-CR- leads to Ig+Ia-CR- leads to Ig+Ia+CR- leads to Ig+Ia+CR+.
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PMID:Ontogeny of murine B lymphocytes: sequence of B-cell differentiation from surface-immunoglobulin-negative precursors to plasma cells. 108 27

Strain A/J mice made secondary indirect plaque-forming cell (PFC) responses to azobenzenearsonate (ABA) conjugates of giant keyhole limpet hemocyanin (KLH), a thymic-dependent antigen, but not to conjugates of Ficoll, a T-independent antigen. ABA-Ficoll was also unable to elicit a response in animals primed with ABA-KLH, which have an expanded anti-ABA memory cell pool. On the other hand, ABA-Ficoll rendered mice unresponsive to ABA-KLH when administered before priming or boosting with the T-dependent immunogen. Hence, the T-independent antigen was able to tolerize but unable to trigger B-memory cells responsive to the T-dependent antigen. A/J mice immunized with dinitrophenyl conjugates of Ficoll or bovine IgG (BGG) made vigorous IgM and IgG PFC responses. PFC responses to ABA-KLH and 2,4-dinitrophenyl (DNP)-BGG were abrogated by depleting mice of C3 with cobra venom factor, whereas the IgM and IgG PFC responses to DNP-Ficoll were unaffected. B lymphocytes were fractionated on the basis of receptors for C3 and the subpopulations were assayed for in vitro PFC responses to DNP-Ficoll. Very little response was obtained from complement receptor lymphocyte [CRL(+)] B cells, whereas CRL(-) cells were more responsive than unfractionated B cells. Both populations responded to a polyclonal B-cell mitogen (lipopolysaccharide). On the other hand, the in vitro PFC response to a T-dependent antigen (sheep erythrocytes) correlated with the presence of CRL(+) B cells in the cultures. However, a minor component of this response, sensitive to anti-Thy-1 serum, was made by CRL(-) B cells, indicating the existence of subpopulations of T-dependent B cells with different signalling requirements. The results suggest that most B cells responsive to T-dependent antigens possess receptors for C3 and that C3 plays an obligatory role in the response of these cells. A distinct subpopulation of B cells which lack C3 receptors respond to T-independent antigens. The precursors of PFC for the ABA epitope reside largely or exclusively in the CRL(+) compartment in A/J mice, whereas precursors for the DNP determinant are found in both compartments.
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PMID:Murine B-cell subpopulations responsive to T-dependent and T-independent antigens. 108 26

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


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