Publications by authors named "M Goodhardt"

Article Synopsis
  • Males and females exhibit significant differences in immune responses, with males being more vulnerable to infections and females being more prone to autoimmune diseases.
  • Disruption of X-chromosome inactivation (XCI) in female mice led to the reactivation of genes associated with the TLR7 signaling pathway, resulting in inflammatory signs resembling lupus.
  • The study suggests that improper regulation of XCI contributes to autoimmune diseases in females by affecting TLR7 signaling in immune cells.
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Article Synopsis
  • Scientists are trying to understand how certain immune cells, called lymphocytes, develop in our bodies.
  • They found that there are different paths these cells can take, and new types of cells called multi-lymphoid progenitors (MLPs) form before becoming either NK, ILC, T cells, or B cells.
  • The way these cells grow and develop is really different depending on the kind of immune cell they will become, and the scientists discovered new important steps and controls in this process.
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Changes in lymphocyte production patterns occurring across human ontogeny remain poorly defined. In this study, we demonstrate that human lymphopoiesis is supported by three waves of embryonic, fetal, and postnatal multi-lymphoid progenitors (MLPs) differing in CD7 and CD10 expression and their output of CD127 early lymphoid progenitors (ELPs). In addition, our results reveal that, like the fetal-to-adult switch in erythropoiesis, transition to postnatal life coincides with a shift from multilineage to B lineage-biased lymphopoiesis and an increase in production of CD127 ELPs, which persists until puberty.

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Recent data have shown that liver fibrosis can regress even at later stages of cirrhosis and shifting the immune response from pro-inflammatory towards a resolutive profile is considered as a promising option. The immune regulatory networks that govern the shift of the inflammatory phenotype and thus potential reversal of liver fibrosis are lesser known. Here we show that in precision-cut human liver slices obtained from patients with end-stage fibrosis and in mouse models, inhibiting Mucosal-Associated Invariant T (MAIT) cells using pharmacological or antibody-driven approaches, limits fibrosis progression and even regresses fibrosis, following chronic toxic- or non-alcoholic steatohepatitis (NASH)-induced liver injury.

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Chimeric antigen receptor T cells (CAR-T) have provided promising results in multiple myeloma (MM). However, many patients still relapse, pointing toward the need of improving this therapy. Here, we analyzed peripheral blood T cells from MM patients at different stages of the disease and investigated their phenotype and capacity to generate functional CAR-T directed against CS1 or B Cell Maturation antigen.

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