Disease relevance of Lymphocyte Activation

• To determine whether expression of DR was required for melanoma cells to be stimulatory, we first treated a stimulating cell line of DR3 allospecificity with anti-DR3-specific serum and demonstrated marked inhibition of its capacity to provoke blastogenesis [1].
• Mitogen-induced blastogenesis and receptor mobility inhibition by breast cancer serum with elevated orosomucoid (alpha 1-acid glycoprotein) levels [2].
• Human lymphocyte blastogenesis responses to mouse mammary tumor virus [3].
• Pseudomonas aeruginosa and its products have been shown to inhibit mitogen-induced human lymphocyte blastogenesis as measured by [3H]TdR uptake [4].
• The addition of inactivated preparations of purified human T cell lymphotropic virus (HTLV-III) was found to inhibit normal human lymphocyte phytohemagglutinin (PHA)-induced blastogenesis but had no effect on concanavalin A (Con A), pokeweek mitogen, or allogeneic stimulation [5].

Psychiatry related information on Lymphocyte Activation

• Individual differences in IC50s for prednisolone, methylprednisolone, cyclosporine, and tacrolimus on blastogenesis of PBMCs from UC patients were spread from 11.0 to 1000, 0.6 to 1000, 0.01 to 1000, and 0.001 to 4.6 ng/ml, respectively [6].

High impact information on Lymphocyte Activation

• No correlation could be demonstrated between the plasma salicylic acid level and the degree of suppression of blastogenesis [7].
• The anergic V beta 6 T-helper cells express IL-2 receptors and undergo limited blastogenesis in vitro upon stimulation, but do not produce IL-2, in marked contrast to V beta 6 cells from naive mice [8].
• AAG has the ability to inhibit certain lymphocyte re-activities including blastogenesis in response to concanavalin A, phytohaemagglutinin and allogeneic cells, and these inhibitory effects are enhanced in association with desialisation [9].
• While these treatments did not render macrophages stimulatory for an MLR in purified CD4+ cells, blastogenesis of CD4+ cells was observed when the MLR involved bulk T cells [10].
• Anti-LFA-1 disassembles newly formed DC-T cell aggregates, whereas anti-CD4 inhibits blastogenesis without disrupting the cluster [11].

Chemical compound and disease context of Lymphocyte Activation

• A crude cell wall-rich fraction of Listeria monocytogenes contains a substance or substances which cause blast transformation and thymidine incorporation by mouse spleen cells [12].
• Immune responses and immunoregulation in relation to human schistosomiasis in Egypt. II. Cimetidine reversal of histamine-mediated suppression of antigen-induced blastogenesis [13].
• These results indicate that marked alterations of immune competence as measured by blastogenesis of spleen cells to Escherichia coli LPS and to a mitogen such as Con A may occur after implantation of an osmotic pump, with or without continuous infusion of endotoxin [14].
• These data suggest that the decreased blastogenesis in certain melanoma patients is due to an increase in PGE2 production by monocytes, along with an increase in lymphocyte sensitivity to its effects [15].
• Dietary deficiency of vitamin E and selenium had no discernible effects on alveolar macrophage function, as measured by cell-mediated antibody-dependent cytolysis, killing of Staphylococcus aureus or regulation of T-lymphocyte blastogenesis [16].

Biological context of Lymphocyte Activation

• Specifically, impaired blastogenesis could be dissociated from alloantigen-specific induction of the B cell activation molecule CD23, IL-4 release, and inositol lipid hydrolysis [17].
• After s.c. injection of peptide in adjuvant the entire Ag-specific population up-regulated IL-2 receptor alpha-chain expression, underwent blast transformation, and developed a memory-surface phenotype [18].
• The antigen recognized by the 4F2 monoclonal was expressed early in the G1 phase of the cell cycle and correlated with blast transformation; this was demonstrated by stimulating resting B cells with a low concentration of anti-mu sufficient for cellular activation but not proliferation [19].
• When peptide was administered i.v. without adjuvant, 50% of the Ag-specific cells expressed IL-2, but the peak of expression occurred before IL-2 receptor alpha-chain up-regulation, and only a minority of the Ag-specific T cells underwent blast transformation [18].
• Changes were also observed in uridine incorporation, total cell number, and blast transformation, indicating that the effect was not on thymidine transport or pool size per se [20].

