@article{lutz_filamins_2025b,

title = {[Filamins, T helper 2 lymphocytes and asthma : A matter of balance]},

author = {Pierre G. Lutz and Isabelle Lamsoul},

doi = {10.1051/medsci/2025032},

issn = {1958-5381},

year  = {2025},

date = {2025-03-01},

urldate = {2025-03-01},

journal = {Medecine Sciences: M/S},

volume = {41},

number = {3},

pages = {232–235},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid39344864,

title = {Canine exfoliative cutaneous lupus erythematosus in two mixed breed littermates},

author = {Mirabela Oana Dumitrache and Aurora Livia Ursache and Corina Toma and Andrada Negoescu and Stefan Jonas Rietmann and Tosso Leeb and Marie-Christine Cadiergues},

doi = {10.1111/vde.13301},

issn = {1365-3164},

year  = {2025},

date = {2025-02-01},

urldate = {2025-02-01},

journal = {Vet Dermatol},

volume = {36},

number = {1},

pages = {99--103},

abstract = {Canine exfoliative cutaneous lupus erythematosus (ECLE) is the rarest variant of cutaneous lupus in dogs and has strong breed predilections. This report presents the clinical, histopathological and immunohistochemical features of two ECLE cases in mixed breed littermates and confirms the expected genetic mutation. A therapeutic response to oclacitinib also is documented.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid38743041,

title = {The },

author = {Carle Paul and Alexander J Stratigos and Tamar Nijsten and Paolo Gisondi and Carmen Salavastru and Martin Röecken and Charles Taieb and Francesca Sampogna and Myrto Trakatelli and Luis Puig and Marie A Richard},

doi = {10.23736/S0026-4806.24.09262-0},

issn = {1827-1669},

year  = {2025},

date = {2025-02-01},

urldate = {2025-02-01},

journal = {Minerva Med},

volume = {116},

number = {1},

pages = {81--83},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid39955774,

title = {Dendritic cell phagosomes recruit GRASP55 for export of antigen-loaded MHC molecules},

author = {Ignacio Cebrian and Sofía Dinamarca and María Jesús Pena Rodríguez and Elena Priego and Nathalie Brouwers and Martina Barends and Jamina Brunnberg and Robert Tampé and Nicolas Blanchard and David Sancho and Vivek Malhotra},

doi = {10.1016/j.celrep.2025.115333},

issn = {2211-1247},

year  = {2025},

date = {2025-02-01},

journal = {Cell Rep},

volume = {44},

number = {2},

pages = {115333},

abstract = {Dendritic cells (DCs) present exogenous antigens via major histocompatibility complex class I (MHC-I) and MHC class II (MHC-II) molecules, activating CD8 and CD4 T cells. A critical but poorly understood step in this process is the trafficking of peptide-loaded MHC molecules from the endocytic system to the cell surface. In this study, we demonstrate that the Golgi reassembly-stacking protein of 55 kDa (GRASP55), which has been shown to have no role in stacking, is essential for antigen presentation. Using soluble, bead-coated, and bacterial-bound antigens, we found significantly impaired exogenous antigen presentation in GRASP55-deficient bone-marrow-derived DCs (BMDCs). Notably, GRASP55 was recruited to late phagosomes, and our data suggest that it is crucial for sorting MHC-I and MHC-II molecules, facilitating their trafficking to the plasma membrane. Our findings highlight the vital role of GRASP55 in the intracellular transport of MHC molecules bound to their respective peptides during exogenous antigen presentation.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Talpin2025,

title = {Mimicry-based strategy between human and commensal antigens for the development of a new family of immune therapies for cancer},

