Low doses of IgG from atopic individuals can modulate in vitro IFN-γ production by human intra-thymic TCD4 and TCD8 cells: An IVIg comparative approach.

The regulatory effect of allergic responses induced by IgG antibodies on human intra-thymic cells has not been reported in the literature. The aim of this study was to evaluate the possible differential effect of purified IgG from atopic and non-atopic individuals on human intra-thymic αβT cell cytokine production. Thymic tissues were obtained from 14 patients who were less than 7 d old. Additionally, blood samples were collected from atopic and non-atopic volunteers. Thymocytes and peripheral blood mononuclear cells were cultured with purified atopic or non-atopic IgG, and intracellular cytokine production was assessed. Purified IgG did not influence the frequency or viability of human intra-thymic αβT cells. Purified non-atopic IgG induced greater IFN-γ production by intra-thymic CD4+CD8+ T cells than did the mock treatment and atopic IgG. A similar effect of purified non-atopic IgG on TCD8 cells was observed compared with the mock treatment. Atopic IgG inhibited IFN-γ and TGF-β production by intra-thymic TCD4 cells. Treatment with intravenous immunoglobulin resulted in intermediate levels of IFN-γ and TGF-β in intra-thymic TCD4 cells compared with treatment with atopic and non-atopic IgG. Peripheral TCD4 cells from non-atopic individuals produced IFN-γ only in response to atopic IgG. This report describes novel evidence revealing that IgG from atopic individuals may influence intracellular IFN-γ production by intra-thymic αβT cells in a manner that may favor allergy development.

Citation

Fábio da Ressureição Sgnotto, Marília Garcia de Oliveira, Aline Aparecida de Lima Lira, Luciana Bento-de-Souza, Alberto José da Silva Duarte, Jefferson Russo Victor. Low doses of IgG from atopic individuals can modulate in vitro IFN-γ production by human intra-thymic TCD4 and TCD8 cells: An IVIg comparative approach. Human vaccines & immunotherapeutics. 2017 Jul 03;13(7):1563-1572

PMID: 28441069

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