Publications by authors named "Quentin Marquant"

Severe defects in human IFNγ immunity predispose individuals to both Bacillus Calmette-Guérin disease and tuberculosis, whereas milder defects predispose only to tuberculosis. Here we report two adults with recurrent pulmonary tuberculosis who are homozygous for a private loss-of-function TNF variant. Neither has any other clinical phenotype and both mount normal clinical and biological inflammatory responses.

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Article Synopsis
  • Researchers have created a new ex vivo model using lung transplant methods to study how SARS-CoV-2 infects human lungs, addressing limitations of animal models and lab systems.
  • The study used single-cell RNA sequencing to determine that the virus primarily targets alveolar macrophages (AMs) and monocyte-derived macrophages (MoMacs), with MoMacs showing a stronger inflammatory response.
  • Findings indicate that the Wuhan strain of SARS-CoV-2 is more effective than the D614G variant, and understanding how the virus interacts with lung macrophages could inform prevention strategies.
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Article Synopsis
  • Conventional immunosuppressants are not effective for treating asthma related to Eosinophilic Granulomatosis with Polyangiitis (EGPA).
  • Tezepelumab, a monoclonal antibody targeting thymic stromal lymphopoietin (TSLP), has shown promise in improving asthma symptoms in patients with severe refractory EGPA-related asthma.
  • Despite improvements in symptoms and asthma control, there are concerns about potential rebound eosinophilia and related complications due to TSLP inhibition, as observed in similar treatments.
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Microbiota studies have dramatically increased over these last two decades, and the repertoire of microorganisms with potential health benefits has been considerably enlarged. The development of next generation probiotics from new bacterial candidates is a long-term strategy that may be more efficient and rapid with discriminative in vitro tests. strains have received attention regarding their antimicrobial potential against pathogens of the upper and, more recently, the lower respiratory tracts.

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Background: Inflammasomes are large protein complexes that assemble in the cytosol in response to danger such as tissue damage or infection. Following activation, inflammasomes trigger cell death and the release of biologically active forms of pro-inflammatory cytokines interleukin (IL)-1β and IL-18. NOD-like receptor family pyrin domain containing 6 (NLRP6) inflammasome is required for IL-18 secretion by intestinal epithelial cells, macrophages, and T cells, contributing to homeostasis and self-defense against pathogenic microbes.

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Respiratory syncytial virus (RSV) is the main cause of acute respiratory infections in young children and also has a major impact on the elderly and immunocompromised people. In the absence of a vaccine or efficient treatment, a better understanding of RSV interactions with the host antiviral response during infection is needed. Previous studies revealed that cytoplasmic inclusion bodies (IBs), where viral replication and transcription occur, could play a major role in the control of innate immunity during infection by recruiting cellular proteins involved in the host antiviral response.

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Tuberculosis exacts a terrible toll on human and animal health. While (Mtb) is restricted to humans, (Mb) is present in a large range of mammalian hosts. In cattle, bovine TB (bTB) is a noticeable disease responsible for important economic losses in developed countries and underestimated zoonosis in the developing world.

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Respiratory Syncytial Virus (RSV) is the major cause of lower respiratory tract infection in infants, in whom, the sensing of RSV by innate immune receptors and its regulation are still poorly described. However, the severe bronchiolitis following RSV infection in neonates has been associated with a defect in type I interferons (IFN-I) production, a cytokine produced mainly by alveolar macrophages (AMs) upon RSV infection in adults. In the present study, neonatal C57BL/6 AMs mobilized very weakly the IFN-I pathway upon RSV infection in vitro and failed to restrain virus replication.

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The gut microbiota contributes to shaping efficient and safe immune defenses in the gut. However, little is known about the role of the gut and/or lung microbiota in the education of pulmonary innate immune responses. Here, we tested whether the endogenous microbiota in general can modulate the reactivity of pulmonary tissue to pathogen stimuli by comparing the response of specific-pathogen-free (SPF) and germ-free (GF) mice.

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Background: Protein kinase C (PKC) θ, a serine/threonine kinase, is involved in T2 cell activation and proliferation. Type 2 innate lymphoid cells (ILC2s) resemble T2 cells and produce the T2 cytokines IL-5 and IL-13 but lack antigen-specific receptors. The mechanism by which PKC-θ drives innate immune cells to instruct T2 responses in patients with allergic lung inflammation remains unknown.

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