Ludimila Souza Santos1,2, Fábio da Ressureição Sgnotto3, Thamires Rodrigues de Sousa2, Raquel Leão Orfali2, Valéria Aoki2, Alberto José da Silva Duarte4,2, Jefferson Russo Victor1,2
1Division of Environmental Health Faculdades Metropolitanas Unidas (FMU) Laureate International Universities São Paulo Brazil
2Laboratory of Medical Investigation LIM‐56 Division of Clinical Dermatology Medical School University of São Paulo São Paulo Brazil
3Division of Hematology Medical School University of Sao Paulo Sao Paulo Brazil
4Division of Pathology Medical School University of São Paulo São Paulo Brazil
Tóm tắt
AbstractBackgroundAtopic dermatitis (AD) pathogenesis still needs to be elucidated, but invariant natural killer T (iNKT) cell involvement was already described by several groups. Our group has demonstrated that IgG antibodies purified from AD patients can modulate cytokine production by thymic T cells. Here we aimed to investigate if IgG from AD patients can modulate infant non‐atopic thymic iNKT cells cytokine production in order to collaborate with the elucidation of AD development in infancy.MethodsThymic tissues were obtained from children from non‐atopic mothers, and IgG was purified from AD patients diagnosed as moderate or severe and, as controls, from subjects clinically classified as non‐atopic individuals. PBMCs from non‐atopic individuals were also used in this study.ResultsOur results demonstrated that IgG from AD patients could induce non‐atopic children thymic iNKT cells to produce higher levels of intracellular IL‐4, IL‐10, and IL‐17 when compared to all control conditions. No effect was observed in non‐atopic adults peripheral iNKT. We also observed that IgG from AD patients induces an increase in the expression of CD4 and Rorγt transcription factor in non‐atopic children thymic iNKT cells compared to the condition of all controls.ConclusionsThese observations suggest that IgG from AD patients can induce a cytokine profile by thymic iNKT cells from non‐atopic infants compatible with the observations in AD development, which can collaborate with the elucidation of AD pathogenesis.