author = {Alice Talpin and Ana Maia and Jean-Marie Carpier and Guillaume Kulakowski and Lucie Aubergeon and Jerome Kervevan and Camille Gaal and Francesco Strozzi and Coline Billerey and Ludivine Amable and Tifanny Mersceman and Alexandrine Garnier and Càtia Oliveira and Carolina Calderon and Diana Bachrouche and Chloé Ventujol and Léa Bernard and Amandine Manteau and Jennifer Martinez and Michaël Bonnet and Julie Noguerol and Karl Laviolette and Laura Boullerot and Marine Malfroy and Gregoire Chevalier and Olivier Adotevi and Olivier Joffre and Ahmed Idbaih and Maria Vieito and Francois Ghiringhelli and Agostina Stradella and Ghazaleh Tabatabai and Michael C Burger and Iris Mildenberger and Ulrich Herrlinger and David A. Reardon and Wolfgang Wick and Cecile Gouttefangeas and Christophe Bonny and Laurent Chene and Joao Gamelas Magalhaes},

doi = {10.1136/jitc-2024-010192},

issn = {2051-1426},

year  = {2025},

date = {2025-02-00},

journal = {J Immunother Cancer},

volume = {13},

number = {2},

publisher = {BMJ},

abstract = {BackgroundMolecular mimicry between commensal bacterial antigens and tumor-associated antigens (TAAs) has shown potential in enhancing antitumor immune responses. This study leveraged this concept using commensal bacterial antigens, termed OncoMimics, to induce TAA-derived peptide (TAAp)-specific cross-reactive cytotoxic T cells and improve the efficacy of peptide-based immunotherapies.MethodsThe discovery of OncoMimics primarily relied on a bioinformatics approach to identify commensal bacteria-derived peptide sequences mimicking TAAps. Several OncoMimics peptide (OMP) candidates were selected in silico based on multiple key parameters to assess their potential to elicit and ameliorate immune responses against TAAs. Selected OMPs were synthesized and tested for their affinity and stability on the major histocompatibility complex (MHC) in vitro and for their capacity to elicit cross-reactive OMP-specific/TAAp-specific CD8+T cell responses in human leukocyte antigen (HLA)-A2-humanized mice, human peripheral blood mononuclear cells (PBMC) and patients with cancer.ResultsSelected OMPs demonstrated superior HLA-A2 binding affinities and stabilities compared with homologous TAAps. Vaccination of HLA-A2-humanized mice with OMPs led to the expansion of OMP-specific CD8+T cells that recognize both OMPs and homologous TAAps, exhibiting cytotoxic capacities towards tumor antigens and resulting in tumor protection in a prophylactic setting. Using PBMCs from HLA-A2+healthy donors, we confirmed the ability of OMPs to elicit potent cross-reactive OMP-specific/TAAp-specific CD8+T-cell responses. Interestingly, we observed a high prevalence of OMP-specific T cells across donors. Cytotoxicity assays revealed that OMP-stimulated human T cells specifically targeted and killed tumor cells loaded with OMPs or TAAps. Preliminary data from an ongoing clinical trial (NCT04116658) support these findings, indicating that OMPs elicit robust OMP-specific/TAAp-specific CD8+T cell responses in patients. Initial immunomonitoring data revealed sustained T-cell responses over time, with T cells maintaining a polyfunctional, cytotoxic and memory phenotype, which is critical for effective antitumor activity and long-term immune surveillance.ConclusionsThese findings suggest that leveraging naturally occurring commensal-derived antigens through OMPs could significantly remodel the tumor immune landscape, offering guidance for a promising strategy for cancer peptide-based immunotherapies.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{nokey,

title = {Polarization of circulating follicular helper T cells correlates with bullous pemphigoid severity. },

author = {Pérals C and le Jan S and Muller C and Le Naour R and Bernard P and Viguier M and Fazilleau N },

doi = {10.1093/bjd/ljae355},

year  = {2025},

date = {2025-01-24},

urldate = {2025-01-24},

journal = {British Journal of Dermatology},

volume = {192},

number = {2},

pages = {283-292},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{nokey,

title = {Assessing IgE and basophil activity in blood samples from nonhuman primates},

author = {Cyprien Pecalvel and Aurélie Mougel and Edouard Leveque and Katia Lemdani and Vincent Serra and Laurent Guilleminault and Laurent L Reber},

