Background The precise mechanism involved in the acquisition of the IL‐17+ profile of γδT cells, the ligands responsible for this change, and whether this default is acquired during intrathymic maturation need to be elucidated. Objective This study aimed to evaluate whether IL‐17‐producing γδT cells are present in the airways of tolerant offspring from allergen‐sensitized mothers and the possible implication of maternal IgG in the generation of these cells. Methods Female mice were immunized or not, and the allergic response, frequency of γδT cell subsets and cytokine production of the offspring were analysed by flow cytometry. The effects of passive in vivo transfer of purified IgG were investigated in offspring. A translational approach was employed to analyse γδT cells in the thymus and PBMCs from humans. Results Maternal immunization reduced the frequency of spontaneous IL‐17‐producing γδT cells in the thymus, spleen and lung of offspring. This effect was mimicked by the in vivo treatment of females with purified IgG. IgG directly interacted with γδT cell membranes. The modulatory effect of human IgG on human infant intrathymic and adult peripheral γδT cells showed similarities to murine γδT cells, which is rarely reported in the literature. Conclusions & Clinical Relevance Together, our results reveal that IgG from potentially tolerant atopic mothers can influence offspring thymic IL‐17‐producing γδT cell maturation. Furthermore, we suggest that IgG is an unprecedented modulatory factor of murine and human γδT cells. These observations may support the future development of IgG‐based immunoregulatory therapeutic strategies.

IgG modulates abT cell cytokine production during the maturation process in human thymus.We aimed to investigate whether IgG from atopic dermatitis (AD) patients can modulate in vitro cytokine production of infant intra-thymic TCD4 and TCD8 cells. Thymic tissue was obtained from newborn children from non-atopic mothers, and thymocytes were cultured for 6 days with purified IgG from AD patients, with IVIg or mock conditions as controls. Cells were gated as double positive T cells (TDP-CD4+CD8+), TCD4 cells or TCD8 cells, and levels of IL-17, IFN-g, TNF-a, IL-4, IL-10 and TGF-b were evaluated by flow cytometry. IgG of AD individuals induced enhanced IL-17 (p 0.05) and IL-10 (p 0.05) production by intrathymic TDP, TCD4 and TCD8 cells of infants, and of TGF-b (p 0.05), in TDP and TCD8 cells. Moreover, IgG from AD patients reduced IFN-g production (p 0.05) in TCD4 cells. IgG of AD patients can stimulate cytokine production in infant thymocytes and resembles the peripheral profile observed in adults. These findings suggest a novel mechanism that can contribute to AD pathogenesis. Atopic dermatitis (AD) is a chronic inflammatory skin disease with skin colonization by Staphylococcus aureus. Interleukin (IL)-22 triggers antimicrobial peptide (AMP) elaboration and enhances immunune responses. In AD, IL-22 is related to epidermal hyperplasia, keratinocyte apoptosis, and inhibition of AMP production. We aimed to evaluate the impact of staphylococcal enterotoxins (SEA and SEB) on the Tc22/Th22 induction in the peripheral blood of AD patients and on CD4 + /CD8 + T cells expressing IL-22 in AD skin. Our study showed inhibition of SEA and SEB response by Th22 cells (p 0.05) in AD patients, and an enhanced response to the bacterial stimuli by Tc22 cells (p 0.05). In AD skin, we detected increased IL-22 transcript expression and T lymphocytes expressing IL-22 (p 0.01). Together, our results provide two major findings in response to staphylococcal enterotoxins in adults with AD: dysfunctional CD4 + IL-22 secreting T cells and increased Tc22 cells. Our hypothesis reinforces the relevance of CD8 T cells modulated by staphylococcal enterotoxins as a potential source of IL-22 in adults with AD, which is relevant for the maintenance of immunological imbalance. 033Increased expression of IL-31, IL-31RA and OSMRb in bullous pemphigoid I Bullous pemphigoid (BP) is characterized by intense pruritus. Serum levels and tissue expression of Interleukin-31 (IL-31) have been found to be increased in pruritic skin disorders such as atopic eczema (AE) and prurigo nodularis (PN). We aimed to investigate the expression of IL-31 and its receptors [IL-31 receptor alpha (IL-31RA) and oncostatin M receptor beta (OSMRb)] in the skin of classical and atypical forms of BP patients. Immunohistochemical staining was performed in biopsy specimens of 16 BP patients (8 classical BP, 5 eczema-like BP, 3 pemphigoid nodularis) and compared with 4 AE, 2 PN and 5 normal skin samples. The stained slides were scanned and computer-assisted analysis of expression was per...