Protein basophil activation

Alam, R-, Forsythe, P.A., Stafford, S., Lett-Brown, M.A. and Grant, J.A. (1992). Macrophage inflammatory protein-la activates basophils and mast cells. J. Exp. Med. 176, 781-786. 

Patella Y Casolaro Y Bjorck L, Marone G Protein L. A bacterial Ig-binding protein that activates human basophils and mast cells. J Immunol 1990 145 3054-3061. 

Preincubation of protein A with human monoclonal IgM VH3 + concentration-dependently inhibited histamine release from basophils (fig. 4). In contrast, a monoclonal IgM VH6+ did not affect the histamine-releasing capacity of protein A. Based on these results, it appears that protein A activates basophils by interacting with IgE VH3 +. 

This chapter highlights the mechanisms responsible for mast cell activation during anaphylactic responses to environmental substances. In addition to discussing in detail the activation of mast cells and basophils by IgE and antigen, we also will describe how mouse models have been used to analyze the importance of various proteins, cells, mediators and activation mechanisms in the expression of anaphylaxis in that species. 

There may be substantial variation both within and among species (e.g., in mice vs. humans) in the expression of various proteins, receptors and/or ligands that influence the activation of mast cells (or basophils or other potential effector cell types), or that can regulate the responsiveness of end organ target cells (e.g., bronchial or gastrointestinal smooth muscle cells, vascular endothelial cells) to potential mediators of anaphylaxis derived from mast cells. 

Several other cell types have also been shown to secrete histamine-releasing activity, some of which may be peptide in nature (although more work is necessary for a definitive characterization). For example, human lung macrophages cultured for 24 h have been shown to release a soluble factor (12 and 30 kDa) that stimulates isolated human lung mast cells and human basophils to release histamine [ 145]. The generation and release of this factor developed over time (> 1 h) and was blocked by cycloheximide, indicating that protein... 

Bueb JL, Mousli M, Bronner C, Rouot B, Landry Y (1990) Activation of Gi-Uke proteins, a receptor-independent effect of kinins in mast cells. Mol Pharmacol 38 816—822 Burde R, Dippel E, Seifert R (1996) Receptor-independent G protein activation may account for the stimulatory effects of first-generation Hl-receptor antagonists in HL-60 cells, basophils, and mast cells. Biochem Pharmacol 51 125—131... 

Endogenous histamine has a modulating role in a variety of inflammatory and immune responses. Upon injury to a tissue, released histamine causes local vasodilation and leakage of plasma-containing mediators of acute inflammation (complement, C-reactive protein) and antibodies. Histamine has an active chemotactic attraction for inflammatory cells (neutrophils, eosinophils, basophils, monocytes, and lymphocytes). Histamine inhibits the release of lysosome contents and several T- and B-lymphocyte functions. Most of these actions are mediated by H2 or H4 receptors. Release of peptides from nerves in response to inflammation is also probably modulated by histamine, in this case acting through presynaptic H3 receptors. 

Gao Z, Li BS, Day YJ, Linden J (2001) A3 adenosine receptor activation triggers phosphorylation of protein kinase B and protects rat basophilic leukemia 2H3 mast cells from apoptosis. Mol Pharmacol 59 76-82... 

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