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)

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.
 ...
PMID:Suppression of polyclonal antibody production in Trypanosoma cruzi-infected mice by treatment with anti-L3T4 antibodies. 295 44

We have analyzed the role of cognate interaction with helper T cells (Th) in support of resting B cell differentiation to plaque formation. Co-culture of histoincompatible resting B cells and resting Th cells resulted in the induction of plaque-forming cells when dimeric but not monomeric fragments of anti-T cell receptor (TcR) antibody were added to culture. The efficiency of B cell activation was comparable to that supported by lipopolysaccharide and lectin-mediated Th-B cell conjugate formation. Further, if resting Th cells were preactivated with antigen and histocompatible antigen-presenting cells, the requirement for addition of anti-TcR to mixtures of histoincompatible Th and B cells was obviated. These results demonstrate that TcR-mediated Th recognition of major histoincompatibility complex class II/antigen composites on the resting B cell membrane does not provide obligate signals for B cell differentiation to plaque formation. We are left with two possibilities. Either the entire process of Th cell-dependent induction of resting B cell differentiation is mediated by soluble lymphokines or if Th-B cell contact is mandatory, it is mediated through nonpolymorphic cell surface determinants.
 ...
PMID:T helper cell-dependent induction of resting B cell differentiation need not require cognate cell interactions. 296 44

Natural suppressor (NS) cells are capable of suppressing immunological responses in a nonspecific manner. Previously, we have described NS cells in the spleens of mice undergoing chronic graft-versus-host disease (GVHD) and also in normal B10.D2 bone marrow (BM). NS cells obtained from these environments appear dependent upon lymphokines for their ability to manifest suppression. In this report, with anti-IFN-gamma antibody, we show that IFN-gamma is necessary for NS cell activation. Anti-IFN-gamma antibody is able to remove the ability of NS cells to suppress a concanavalin A (Con A) proliferation assay. Also, anti-IFN-gamma antibody removes the ability of rIL-2, lectin-free Con A supernate (CAS), and recombinant IFN-gamma (rIFN-gamma) to enhance NS suppression of lipopolysaccharide response. By these criteria, IFN-gamma is required for NS cell activation, and rIL-2 may act indirectly by its ability to stimulate IFN-gamma synthesis. These results are discussed in the context of the immuno-suppression seen in human BM transplantation.
 ...
PMID:Evidence that IFN-gamma is responsible for natural suppressor activity in GVHD spleen and normal bone marrow. 296 35

The present study focuses on the effect of lipopolysaccharide (LPS) on the cellular events leading to T-cell activation by concanavalin A (Con A). Interleukin 2 (Il-2) production is much reduced in Con A-stimulated cultures of spleen cells derived from LPS-treated mice. This depressed Il-2 synthesis is not related to the eventual activity of LPS-activated suppressive B cells. Rather, it reflects an ineffective collaboration between adherent cells and T lymphocytes. The low level of Il-2 produced by LPS-sensitized spleen cells is sufficient for lectin-induced T-cell proliferation. Moreover, acquisition of responsiveness to Il-2 is unaltered by LPS. No strict correlation was found between the deficiency in Il-2 production and the inability of LPS-sensitized spleen cells to generate a thymus-dependent response. Less time (5 hr) is needed for LPS to exert its inhibitory effect on an anti-sheep red blood cell response than on Il-2 synthesis (at least 24 hr). Results are discussed in terms of cellular interactions implicated in a polyclonal T-cell response and with regard to the contribution of Il-2 to the LPS-induced immune unresponsiveness.
 ...
PMID:Effect(s) of lipopolysaccharide on lectin-induced T-cell activation. 309 Dec 72

