Publications by authors named "P GRENOT"

Article Synopsis
  • The study investigates a specific genetic variant in the IP3 receptor that results in a significant disorder affecting multiple systems, characterized by immunodeficiency and disturbed calcium release in cells.
  • The variant (c.7570C>T, p.Arg2524Cys) leads to cellular defects, particularly impacting T cells, and is shown to affect calcium regulation and mitochondrial function, evidenced in laboratory models.
  • Patients exhibited a range of symptoms beyond immunodeficiency, such as ectodermal dysplasia and short stature, suggesting that this genetic mutation plays a unique and broader role in disease compared to previously documented cases.
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After entering the adult thymus, bipotent T-cell progenitors give rise to αβ or γδ T cells. To determine whether the γδ T-cell receptor (TCR) has an instructive role in γδ T-cell lineage commitment or only "confirms" a pre-established γδ Τ-cell lineage state, we exploited mice lacking expression of LAT, an adaptor required for γδ TCR signaling. Although these mice showed a T-cell development block at the CD4 CD8 double-negative third (DN3) stage, 0.

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In both multiple sclerosis and its model experimental autoimmune encephalomyelitis (EAE), the extent of resident microglia activation and infiltration of monocyte-derived cells to the CNS is positively correlated to tissue damage. To address the phenotype characterization of different cell subsets, their spatio-temporal distributions and contributions to disease development we induced EAE in Thy1-CFP//LysM-EGFP//CD11c-EYFP reporter mice. We combined high content flow cytometry, immunofluorescence and two-photon imaging in live mice and identified a stepwise program of inflammatory cells accumulation.

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Dendritic cells (DCs) are instrumental in the initiation of T cell responses, but how thymic and peripheral tolerogenic DCs differ globally from Toll-like receptor (TLR)-induced immunogenic DCs remains unclear. Here, we show that thymic XCR1(+) DCs undergo a high rate of maturation, accompanied by profound gene-expression changes that are essential for central tolerance and also happen in germ-free mice. Those changes largely overlap those occurring during tolerogenic and, more unexpectedly, TLR-induced maturation of peripheral XCR1(+) DCs, arguing against the commonly held view that tolerogenic DCs undergo incomplete maturation.

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Background: Congenital cytomegalovirus infections are a leading cause of neurodevelopmental disorders in human and represent a major health care and socio-economical burden. In contrast with this medical importance, the pathophysiological events remain poorly known. Murine models of brain cytomegalovirus infection, mostly neonatal, have brought recent insights into the possible pathogenesis, with convergent evidence for the alteration and possible involvement of brain immune cells.

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