Regulatory effects of human IgE-binding factors in the IgE synthesis by human and rat lymphocytes.
We have previously established human T cell hybridomas which produce IgE-binding factors. Incubation of one of the T cell hybridomas, 166A2, with human IgE dimer in the presence of 1 microgram/ml bradykinin resulted in the formation of IgE-binding factors having affinity for lentil lectin. The factors selectively enhanced both IgE-forming cell responses of rat mesenteric lymph node (MLN) cells and spontaneous IgE synthesis by human peripheral blood B cells of atopic patients, without affecting the IgG response. The same factors that enhanced IgE synthesis of B cells from atopic patients also enhanced IgE synthesis induced under bystander conditions by activated alloreactive T cells. Fractionation of the affinity-purified IgE-binding factors by gel filtration revealed three molecular mass species, i.e., 60 kDa, 30 kDa and 15 kDa. The 60-kDa and 15-kDa IgE-binding factors selectively enhanced both the spontaneous IgE synthesis by B cells of atopic patients and IgE response of rat MLN cells. In contrast, the 30-kDa IgE-binding factors had only marginal enhancing effects on the IgE synthesis by both human B cells and rat MLN cells. When the 166A2 hybridoma cells were incubated with IgE dimer in the presence of glycosylation-inhibiting factor (GIF), essentially all IgE-binding factors formed by the cells had affinity for peanut agglutinin (PNA) but for neither lentil lectin nor concanavalin A. All of the 60-kDa, 30-kDa and 15-kDa species, having affinity for PNA, selectively suppressed the potentiating factor-enhanced IgE response of rat MLN cells. The factors also suppressed the IgE synthesis of human B cells from atopic patients when the synthesis was enhanced by IgE-potentiating factor. The results indicate that human IgE-binding factors regulate IgE synthesis by both human and rat lymphocytes.
Kisaki
T
T
Subdepartment of Immunology, Johns Hopkins University School of Medicine, Baltimore, MD.
Leung
D Y
DY
Jardieu
P
P
Geha
R S
RS
Ishizaka
K
K
D000818:Animals; D000921:Antibody-Producing Cells / Q000502:physiology*; D001920:Bradykinin / Q000494:pharmacology; D002460:Cell Line; D002999:Clone Cells; D006031:Glycosylation; D006801:Humans; D006969:Hypersensitivity, Immediate / Q000276:immunology; D007073:Immunoglobulin E / Q000096:biosynthesis*; D007074:Immunoglobulin G / Q000096:biosynthesis; D066298:In Vitro Techniques; D008222:Lymphokines / Q000502:physiology*; D009000:Monocytes / Q000502:physiology; D029584:Prostatic Secretory Proteins; D051381:Rats; D013491:Suppressor Factors, Immunologic / Q000502:physiology; D013601:T-Lymphocytes / Q000502:physiology*
D007074:Immunoglobulin G; D008222:Lymphokines; D029584:Prostatic Secretory Proteins; D013491:Suppressor Factors, Immunologic; C043076:beta-microseminoprotein; C013059:immunoglobulin-binding factors; D007073:Immunoglobulin E; D001920:Bradykinin