The production of and responsivity to leukocyte-derived lymphokine-rich culture supernatants (SNs) was examined during the ontogeny of the frog, Xenopus. Thymocytes and splenocytes from adult frogs are capable of responding to the T-cell mitogen, phytohemagglutinin-P (PHA). Larval thymocytes are unresponsive to this lectin, whereas larval splenocytes are not. PHA-unresponsive thymocytes can be costimulated with PHA plus either a T-cell growth factor (TCGF)-rich SN or an interleukin-1 (IL-1)-rich SN (from cultures of lipopolysaccharide (LPS)-treated macrophage-enriched peritoneal cells (PCs). Stimulation of larval thymocytes with PHA does not produce a TCGF-rich SN as assayed by proliferation of lymphoblasts. Larval as well as adult splenocytes treated with PHA, however, do produce TCGF. These data are consistent with the hypothesis that the factor limiting mitogen responsiveness of larval thymocytes is the ability of cell populations in the thymus to produce rather than respond to either IL-1 or IL-2.
 ...
PMID:The ontogeny of interleukin production and responsivity in the frog, Xenopus. 325 26

Cyclophosphamide injections to mice following T cell mitogen (lectins from Lens culinaris and concanavalin A) were shown to suppress (20-40-fold) thymus-dependent response to SRBC. At the same time no damage-specific and polyclonal response to thymus-independent antigen and polyclonal activator of B cells--lipopolysaccharide--has been observed. Injections of lectin and cyclophosphamide to mice prevented the onset of DTH reaction to SRBC and induction of antigen-specific DTH suppressor cells. Thus, cyclophosphamide injection after T cell mitogen leads to T-cell anergy, with B-cell activity remaining unchanged.
 ...
PMID:[T-cell immunodeficiency in mice receiving lectin and cyclophosphamide]. 326 Nov 77

Monoclonal antibodies (MAbs) reacting with bovine (2) ovine (3), murine (1) or human (1) Class II MHC antigens were examined for reactivity with bovine peripheral blood leucocytes (PBL) and lymph node cells (LNC) by immunofluorescence, immunoprecipitation and the capacity to inhibit mixed lymphocyte responses (MLR), lectin- and antigen-induced blastogenesis. The 6 MAbs identified comparable percentages of Class II positive lymphocytes in PBL (40.8 to 54.2%) and LNC (6 to 11.5%) regardless of BoLA-A phenotype. Immunohistological staining of Class II MAb was localized principally to the lymphoid follicles in lymph nodes and to isolated epithelial reticular cells in the thymus. The anti-Class II MAb immunoprecipitated alpha- and beta- chains of 26-29K and 32-34K, respectively. These MAb inhibited proliferative responses in the MLR by between 25 and 74%, and diminished blastogenesis induced by specific antigens (purified protein derivative + PPD and ovalbumin) and B-lymphocyte mitogens (PPD, lipopolysaccharide and dextran sulphate) by between 45 and 75%, regardless of BoLA-A phenotype. In contrast, proliferation in response to concanavalin A and phytohaemagglutinin were unaffected by the anti- Class II MAb. Similarly these MAb did not affect lysis by cytotoxic T-lymphocytes, the activity of which was depressed by anti-Class I MAbs and monospecific alloantisera.
 ...
PMID:A functional and biochemical analysis of bovine class II MHC antigens using monoclonal antibodies. 332 60

B lymphocytes, preactivated by lipopolysaccharide (LPS), could be triggered to growth by a strain of Mycoplasma arginini, while the level of immunoglobulin (Ig) secretion, quantitated as the number of plaque-forming cells (PFC), was low. The PFC response could be increased by the addition of conditioned media (CM) from lectin-activated spleen cells or T cell tumour EL-4 to the culture of preactivated B cells. CM did not by itself induce a significant amount of PFC in the cultures of LPS-preactivated B cells. The maturation enhancing activity was distinct from IL-2 and B cell growth factor as judged by gel exclusion chromatography.
 ...
PMID:Enhancement of immunoglobulin secretion by the lymphokine-like activity of a Mycoplasma arginini strain. 348 65

