Santos, Ludimila S.
Sgnotto, Fabio da Ressureicao
Sousa, Thamires R.
Orfali, Raquel L.
da Silva Duarte, Alberto Jose
Victor, Jefferson R.
Total Authors: 7
 Laureate Int Univ, FMU, Div Environm Hlth, Sao Paulo - Brazil
 Univ Sao Paulo, Sch Med, Div Clin Dermatol, Lab Med Invest LIM 56, Ave Dr En eas de Carvalho Aguiar 500, 3rd Floor, BR-05403000 Sao Paulo - Brazil
 Univ Sao Paulo, Div Hematol, Sch Med, Sao Paulo - Brazil
 Univ Sao Paulo, Sch Med, Div Pathol, Sao Paulo - Brazil
Total Affiliations: 4
INTERNATIONAL JOURNAL OF DERMATOLOGY;
Web of Science Citations:
Background Atopic 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. Methods Thymic 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. Results Our 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 Ror gamma t transcription factor in non-atopic children thymic iNKT cells compared to the condition of all controls. Conclusions These 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. (AU)