Dermatologic and ocular diseases
Effects of complement inactivation and IgG depletion on skin reactivity to autologous serum in chronic idiopathic urticaria,☆☆

https://doi.org/10.1067/mai.2000.108913Get rights and content

Abstract

Background: Intradermal injection of autologous serum elicits a wheal-and-flare response in about 60% of patients with chronic idiopathic urticaria (CIU). This reactivity has been attributed to the presence of IgG autoantibodies directed against IgE or the α-chain of the high-affinity IgE receptor (FcϵRIα) expressed on basophils and mast cells, leading to the hypothesis that at least some forms of CIU could be sustained by an autoimmune process. Objectives: The aim of this study was to investigate the relationship between the presence of anti-IgE or anti-FcϵRI antibodies and the ability to induce wheal-and-flare responses in CIU sera selected for the capacity to give a positive skin test response. Methods: Fifteen patients with CIU and a positive skin test response to autologous serum were injected intradermally with native serum and with serum heated at 56°C for 30 minutes and then adsorbed on Sepharose-protein G to obtain IgG depletion. Serum levels of anti-IgE and anti-FcϵRIα antibodies were measured by ELISA by using purified IgE and recombinant RIα-soluble double-fusion protein RIα-human serum albumin-RIα, respectively. The histamine-releasing activity of sera was tested by using ELISA with whole human blood from a healthy donor. Results: All patients had positive cutaneous responses to native serum injection. Anti-FcϵRIα antibodies were present in 14 of 15 native sera, only two of which were able to induce in vitro basophil degranulation. On the contrary, detectable amounts of anti-IgE antibodies were not found in any serum. IgG depletion by protein G resulted in complete (10/14 samples) or considerable (4/14 samples) removal of anti-FcϵRIα antibodies. The two sera endowed with functional activity lost their capacity to trigger histamine release from basophils after heating and protein G adsorption. Nonetheless, heat-decomplemented/IgG-depleted sera elicited wheal-and-flare reactions comparable with those observed with untreated sera. Conclusions: These results strongly suggest that skin reactivity to autologous serum could be due to as yet unidentified non–Ig reactants present in the sera of patients with CIU. (J Allergy Clin Immunol 2000;106:567-72.)

Section snippets

Study population

Fifteen patients with severe CIU and a positive skin test response to autologous serum (14 women and 1 man; age range, 19-58 years) were selected from our CIU patient cohort, which was composed of 132 individuals, 72 of whom had positive reactions to intradermal injection of autologous serum. The duration of urticaria ranged from 6 to 48 months, and all patients were under treatment with cetirizine associated in some cases with steroids. At the time of the study, none of the patients had been

Results

In all patients the prick test with histamine elicited positive results, whereas the injection of plain saline always elicited negative results. When autologous serum was injected, significant wheal-and-flare responses were observed in all 15 patients studied (Table I).

None of the native sera showed detectable amounts of anti-IgE autoantibodies (data not shown); on the contrary, it was possible to demonstrate the presence of variable amounts of anti-FcϵRIα antibodies in 14 of 15 sera, ranging

Discussion

In this study we extend the knowledge about the presence of anti-FcϵRIα IgG antibodies in the sera from patients with CIU and a positive skin test response to autologous serum. Moreover, we show, for the first time, that heat-decomplemented/IgG-depleted sera retain the ability to induce wheal-and-flare reactions.

The finding of anti-IgE and anti-FcϵRIα autoantibodies in sera of patients with CIU has been repeatedly reported. Anti-IgE antibodies, isolated3, 4, 5 or in association with anti-FcϵRIα

Acknowledgements

We thank Dr Rita Zamarchi and Raffaele Bendo, University of Padova, for their technical assistance.

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Supported in part by grants from Ministero dell’Università e della Ricerca Scientifica e Tecnologica, 60%.

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Reprint requests: Umberto Fagiolo, MD, Dipartimento di Scienze Mediche e Chirurgiche, Università degli Studi di Padova, Via Giustiniani, 2, 35128 Padova, Italy. fax +(39)049 821 2151; E-mail [email protected]

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