Phytohaemagglutinin (PHA) receptor glycoproteins purified by affinity chromatography from porcine splenic lymphocytes, were reconstituted into vesicles made of phosphatidylcholine and phosphatidylserine, concomitantly with Sendai virus fusogenic proteins HN and F. The vesicles were used as a vehicle to insert the PHA receptor glycoproteins into a highly enriched population of porcine B lymphocytes. Fluorescence analyses showed that 52 +/- 2% of the reconstituted B cells had incorporated the lectin receptors. The modified B lymphocytes were assayed for their response (tritiated thymidine incorporation into nucleic acids) to PHA, concanavalin A (Con A), or to lipopolysaccharide (LPS). The results showed that porcine B cells fused with vesicles containing only viral fusogenic proteins failed to respond to either PHA or Con A. Tritiated thymidine incorporation was similar to background values. The cells did, however, respond to LPS with values of label incorporation similar to those observed in the case of pre-fused B lymphocytes. When purified B lymphocytes were fused with vesicles containing PHA receptors and viral fusogenic proteins, assays of thymidine incorporation showed a statistically significant (P less than 0.001) and specific response of the modified cells to PHA stimulation. Reconstituted cells cultured in the presence of PHA incorporated approximately nine times more radioactive label than pre-fused cells or cells fused with vesicles containing only fusogenic viral proteins. In marked contrast, reconstituted B lymphocytes did not show any significant label incorporation above background level in response to Con A, but they retained their ability to respond to LPS. Our findings suggest that B lymphocytes can be made to respond specifically to PHA by insertion of appropriate lymphocyte-derived receptors.
 ...
PMID:B lymphocytes respond specifically to phytohaemagglutinin after liposome-dependent transfer of purified phytohaemagglutinin receptors. 349 68

Poikilotherms are now known to increase their survival by behaviorally induced fevers in response to pathogenic infection. Increased host resistance to viral and bacterial infections has also been noted in homeotherms whose body temperature has been elevated by manipulation of ambient temperature. These observations suggest that fever may increase host resistance by augmenting acquired immunity; thus, this highly conserved response during evolution may provide a survival advantage against environmental pathogens. This possibility has prompted us to investigate the influence of a temperature characteristic of a modest fever in humans (39 degrees C) on T-cell proliferation and function. Our studies revealed that T-cell mitogenesis was enhanced when cultures were incubated at the febrile temperature (39 degrees C). Analysis of T-cell subsets demonstrated that temperature enhanced the mitogenic (Concanavalin A) response of Lyt-1+23- splenocytes; in contrast, hyperthermia was deleterious to lectin-driven proliferation of the Lyt-1-23+ population even in the presence of large quantities of recombinant interleukin-2 (rIL-2). B-cell mitogenesis was invariably inhibited by hyperthermia over a broad range of concentrations of lipopolysaccharide (LPS). Although T-cell mitogenesis was enhanced at the febrile temperature, T-cell proliferation induced by alloantigens or by a murine pathogen, Sendai virus (SV), was diminished at the febrile temperature. Hyperthermia inhibited SV-induced proliferation of Lyt-1+23- lymphocytes, indicating that a febrile temperature can either augment or inhibit T-cell proliferation of the same T-cell subset depending upon the activation signal (i.e., lectin or antigen). Because effector cell development depends upon antigen-induced clonal expansion (proliferation), we evaluated the influence of temperature on primary cytotoxic thymus (T)-derived lymphocyte (CTL) responses against alloantigens and secondary CTL responses against SV under afebrile and febrile conditions. We consistently observed that the induction of alloreactive and virus-specific CTL was diminished in cultures incubated at the elevated temperature, suggesting that a thermosensitive event(s) exists in the progression of CTL derived from either CTL precursors (CTLp) or memory CTL. Furthermore, hyperthermia reduced the number of SV-specific CTL detectable by limiting dilution analysis, suggesting that another event independent of clonal expansion was thermolabile during effector cell development. In view of these results, we suggest that it may be premature to conclude that the observed increase in host resistance induced by a febrile state is mediated by enhanced cell-me
 ...
PMID:Analysis of T-cell subset proliferation at afebrile and febrile temperatures: differential response of Lyt-1+23- lymphocytes to hyperthermia following mitogen and antigen stimulation and its functional consequence on development of cytotoxic lymphocytes. 349 61


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>