PubMed · 2484956
The source did not provide an abstract. Follow the original record for more information.
Explore connections, maps & timelines
B M Czarnetzki. 1989. Urticaria.. https://pubmed.ncbi.nlm.nih.gov/2484956/
Cite the original work for its findings. Save a collection to share your selection of sources.
KEEP EXPLORING
The inflammatory response that is often associated with asthma is characterized by the recruitment of eosinophils, basophils, and lymphocytes. Until recently, profiling the basophil and defining its functional characteristics have been difficult. With the advent of some new tools, there is a steadily increasing body of information on the presence and potential activities of the basophil. Although the precise role of these cells in airway diseases, such as asthma, remain unclear, relatively accurate enumeration is now possible. Coupled with new insights into cytokine secretion from these cells, a more accurate picture of the dynamics of this specialized form of inflammation is available for refining our hypotheses regarding its regulation.
BACKGROUND: Histamine release in chronic urticaria is initiated by cross-linking of the alpha subunit of FcepsilonRI by means of IgG antibody, followed by complement activation. OBJECTIVE: We sought to further elucidate the mechanism by which complement augments histamine release and to assess the role of C5a. METHODS: We first quantitated the ability of purified C5a to initiate basophil histamine release and to be inhibited by antibody directed to the C5a receptor. Using this antibody, we quantitated its ability to inhibit histamine release induced by sera from patients with chronic urticaria. We also compared the ability of normal serum, C5-depleted serum, and C5-depleted serum after reconstitution with C5 to augment histamine release by IgG isolated from patients with chronic urticaria. RESULTS: As the concentration of C5a was increased up to 50 ng/mL, the percentage of histamine release increased and reached a plateau of 40% to 50%; this was inhibited by antibody to the C5a receptor. Preincubation of basophils with antibody to the C5a receptor inhibited basophil histamine release from 15 sera tested, with a range of 4% to 39%. Histamine release caused by patient IgG was augmented when normal serum was added but not when C5-depleted serum was substituted for normal serum. Augmentation of histamine release by patient IgG was again obtained when C5-depleted serum was reconstituted with C5. CONCLUSION: Our conclusion is that pathogenic IgG cross-links the IgE receptor directly to cause histamine release, and activation is augmented by complement. C5a is the complement agonist that is responsible for the augmented histamine release.
Basophils are rare, circulating leukocytes derived from hematopoietic CD34+ progenitors. The identification of cytokines promoting their development in vitro has led to substantial advances in understanding their differentiation process. An important role could be assigned to interleukin-3 (IL-3), which supports the maturation of hematopoietic progenitors into basophils in vitro and in vivo. In contrast to other myeloid lineages, a specific basophil growth factor has not yet been discovered. Furthermore, it is still unclear whether basophils possess a lineage-restricted progenitor or whether they share a common ancestor with mast cells (MC), eosinophils, or even megakaryocytes. Partial answers to these questions could be provided using in vitro culture systems or taking advantage of hematological disorders, such as chronic and acute myeloid leukemia (CML and AML), some myelodysplastic syndromes, and the very rare acute basophilic leukemia in which basophilic differentiation occurs.