By Novartis Foundation(eds.)
The ebook provides contemporary advances in relation to the criteria and mechanisms that keep watch over the expansion, differentiation and serve as of mast cells and basophils; dialogue of recent applied sciences used to check those cells, and integration of the fundamental clinical findings within the context of healing probabilities for the therapy of illnesses similar to allergic irritation and autoimmune disorder that are mediated, partly, by means of those granulocytes.Content:
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Extra resources for Mast Cells and Basophils: Development, Activation and Roles in Allergic/Autoimmune Disease: Novartis Foundation Symposium 271
V. administration of the ‘cytokinergic’ SPE-7 IgE monoclonal antibodies 18 h before the mice were sacrificed resulted in dose-related increases in the levels of these cytokines. IgE ANTIBODIES ENHANCE CONTACT SENSITIVITY RESPONSES 21 IL-1b TNFa mRNA % WT SPE7 SPE7 MCP-1 IL-6 mRNA % WT SPE7 SPE7 FIG. 4. Defective sensitization in the absence of IgE is associated with reduced gene expression. v. injection of monoclonal IgE antibody, SPE-7. Taken together, these findings suggested that the cytokine milieu of IgE-/- skin is not optimally supportive of immune sensitization to haptens.
Austen: Some will be on the mast cells because that’s the highest affinity place to catch it. Oettgen: We know the injected IgE is cleared very quickly, but we can’t distinguish from this destruction versus binding to mast cells, as you say. We haven’t labelled mast cells with anti-IgE. Razin: It is easy to do. You can label IgE and follow it. Metcalfe: If you take mast cells from IgE-negative mice and grow them up in the presence of IgE, is it possible to inject these IgE-positive mast cells from the same mouse back into the skin and then sensitize?
It seems that these experiments suggest there may be another mechanism by which one gets spreading, due to enhanced sensitization of some of the cells that lead to the effector cells. Metcalfe: Focusing on effector cells, I would think would lead to a similar conclusion; that the early treatment of inflammation, say with steroids, would have a beneficial effect on early sensitization. Have you examined how long it takes to sensitize from when the sensitizing agent is applied? This would provide some insight into the processes.