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 role of T and B lymphocytes in rejection of cardiac allografts bearing isolated major histocompatibility complex (MHC) subregion RT1.B/D encoded class II "Ia" disparities was investigated using natural and congenic recombinant inbred rats (RP, PVG RT1r1). RT1.B/D-disparate heart grafts were shown in 3 strain combinations (RP leads to WF, WF leads to [RP x PVG RT1l] F1, and PVG RT1r1 leads to PVG RT1 alpha) to induce a brisk humoral response (complement-dependent cytotoxicity [CDC] titers greater than 2(6] with specificity for class II determinants as evidenced by strain and tissue distribution of susceptible targets. Cytotoxic T cells (Tc) generated in parallel effected equivalent lysis (in the 4-hr 51Cr-release LMC assay) of con A and lipopolysaccharide (LPS) blasts of the same strains. Specificity of Tc for class II determinants was demonstrable by specific inhibition of killing (congruent to 50%) by anti-Ia antibody preparations (monoclonal 0X4 and antiserum ATH anti-ATL) with specificity for class II products of MHC subregions RT1.B and RT1.D, respectively. Adoptive transfer studies revealed that antibody and cytotoxic effectors (W3/25+, OX8+) with specificity for class II "Ia" determinants, though potentially injurious, are not required for rejection of cardiac allografts transplanted across isolated RT1.B/D disparities (RP leads to WF) because transfer even of small numbers (0.5 X 10(6] of helper T cells (W3/25+, OX8-) previously shown to be responsible for adoptive transfer of delayed type hypersensitivity to alloantigen, effected rejection in the absence of detectable antibody or Tc. In the immune response to alloantigen both cytotoxic T cell generation and a humoral immune response develop in parallel with that other form of cellular immunity, akin to classic delayed or tuberculinlike hypersensitivity, itself potentially a potent effector mechanism in organ allograft rejection.
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PMID:Immune mechanisms in organ allograft rejection. III. Cellular and humoral immunity in rejection of organ allografts transplanted across MHC subregion disparity RT1.B (RT1.D). 635 8

Mice mount a normal primary antibody response on stimulation with the thymic-independent antigen trinitrophenylated lipopolysaccharide (TNP-LPS). Although we have previously reported the generation of functional B-memory lymphocytes to TNP-LPS, this memory response was only observed in few mouse strains. Here we have used congeneic mouse strains in an attempt to locate the genetic regions involved in the memory response. We show that genes of the major histocompatibility complex (MHC) do not have a critical role but that genes coding for the variable region of immunoglobulin heavy chains or gene(s) closely linked to them are required for memory cell induction by TNP-LPS.
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PMID:Igh-V or closely linked gene(s) control immunological memory to a thymus-independent antigen. 640 46

It has previously been shown that activated murine T lymphocytes express intracellular vesicles containing the class I major histocompatibility complex (MHC) antigen H-2K. Evidence has also been provided that such vesicles may be part of a cellular pathway of spontaneous H-2K antigen internalization and recycling, which is specific to T-lymphoid cells. Dual fluorescence flow cytometry has now been used to establish that H-2K antigen is acidified upon internalization in concanavalin A-stimulated but not lipopolysaccharide-stimulated murine splenocytes, thus providing further support that in T lymphoblasts this class I MHC antigen may travel intracellular routes similar to those reported for other cell surface receptors.
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PMID:Acidification of internalized class I major histocompatibility complex antigen by T lymphoblasts. 643 85

