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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

Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21224.No affiliation info availableNo affiliation info availableNo affiliation info available

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_ L2 - https://www.jimmunol.org/lookup/pmidlookup?view=long&pmid=1376345 DB - PRIME DP - Unbound Medicine ER -