Anatomical context of Lymphocyte Activation

• The first detectable increase in CD25 expression and blast transformation was in the peritoneal cavity beginning days 5 and 6 [21].
• Anti-SEA responses include lymphocyte blastogenesis, the production of the lymphokine eosinophil stimulation promoter (ESP), hemagglutinating antibody, heat-labile and heat-stable, 72-hr passive cutaneous anaphylaxis (PCA) antibodies, and pronounced peripheral blood eosinophilia [22].
• MDF activity was stable at 56 degrees C for 30 min but more, supernatants of stimulated monocytes by lipopolysaccharide or silica particles failed to show ECF-producing activity, whereas they showed evident lymphocyte-activation activity [23].
• The administration of high dosages of estradiol cypionate produced no measurable effect on the total or differential leukocyte count, neutrophil function, lymphocyte blastogenesis, or blood cortisol levels [24].
• During the first 5 days after subcutaneous tumor injection, alveolar macrophages were stimulatory to Con A blastogenesis of normal spleen cells [25].

Associations of Lymphocyte Activation with chemical compounds

• Inclusion in serum-free or serum-containing medium of the optimal concentration (5 x 10(-5) M) of either 2-ME or alpha TG resulted in highly significant uptake and incorporation of tritiated thymidine ([3H]TdR) into DNA and in morphological blast transformation [26].
• Furthermore, purified IL-2 failed to correct PPD-induced blastogenesis in patients [27].
• Sonicates of spleen cells which had been activated with optimal concentrations of 2-ME for 24 h and then washed extensively, stimulated the uptake of tritiated thymidine and morphological blast transformation of fresh, unstimulated cells [28].
• Evidence is presented that the majority of mouse spleen cells binding tritium-labeled POL undergoes blastogenesis after antigen capping, antigen shedding, and receptor reformation [29].
• An extracellular product of group A streptococci which induces lymphocyte blastogenesis has been purified to homogeneity by DEAE-cellulose and CM-cellulose chromatography [30].

Gene context of Lymphocyte Activation

• Lymphokine secretion and blast transformation are similarly reduced when active accessory ligand-receptor interactions are blocked in the dendritic cell-stimulated allogeneic MLR [31].
• We demonstrate herein that in addition to their IFN-gamma production, NKT lymphocytes stimulated with IL-12 plus IL-18 in vitro underwent activation in terms of CD69 expression, blast transformation, and proliferation [32].
• However, CD4 mAbs decreased neither the number of blast cells nor the expression of CD25 (the alpha chain of IL-2 receptor), indicating that initial activation events leading to blast transformation were not affected [33].
• Adding IVIg 24 h after SPE-A stimulation also resulted in reduced blast transformation and decreased synthesis of IFN-gamma and TNF-beta [34].
• These data suggest that hrIL-1ra exhibits a dose-response inhibition of lymphocyte blastogenesis induced by Con A, probably through the down-regulation of IL-1 synthesis necessary as an early signal for T-cell activation and IL-2 production [35].

Analytical, diagnostic and therapeutic context of Lymphocyte Activation

• Sensitized cells were also examined for their ability to respond to purified protein derivative (PPD) by blastogenesis, migration inhibitory factor release (MIP), and lymphotoxin (LT) production, both before and after treatment with HTLA and complement [36].
• The LPCA assay correlated closely with the blast transformation and MIF tests in which cells were used from more strongly sensitized donors who reacted in skin tests with lower doses of tuberculin (1 or 10 TU) [37].
• T/B lymphocyte ratios, lymphocyte blastogenesis (LB) with PHA and with cancer antigen preparations were carried out from two to four weeks after cancer surgery, and immediately after eight weeks of immunostimulation with a tumor-specific vaccine [38].
• Allograft survival appeared to be directly related to the immunosuppressive activity of patient sera on phytohemagglutinin-induced blastogenesis of normal lymphocytes in vitro [39].
• The administration of steroid caused significant immunosuppression in most animals as measured by inhibition of splenocyte blastogenesis induced with phytohemagglutinin [40].

References