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Anti-human IgG causes basophil histamine release by acting on IgG-IgE complexes bound to IgE receptors.
J Immunol. 1992 Jun 15; 148(12):3929-36.JI

Abstract

We have reexamined the ability of anti-human IgG antibodies to induce histamine release from human basophils. A panel of purified murine mAbs with International Union of Immunological Societies-documented specificity for each of the four subclasses of human IgG was used. Of the 24 allergic subjects studied, the basophils of 75% (18/24) released greater than 10% histamine to one or more anti-IgG1-4 mAb, whereas none of the 13 nonatopic donor's basophils released histamine after stimulation with optimal amounts of anti-IgG mAb. The basophils of 85% (11/13) of the nonatopic donors did respond to anti-IgE challenge, as did 92% (22/24) of the atopic donor cells. Histamine release was induced most frequently by anti-IgG3, and 10/18 anti-IgG responder cells released histamine with mAb specific for two or more different subclass specificities. The rank order for induction of histamine release was anti-IgG3 greater than anti-IgG2 greater than IgG1 greater than anti-IgG4. As in our previous study using polyclonal anti-IgG, 100- to 300-micrograms/ml quantities of the anti-IgG mAb were required for maximal histamine release, about 1000-fold higher than those for comparable release with anti-human IgE. Specificity studies using both immunoassays and inhibition studies with IgE myeloma protein indicated that anti-IgG induced histamine release was not caused by cross-reactivity with IgE. Ig receptors were opened by lactic acid treatment so that the cells could be passively sensitized. Neither IgE myeloma nor IgG myeloma (up to 15 mg/ml) proteins could restore the response to anti-IgG mAb. However, sera from individuals with leukocytes that released histamine upon challenge with anti-IgG mAb could passively sensitize acid-treated leukocytes from both anti-IgG responder and nonresponder donors for an anti-IgG response. The only anti-IgG mAb that induced release from these passively sensitized cells were those to which the serum donor was responsive. Sera from non-IgG responders could not restore an anti-IgG response. These data led to the hypothesis that the IgG specific mAb were binding to IgG-IgE complexes that were attached to the basophil through IgE bound to the IgE receptor. This was shown to be correct because passive sensitization to anti-IgG could be blocked by previous exposure of the basophils to IgE. We conclude that anti-IgG-induced release occurs as a result of binding to IgG anti-IgE antibodies and cross-linking of the IgE receptors on basophils.

Authors+Show Affiliations

Lichtenstein LM
Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21224.
Kagey-Sobotka A
No affiliation info available
White JM
No affiliation info available
Hamilton RG
No affiliation info available

MeSH

Antibodies, Anti-IdiotypicAntigens, Differentiation, B-LymphocyteBasophilsDose-Response Relationship, ImmunologicHistamine ReleaseHumansHypersensitivityImmunization, PassiveImmunoglobulin EImmunoglobulin GMacromolecular SubstancesReceptors, FcReceptors, IgESignal Transduction

Pub Type(s)

Journal Article
Research Support, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

1376345

Citation

Lichtenstein, L M., et al. "Anti-human IgG Causes Basophil Histamine Release By Acting On IgG-IgE Complexes Bound to IgE Receptors." Journal of Immunology (Baltimore, Md. : 1950), vol. 148, no. 12, 1992, pp. 3929-36.
Lichtenstein LM, Kagey-Sobotka A, White JM, et al. Anti-human IgG causes basophil histamine release by acting on IgG-IgE complexes bound to IgE receptors. J Immunol. 1992;148(12):3929-36.
Lichtenstein, L. M., Kagey-Sobotka, A., White, J. M., & Hamilton, R. G. (1992). Anti-human IgG causes basophil histamine release by acting on IgG-IgE complexes bound to IgE receptors. Journal of Immunology (Baltimore, Md. : 1950), 148(12), 3929-36.
Lichtenstein LM, et al. Anti-human IgG Causes Basophil Histamine Release By Acting On IgG-IgE Complexes Bound to IgE Receptors. J Immunol. 1992 Jun 15;148(12):3929-36. PubMed PMID: 1376345.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Anti-human IgG causes basophil histamine release by acting on IgG-IgE complexes bound to IgE receptors. AU - Lichtenstein,L M, AU - Kagey-Sobotka,A, AU - White,J M, AU - Hamilton,R G, PY - 1992/6/15/pubmed PY - 1992/6/15/medline PY - 1992/6/15/entrez SP - 3929 EP - 36 JF - Journal of immunology (Baltimore, Md. : 1950) JO - J Immunol VL - 148 IS - 12 N2 - We have reexamined the ability of anti-human IgG antibodies to induce histamine release from human basophils. A panel of purified murine mAbs with International Union of Immunological Societies-documented specificity for each of the four subclasses of human IgG was used. Of the 24 allergic subjects studied, the basophils of 75% (18/24) released greater than 10% histamine to one or more anti-IgG1-4 mAb, whereas none of the 13 nonatopic donor's basophils released histamine after stimulation with optimal amounts of anti-IgG mAb. The basophils of 85% (11/13) of the nonatopic donors did respond to anti-IgE challenge, as did 92% (22/24) of the atopic donor cells. Histamine release was induced most frequently by anti-IgG3, and 10/18 anti-IgG responder cells released histamine with mAb specific for two or more different subclass specificities. The rank order for induction of histamine release was anti-IgG3 greater than anti-IgG2 greater than IgG1 greater than anti-IgG4. As in our previous study using polyclonal anti-IgG, 100- to 300-micrograms/ml quantities of the anti-IgG mAb were required for maximal histamine release, about 1000-fold higher than those for comparable release with anti-human IgE. Specificity studies using both immunoassays and inhibition studies with IgE myeloma protein indicated that anti-IgG induced histamine release was not caused by cross-reactivity with IgE. Ig receptors were opened by lactic acid treatment so that the cells could be passively sensitized. Neither IgE myeloma nor IgG myeloma (up to 15 mg/ml) proteins could restore the response to anti-IgG mAb. However, sera from individuals with leukocytes that released histamine upon challenge with anti-IgG mAb could passively sensitize acid-treated leukocytes from both anti-IgG responder and nonresponder donors for an anti-IgG response. The only anti-IgG mAb that induced release from these passively sensitized cells were those to which the serum donor was responsive. Sera from non-IgG responders could not restore an anti-IgG response. These data led to the hypothesis that the IgG specific mAb were binding to IgG-IgE complexes that were attached to the basophil through IgE bound to the IgE receptor. This was shown to be correct because passive sensitization to anti-IgG could be blocked by previous exposure of the basophils to IgE. We conclude that anti-IgG-induced release occurs as a result of binding to IgG anti-IgE antibodies and cross-linking of the IgE receptors on basophils. SN - 0022-1767 UR - https://www.unboundmedicine.com/medline/citation/1376345/Anti_human_IgG_causes_basophil_histamine_release_by_acting_on_IgG_IgE_complexes_bound_to_IgE_receptors_ DB - PRIME DP - Unbound Medicine ER -