The antigen-binding T cell factor PCl-F sensitizes mast cells for in vitro release of serotonin. Comparison with monoclonal IgE antibody.
Picryl chloride factor (PC1-F) is an antigen (TNP hapten)-binding T cell factor that initiates PC1 contact sensitivity (CS). PC1-F initiates PC1 CS by mediating an early 2-h skin swelling reaction that is due to local release of the vasoactive amine serotonin (5-HT) by mast cells, and perhaps other 5-HT-containing cells. Experiments were conducted to determine if PC1-F could sensitize normal mast cells in vitro for subsequent release of 3H-5-HT that had been taken up previously. It was found that PC1-F could sensitize mast cells, inasmuch as incubation with PC1-F, followed by washing, resulted in the ability to release 5-HT by challenge with Ag (TNP-bovine serum albumin), or by an anti-factor mAb called 14-30. As with release induced by anti-TNP IgE mAb PC1-F-induced release required phosphatidyl serine. Mast cell sensitization and activation for 5-HT release by PC1-F was not due to contamination of PC1-F with IgE antibody, because IgE (and not PC1-F) was sensitive to reduction and alkylation. Also, affinity columns linked with 14-30 or anti-IgE showed that the mast cell sensitizing and activating property of PC1-F was clearly separate from that of IgE. PC1-F-induced release was not IgE dependent, because mast cells that were acid-stripped and largely depleted of surface IgE, could then be sensitized by PC1-F. In vivo experiments demonstrated that local challenge with 14-30 antibody induced a 2-h ear swelling reaction in actively contact sensitized mice, or adoptive recipients of sensitized cells, and in normal mice that received PC1-F i.v. These findings suggest that in vitro sensitization of mast cells with PC1-F, and subsequent in vitro release of 5-HT induced by challenge with 14-30 antibodies, correlates with the initiation of PC1 CS in vivo. Therefore, in the initiation of CS by PC1-F, mast cells can be one source of 5-HT, to cause the early, vasoactive phase of CS.
Meade
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R
Department of Medicine, Yale University School of Medicine, New Haven, CT 06510.
Van Lovern
H
H
Parmentier
H
H
Iverson
G M
GM
Askenase
P W
PW
D000042:Absorption; D000478:Alkylation; D000818:Animals; D000911:Antibodies, Monoclonal / Q000502:physiology*; D003877:Dermatitis, Contact / Q000209:etiology / Q000276:immunology; D000939:Epitopes / Q000276:immunology; D007110:Immunity, Active; D007116:Immunization, Passive; D007073:Immunoglobulin E / Q000502:physiology*; D008264:Macrophages / Q000378:metabolism; D008297:Male; D008407:Mast Cells / Q000276:immunology* / Q000378:metabolism; D051379:Mice; D008808:Mice, Inbred CBA; D010853:Picryl Chloride / Q000276:immunology*; D012701:Serotonin / Q000378:metabolism*; D013491:Suppressor Factors, Immunologic / Q000502:physiology*
D000911:Antibodies, Monoclonal; D000939:Epitopes; D013491:Suppressor Factors, Immunologic; D012701:Serotonin; D007073:Immunoglobulin E; D010853:Picryl Chloride