Mast cells descriptions

Our understanding of anaphylaxis has advanced substantially since the original description of this phenomenon in the scientific literature over 100 years ago. There is now little reasonable doubt that the IgE-dependent activation of mast cells and basophils is the key event underlying most examples of allergen-induced anaphylaxis in humans [3-5]. IgE binds to the high-affinity IgE receptor, FcsRI, expressed on the... 

The first description of the mast cell was made in 1863 by Von Recklinhausen, although it was not until 1878 that the cell was named by Paul Ehrlich (Ehrlich, 1878). 

AJthough IgE rheumatoid factors have been identified in both the serum of patients with rheumatoid arthritis (Zuraw et al., 1981) and rheumatoid synovial fluid (De Clerck et al., 1991 Burastero et al., 1993), it is quite likely that IgE-independent modes of mast cell activation operate in non-allergic inflammatory processes. These might include C3a and C5a generated by activation of the complement cascade (Moxley and Ruddy, 1985 Brodeur et al., 1991) by immune complexes containing rheumatoid factors, substance P, and as yet unidentified mediators of mast cell secretion. From the above descriptions of the different mast cell mediators and cytokines it is easy to imagine how these may participate in the development of joint patholt. ... 

The identification in 1937 of the staining properties of heparin with meta-chromatic dyes with the similar staining of the mast cells by Wilander meant the satisfactory identification of the source and location of much of the heparin in the body. Recent descriptions of the mast cells are given by Bloom and Smith . Equally important was the identification of histamine as the other important pharmacologically active component of the mast cell by Riley, Shepherd and West . This is further discussed in the book by Riley . In general, there is a rough correlation between the distribution of heparin, histamine, hyaluronic acid and the mast cells. 

The current descriptions of sensitivity and maximal response are best applied to secretion of histamine. However, a more complete understanding will require further information about the same parameters in the context of lipid and cytokine release. Both of these mediators are critical determinants of the allergic inflammatory response, so that understanding the extent to which new therapeutics need to suppress basophil and mast cell responsiveness will be dependent on new information regarding the relative roles of each of the secreted mediators. Recent studies have indicated that basophil sensitivity is very similar when viewed from the secretion of each of three classes of mediators. This means that if cell surface antigen-specific IgE is present at a density sufficient to initiate only 50% of the maximum histamine release, approximately 50% of the maximal secretion of IL-4 and LTC4 will also be obtained. It remains to be determined whether the equivalent suppression of secretion for each of the three classes of mediators will lead to equivalent reductions for the functional endpoints of the three different mediator classes. 

III. FceRI Expression on Basophils and Mast Cells A. Descriptives... 

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