Disease relevance of Basophils

• Patients with atopic dermatitis and food hypersensitivity were found to have higher rates of spontaneous release of histamine from basophils than controls (mean +/- SE, 35.1 +/- 3.9 percent vs. 2.3 +/- 0.2 percent; P less than 0.001) [1].
• Here we report that one family member, described as monocyte chemotactic protein 1 (MCP-1), strongly activates mature human basophils in a pertussis toxin-sensitive manner [2].
• Deuterium oxide (D2O) greatly increased histamine release (in both groups), indicating that the anti-IgE interacted with the basophils of urticaria patients [3].
• These data suggest that kallikrein-like activity can be generated from human basophils as a direct result of a primary IgE-mediated immune reaction, thus providing a potential link between reactions of immediate hypersensitivity and the plasma and(or) tissue kinin-generating systems [4].
• Mouse lymphoma (WEHI-5) and rat basophil leukemia (RBL-1) cells, when stimulated with calcium ionophore A23187, each produced immunoreactive leukotrienes; and LTC4, LTD4, and LTE4 from RBL-1 cells were individually quantitated by radioimmunoassay after resolution by high-performance liquid chromatography [5].

Psychiatry related information on Basophils

• The negative correlation between anti-IgE and FMP-induced histamine release in unresponsive basophils may suggest individual differences in the ratio of Fc epsilon RI and FMP receptors on the surface of basophils [6].

High impact information on Basophils

• The histamine-releasing activity of the serum was abolished by passive sensitization of basophils with myeloma IgE, enhanced after dissociation of IgE by treatment with lactic acid, and induced by IgG fractions from the serum of all four patients [7].
• The histamine-releasing factor was found to activate basophils through surface-bound IgE [1].
• Since histamine is released only by mast cells and basophils and prostaglandin D2 is not produced by basophils, we suggest that these cells are partly responsible for the late-phase response [8].
• C3a- and C5a-induced thromboxane (TXB2) generation and histamine release from HMC-1 cells and whole-blood basophils were also suppressed by exogenous immunoglobulins [9].
• Mast cells and basophils co-express Fc gamma RIIb, a low affinity receptor containing an immunoreceptor tyrosine-based inhibitory motif and whose co-aggregation with Fc epsilon RI can block Fc epsilon RI-mediated reactivity [10].

Chemical compound and disease context of Basophils

• Bsp-1 staining correlated with toluidine blue-positive basophils in chronic phase CML and with toluidine blue-negative blast cells expressing an immature myeloid phenotype in blast crisis CML and AML [11].
• Effect of disodium cromoglycate on cutaneous basophil anaphylaxis [12].
• In contrast, little 125-I-HF accumulated in cell-mediated reactions rich in basophils--cutaneous basophil hypersensitivity (CBH) reactions to keyhole limpet hemocyanin, ovalbumin, and dinitrochlorobenzene--due in part to less vascular leakage of macromolecules and to decreased formation of urea-insoluble fibrin [13].
• Contact hypersensitivity reactions were elicited by intraluminal application of DNCB to the colon of guinea pigs and were found sometimes to contain large infiltrates of basophils [14].
• Identification of selective basophil chemoattractants in human nasal polyps as insulin-like growth factor-1 and insulin-like growth factor-2 [15].

Biological context of Basophils

• We have demonstrated the presence of specific binding sites for that drug on the membranes of basophils and mast cells and more recently, we have succeeded in isolating the cromoglycate-binding protein from the membranes of RBL-2H3 cells [16].
• These closely associated biochemical changes facilitate the transmission of many signals through membranes, resulting in the generation of adenosine 3',5'-monophophate in many cell types, release of histamine in mast cells and basophils, mitogenesis in lymphocytes, and chemotaxis in neutrophils [17].
• In addition, CRTH2, but not DP, mediates PGD2-dependent cell migration of blood eosinophils and basophils [18].
• We have analyzed the function of the Rho proteins Rac1 and CDC42 in the high affinity receptor for IgE (FcepsilonRI)-mediated phagocytosis using transfected rat basophil leukemia (RBL-2H3) mast cells expressing dominant inhibitory forms of CDC42 and Rac1 [19].
• Aggregation of the receptor with high affinity for IgE (Fc epsilon RI) on the surface of mast cells and basophils stimulates phosphorylation of protein tyrosines, a process in which p53/56lyn kinase has been implicated [20].

Anatomical context of Basophils

• Investigation of the biological effects of the cleavage product, C3a, derived from the third component of complement has generally focused on the effects it exerts as an anaphylatoxin, that is, smooth muscle contraction and histamine release from mast cells and basophils [21].
• The human eotaxin-receptor CCR3, originally described on eosinophils and basophils, was also found to be expressed by TH2 cells [22].
• Interleukin-4 (IL-4) is an immunomodulatory cytokine secreted by activated T lymphocytes, basophils, and mast cells [23].
• MCAF was also shown to activate highly purified human basophils more readily than mixed leukocytes, and its activity was inhibited by a polyclonal rabbit antibody [24].
• Recombinant monocyte chemotactic-activating factor (MCAF) has been shown to induce histamine release from human basophils with a dose response between 10(-9) and 10(-6) M [24].

Associations of Basophils with chemical compounds

• We present a model for the control of immunoglobulin E (IgE)-mediated histamine release from human basophils [25].
• Both mast cells and basophils possess receptors which bind the Fc portion of IgE with high affinity; crosslinking of membrane-bound IgE by allergen results in degranulation of the cell and release of a variety of pharmacologically active mediator including histamine [26].
• Mast cells, basophils and a tumour analogue--rat basophilic leukaemia (RBL) cells--have a surface glycoprotein (R epsilon) which specifically binds monomeric immunoglobulin E (IgE), and aggregation of R epsilon causes secretion [27].
• Basophil variants with impaired cromoglycate binding do not respond to an immunological degranulation stimulus [16].
• IL-5 enhanced basophil histamine release evoked by anti-IgE, formyl-methionyl-leucyl-phenylalanine, or ionophore A23187 at picomolar concentrations [28].

Gene context of Basophils

• IgER-induced IL-4 synthesis and release by basophils cultured with IL-3 was rapid and complete after 6 h [29].
• Thus, MCP-3 was as effective as MCP-1 as an inducer of mediator release, and as effective as RANTES as a stimulus of basophil migration [30].
• Similar basophil GFP expression was found in infected Stat6-/- mice [31].
• High expression of the chemokine receptor CCR3 in human blood basophils. Role in activation by eotaxin, MCP-4, and other chemokines [32].
• Interleukin 4 (IL-4), a critical immunoregulatory cytokine, is produced by a subset of T lymphocytes and cells of the mast cell/basophil lineage [33].

Analytical, diagnostic and therapeutic context of Basophils

• MBP was also detected by immunofluorescence and RIA in cells obtained from a patient with basophil leukemia, although the MBP content for basophil leukemia cells was lower than that for normal basophils [34].
• Cell fractionation studies indicate that the basophil is the source of lipid mediators and that IL-3 affects the basophil response directly [35].
• The two groups were equally sensitive based on skin tests and basophil histamine release [36].
• Immunoprecipitation of the Tac peptide from enriched basophils metabolically labeled with 35S-methionine showed active synthesis of the IL-2 receptor [37].
• In this study, tryptase expression was analyzed in normal and neoplastic basophils by immunoelectron microscopy using antitryptase monoclonal antibody G3 [38].

References