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Background: Skin exposure to chemicals may induce an inflammatory disease known as contact dermatitis (CD). Distinguishing the allergic and irritant forms of CD often proves challenging in the clinic. Methods:To characterize the molecular signatures of chemical-induced skin inflammation, we conducted a comprehensive transcriptomic analysis on the skin lesions of 47 patients with positive patch tests to reference contact allergens and nonallergenic irritants.Results: A clear segregation was observed between allergen-and irritant-induced gene profiles. Distinct modules pertaining to the epidermal compartment, metabolism, and proliferation were induced by both contact allergens and irritants; whereas only contact allergens prompted strong activation of adaptive immunity, notably of cytotoxic T-cell responses. Our results also confirmed that: (a) unique pathways characterize allergen-and irritant-induced dermatitis; (b) the intensity of the clinical reaction correlates with the magnitude of immune activation. Finally, using a machinelearning approach, we identified and validated several minimal combinations of biomarkers to distinguish contact allergy from irritation. Conclusion:These results highlight the value of molecular profiling of chemicalinduced skin inflammation for improving the diagnosis of allergic versus irritant contact dermatitis.

Antigen‐specific T‐cells are essential for protective immunity against SARS‐CoV‐2. We set up a semi‐automated whole‐blood Interferon‐gamma release assay (WB IGRA) to monitor the T‐cell response after stimulation with SARS‐CoV‐2 peptide pools. We report that the WB IGRA is complementary to serological assays to assess SARS‐CoV‐2 immunity.

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In mammals, brain development is critically dependent on proper thyroid hormone signaling, via the TRα1 nuclear receptor. However, the downstream mechanisms by which TRα1 impacts brain development are currently unknown, notably because this receptor is expressed ubiquitously from early stages of development. In order to better define the function of TRα1 in the developing brain, we used mouse genetics to induce the expression of a dominant-negative mutation of the receptor specifically in GABAergic neurons, the main inhibitory neurons in the brain, which were previously identified as sensitive to hypothyroidism. This triggered post-natal epileptic seizures, reflecting a profound impairment of GABAergic neuron maturation in different brain areas. Analysis of transcriptome and TRα1 cistrome also allowed us to identify a small set of genes, the transcription of which is upregulated by TRα1 in GABAergic neurons during post-natal maturation of the striatum and which probably play an important role during neurodevelopment. Thus, our results point to GABAergic neurons as direct targets of thyroid hormone during brain development and suggest that many defects seen in hypothyroid brains may be secondary to GABAergic neuron malfunction. Richard et al. 2019 -T3 and GABAergic neuron maturation

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