url = {https://pubmed.ncbi.nlm.nih.gov/39495093/},

doi = {10.1111/all.16367},

year  = {2025},

date = {2025-01-08},

urldate = {2025-01-08},

journal = {Allergy},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid39833171,

title = {Brucella abortus impairs T lymphocyte responsiveness by mobilizing IL-1RA-secreting omental neutrophils},

author = {Joaquin M Pellegrini and Gabriela González-Espinoza and Raheleh R Shayan and Lisiena Hysenaj and Thomas Rouma and Vilma Arce-Gorvel and Hugues Lelouard and Dimitri Popoff and Yun Zhao and Sean Hanniffy and Amanda Castillo-Zeledón and Maite Loperena-Barber and Javier Celis-Gutierrez and Cyrille Mionnet and Mile Bosilkovski and Javier Solera and Eric Muraille and Elías Barquero-Calvo and Edgardo Moreno and Raquel Conde-Álvarez and Ignacio Moriyón and Jean-Pierre Gorvel and Sylvie Mémet},

doi = {10.1038/s41467-024-55799-2},

issn = {2041-1723},

year  = {2025},

date = {2025-01-01},

urldate = {2025-01-01},

journal = {Nat Commun},

volume = {16},

number = {1},

pages = {862},

abstract = {Immune evasion strategies of Brucella, the etiologic agent of brucellosis, a global zoonosis, remain partially understood. The omentum, a tertiary lymphoid organ part of visceral adipose tissue, has never been explored as a Brucella reservoir. We report that B. abortus infects and replicates within murine omental macrophages. Throughout the chronic phase of infection, the omentum accumulates macrophages, monocytes and neutrophils. The maintenance of PD-L1Sca-1 macrophages, monocytes and neutrophils in the omentum depends on the wadC-encoded determinant of Brucella LPS. We demonstrate that PD-L1Sca-1 murine omental neutrophils produce high levels of IL-1RA leading to T cell hyporesponsiveness. These findings corroborate brucellosis patient analysis of whole blood displaying upregulation of PDL1 and Ly6E genes, and of serum exhibiting high levels of IL-1RA. Overall, the omentum, a reservoir for B. abortus, promotes bacterial persistence and causes CD4 and CD8 T cell immunosuppression by IL-1RA secreted by PD-L1Sca-1 neutrophils.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid38879153,

title = {Prolyl Endopeptidase Is Involved in Filaggrinolysis and Cornification},

author = {Julie Briot and Carole Pons and Aude Foucher and Dominique Goudounèche and Nicolas Gaudenzio and Mark Donovan and Dominique Bernard and Marie-Claire Méchin and Michel Simon},

doi = {10.1016/j.jid.2024.04.028},

issn = {1523-1747},

year  = {2025},

date = {2025-01-01},

urldate = {2025-01-01},

journal = {J Invest Dermatol},

volume = {145},

number = {1},

pages = {98--108.e15},

abstract = {FLG is a well-known biomarker of atopic dermatitis and skin dryness. Its full proteolysis (or filaggrinolysis) produces the major constituents of the natural moisturizing factor. Some proteases/peptidases remain to be identified in this multistep process. Mining 16 omics analyses, we identified prolyl endopeptidase (PREP) as a candidate peptidase. Indirect immunofluorescence and confocal analysis demonstrated its localization in the granular and deep cornified layers, where it colocalized with FLG. Tandem mass spectroscopy and fluorescent quenching activity assays showed that PREP cleaved several synthetic peptides derived from the FLG sequence, at the carboxyl side of an internal proline. Deimination of these peptides increased PREP enzymatic efficiency. Specific inhibition of PREP in reconstructed human epidermis using benzyloxycarbonyl-pro-prolinal induced the accumulation of FLG monomers. Downregulation of PREP expression in reconstructed human epidermis using RNA interference confirmed the impact of PREP on FLG metabolism and highlighted a more general role of PREP in keratinocyte differentiation. Indeed, quantitative global proteomic, western blotting, and RT-qPCR analyses showed a strong reduction in the expression of bleomycin hydrolase, known to be involved in filaggrinolysis, and of several other actors of cornification such as loricrin. Consequently, at the functional level, the transepidermal electric resistance was drastically reduced.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid40698039b,

