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Stories fresh easy learn into IgE, mast cells, and the allergic reaction and the relevance of this paintings to human pathophysiology, and discusses new equipment of therapy. This symposium is exclusive within the IgE box for its breadth of assurance and interdisciplinary nature, and it exhibits the advantages from the present speedy growth of information in mobile biology, immunology, and molecular genetics, in addition to the capability medical importance of this study to medical immunologists and allergologists.


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Mouse BMMC are able to further differentiate and assume a CTMC phenotype after transfer into the serosal cavity of mast celldeficient mice (Kitamura et a1 1986), or by co-culture on 3T3 fibroblasts, where they become safranin positive, synthesize heparin proteoglycan, and demonstrate increased amounts of CPA activity and histamine (Dayton et a1 1988, LeviSchaffer et a1 1986, 1987, Serafin et a1 1987, Stevens et a1 1989). In humans, two mast cell subclasses have also been described on the basis of their predominant serine proteases, although both categories fail to counterstain with safranin and have the same histamine content (Schwartz et a1 1987).

Using this species, two subclasses of MC are defined on the basis of differences in histochemistry, anatomical location, responsiveness to various secretagogues and the spectrum of inflammatory mediators released after immunological activation (Stevens et a1 1986, 1989). The first indication of rat mast cell heterogeneity was based on the difference in histochemical staining of MC found in the connective tissue (CTMC) versus those found in gastrointestinal mucosa (MMC). Upon staining with the cationic dyes alcian blue and safranin red, the MMC exhibited only blue granules while the CTMC exhibited red granules, indicating that the latter cells had counterstained with the safranin.

We have used other monoclonal antibodies directed at CD23, such as Dr Yodoi's, and they did not affect HRF-induced release. AndrP Capron: We believe that there is more heterogeneity among CD23 and the Fc,RII receptor on inflammatory cells than Dr Kishimoto seems to find. This may explain some of the discrepant results. Metzger: In regard to that, you showed us, Professor Kishimoto, some restriction enzyme mapping of the extracellular (C-terminal) domain of CD23 on different cell types, where you concluded that they were all identical; but have you sequenced the extracellular domain of the Fc,RIIb on the monocyte?

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