Normal C57BL/6 (B6) mouse serum was tested in the direct cytotoxicity assay for specific reactivity against lipopolysaccharide (LPS)-stimulated mouse spleen cells. Selective reactivity was found in weanling and adult serum against lymphoblasts from mice that express an antigen encoded by the H-2Kk region of the major histocompatibility complex (MHC). Other strains, congenic with B6 at the MHC, did not exhibit the same alloreactivity. Serum from mice of a congenic strain being derived in our laboratory, which differs from B6 at two unlinked loci, Tla and nu, exhibited similar reactivity against the B6-H-2k LPS-stimulated lymphoblasts, implying that a competent T cell compartment is not necessary for generation of this reactivity. Such reactivities may result from environmental stimulation of the immune system, from internal immunoregulatory controls, or from some combination of these immune stimuli.
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PMID:Allogeneic reactivity in normal mouse serum. 652 Apr 7

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

C3H/HeJ T cells which specifically recognize B cell-surface antigens of the related, major histocompatibility complex-compatible C3H/Tif strain, can be substantially enriched in vitro by long-term exposure (2--6 wk) of primed lymph node cells to the relevant cellular antigens. These enriched T cells contain functional helper cells as demonstrated by their capacity to induce large numbers of Ig-secreting plaque-forming cells (PFC) in cultures of antigenic B cells. The cooperative interaction results in activation of a large fraction of all splenic B cells, with consequent exponential growth and maturation to high rate secretion of IgM, IgG1, and IgG2, but not IgG3. The IgM PFC response includes antibody specificities to a number of different antigens and can be considered, therefore, as polyclonal. The T helper cell-dependent B-cell response is insensitive to inhibition by anti-delta antibodies, and in contrast with lipopolysaccharide-induced PFC responses, is only partially sensitive to the inhibitory effects of anti-mu antibodies. Finally, B-cell activation to growth and maturation by helper T cells strictly required direct T-cell recognition of antigens on the surface of responding B cells, leading us to the conclusions that if any soluble factors are generated in the collaborative process, they are either antigen specific or incompetent to initiate B-cell growth.
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PMID:Specific T helper cells that activate B cells polyclonally. In vitro enrichment and cooperative function. 676 81

The requirements for different activation signals in the generation of plaque-forming cell (PFC) responses by positively selected B (surface immunoglobulin-positive) cells were analyzed in low-density cultures to minimize the possible effects of contaminating T cells. Using this system, it is demonstrated that not only in T helper cell (TH)-dependent but also in lipopolysaccharide (LPS)-dependent (i.e., so-called T-independent) PFC responses, the resting B cells have to receive at least three different signals: (a) a major histocompatibility complex (MHC)-specific TH signal that can be bypassed by LPS, (b) an antigen signal, and (c) a second TH signal medicated by MHC- and antigen-unspecific helper factor(s) for B cell responses (BHF) that cannot by bypassed by LPS. Specifically, contact of surface immunoglobulin-positive cells with cloned allo-I-A-specific TH or LPS induced a polyclonal PFC response without significant proliferation, whereas contact with BHF alone (obtained as supernatants from different cloned TH, EL-4 thymoma cells, or secondary mixed leukocyte culture cells) had no effect. Only when LPS, antigen, and BHF, or, alternatively, allo-TH (producing themselves BHF) and antigen were present did clonally expanded PFC responses occur. Thus, the data indicate that both an LPS (or specific TH) signal and an antigen signal are required to render the B cells responsive to BHF. BHF seems to act essentially as a nonspecific growth factor, whereas differentiation into antibody-secreting cells appears to be a preprogrammed consequence of B cell activation by an LPS or specific TH signal.
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PMID:Requirement for three signals in "T-independent" (lipopolysaccharide-induced) as well as in T-dependent B cell responses. 680 Nov 77

We previously described a cloned cell line that combines information for a unique display of cell surface antigens and specialized function similar to activated natural killer (NK) cells. In addition to conventional cellular targets such as the YAC-1 and MBL-2 lymphomas, this cloned line also lysed lipopolysaccharide-activated B lymphocytes. To determine whether some NK cells can inhibit B cell function, we tested the ability of NK-like clones to suppress Ig secretion in vitro and in vivo. These cloned cells suppressed Ig secretion when they constituted as few as 0.2% of the total cell population and inhibition did not require identity at the H-2 locus. We suggest that some NK cells might recognize non-major histocompatibility complex gene products on activated B lymphocytes and lyse these cells, and this might represent a fundamental cell-cell interaction that regulates antibody secretion by activated B cells.
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PMID:A cloned cell line mediating natural killer cell function inhibits immunoglobulin secretion. 698 Feb 61

