Tatlock H. Lauten

This study identifies norepinephrine as a novel regulator of T-lymphocyte IL-17A expression through a noncanonical pathway involving TGFβ, cAMP, PKA, CREB, and CBP/p300, distinct from the canonical STAT3-dependent pathway.

This study identifies hemoglobin alpha's role in T-lymphocyte activation and mitochondrial function, showing its impact on cytokine production and EAE severity.

This study shows that traumatic stress increases blood pressure sensitivity to angiotensin II via T-lymphocytes, independent of psychopathology, using a mouse model of repeated social defeat stress.

This study investigates the therapeutic potential of beta-adrenergic receptor inhibition in autoimmune diseases by showing its ability to reduce TH17 cells and promote Treg cells in an experimental model of multiple sclerosis.

This study identifies hemoglobin alpha-a1 as a redox-sensitive mitochondrial antioxidant in T-lymphocytes, showing its regulation by redox stress and metabolic state.

This study shows that beta-adrenergic signaling and T-lymphocyte-produced catecholamines are required for IL-17A synthesis, offering new therapeutic targets for PTSD and autoimmune diseases.