A T-cell hybridoma was derived by somatic cell hybridization between concanavalin A-activated BALB/c spleen cells and the AKR thymoma BW 5147. Media conditioned by hybridoma cells, even at high dilutions (1:1,000) support the growth of lipopolysaccharide-stimulated B-cell blasts but not that of T-cell growth factor (TCGF)-reactive T-cells. This activity, herein designated B-cell growth factor (BCGF), has a Mr of approximately equal to 20,000 and it can readily be separated from TCGF (Mr approximately equal to 30,000) by gel filtration. BCGF is constitutively produced by the hybridoma cells, it is removed from conditioned media by incubation with target cells at +4 degrees C, and it is equally effective on B-cell blasts carrying different major histocompatibility complex and Ig haplotypes. BCGF shows no T-cell replacing factor (TRF) activity, and it is poor in supporting the development of Ig-secreting plaque-forming cells in B-cell blast cultures. Terminal maturation, however, can be induced in BCGF-dependent blasts by addition of conditioned media from normal helper T cell cultures, suggesting that two distinct factors are involved in the helper cell-dependent growth and maturation of B lymphocytes.
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PMID:B-cell growth factor: distinction from T-cell growth factor and B-cell maturation factor. 698 88

AKR mice were protected from lethal irradiation and established as long-lived chimeras by transplanting allogeneic C57BL/6 (B6) bone marrow that had been treated in vitro with anti-Thy-1 antiserum without complement. In these chimeras, which were designated [B6 {arrow} AKR], virtually all the thymus and spleen cells were shown to be derived from the B6 donor; several immune functions studied in these chimeras were as follows: (a) The chimeric mice were tolerant of histocompatibility antigens of both donor and recipient strain and nearly fully reactive to antigens of third party, as revealed by Simonsen's splenomegaly assay. The tolerance of these chimeras could not be attributed to suppressor cells but was compatible with clonal depletion. (b) Proliferative responses to concanavalin A, phytohemagglutinin, and lipopolysaccharide as well as natural killer and antibody-dependent cell- mediated cytotoxicity activity of the chimeric mice was normal. (c) Plaque- forming cell (PFC) assays of antibody responses to sheep erythrocytes (SRBC) showed gross deficiency in the primary response of the [B6 {arrow} AKR] and [AKR {arrow} B6] chimeras. By contrast, [B6-H-2(k)(E(k)) {arrow} AKR] H-2-compatible chimeras and [AKR {arrow} AKR] syngeneic marrow transplanted mice had normal primary PFC responses. PFC responses after secondary stimulation with SRBC, however, revealed vigorous direct plaque formation and substantial but somewhat smaller indirect plaque formation in the [B6 {arrow} AKR] chimeras. This observation favors operationally the concept of adaptive differentiation proposed by Katz et al. (44). (d) Analysis of ability of the chimeras to develop and express delayed-type hypersensitivity responses to contact sensitizer (2,4-dinitro-l-fluorobenzene [DNFB]) showed no apparent immunodeficiency of either chimeras to this form of immunization. Development of immunologic tolerance to DNFB, however, was grossly deficient in [B6 {arrow} AKR] chimeras but normal in [AKR {arrow} AKR], [B6 {arrow} B6], and [E(k) {arrow} AKR] chimeras. These findings indicate that full chimeras across major histocompatibility complex have considerable immunologic vigor even though primary immune responses that require histocompatibility between interacting cell types are initially defective.
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PMID:Humoral and cell-mediated immune responses in fully allogeneic bone marrow chimera in mice. 698 46


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