title = {Epidermal lamellar bodies, essential organelles for the skin barrier},

author = {Corinne Leprince and Michel Simon},

doi = {10.3389/fcell.2025.1597884},

issn = {2296-634X},

year  = {2025},

date = {2025-01-01},

urldate = {2025-01-01},

journal = {Front Cell Dev Biol},

volume = {13},

pages = {1597884},

abstract = {Skin lamellar bodies are members of the Lysosome-Related-Organelle (LRO) family, characterized by specific features related to the skin's primary function, i.e., protecting the body from external assaults while minimizing dehydration. In the uppermost living cell layers of the epidermis, the vesicles and tubulovesicular network that make up the « lamellar body system » as identified by electron microscopists, play a crucial role in maintaining the skin barrier. As a secretory compartment, lamellar bodies carry a variety of compounds that, when released in the extracellular space or exposed at the membrane, contribute to the unique hydrophobic structure of the upper epidermis (lipids and lipid metabolism enzymes), regulate desquamation (proteases and inhibitors) and provide anti-microbial defense. The molecular machinery involved in the biogenesis and trafficking of skin lamellar bodies is only beginning to be deciphered, including the Rab11A GTPase, the Myosin5B molecular motor, and the CHEVI complex. This later one is constituted of the Vps33B and VIPAR tethering molecules, whose mutations lead to the ARC and ARKID syndromes. Further studies are needed to identify the key molecules regulating the various stages of LB biogenesis, maturation and exocytosis. It is likely that some of these molecules will be shared with other members of the LRO family. These studies will further enhance our understanding of the relationships between lamellar body trafficking and skin barrier dysfunction.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid39749396,

title = {Novel ABCA12 Missense Variant in a Patient with Congenital Ichthyosis and Palmoplantar Keratoderma},

author = {Pauline Bernard and Nuria Pell and Juliette Mazereeuw-Hautier and Nathalie Jonca},

doi = {10.2340/actadv.v105.42502},

issn = {1651-2057},

year  = {2025},

date = {2025-01-01},

urldate = {2025-01-01},

journal = {Acta Derm Venereol},

volume = {105},

pages = {adv42502},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid40698039,

title = {Epidermal lamellar bodies, essential organelles for the skin barrier},

author = {Corinne Leprince and Michel Simon},

doi = {10.3389/fcell.2025.1597884},

issn = {2296-634X},

year  = {2025},

date = {2025-01-01},

urldate = {2025-01-01},

journal = {Front Cell Dev Biol},

volume = {13},

pages = {1597884},

abstract = {Skin lamellar bodies are members of the Lysosome-Related-Organelle (LRO) family, characterized by specific features related to the skin's primary function, i.e., protecting the body from external assaults while minimizing dehydration. In the uppermost living cell layers of the epidermis, the vesicles and tubulovesicular network that make up the « lamellar body system » as identified by electron microscopists, play a crucial role in maintaining the skin barrier. As a secretory compartment, lamellar bodies carry a variety of compounds that, when released in the extracellular space or exposed at the membrane, contribute to the unique hydrophobic structure of the upper epidermis (lipids and lipid metabolism enzymes), regulate desquamation (proteases and inhibitors) and provide anti-microbial defense. The molecular machinery involved in the biogenesis and trafficking of skin lamellar bodies is only beginning to be deciphered, including the Rab11A GTPase, the Myosin5B molecular motor, and the CHEVI complex. This later one is constituted of the Vps33B and VIPAR tethering molecules, whose mutations lead to the ARC and ARKID syndromes. Further studies are needed to identify the key molecules regulating the various stages of LB biogenesis, maturation and exocytosis. It is likely that some of these molecules will be shared with other members of the LRO family. These studies will further enhance our understanding of the relationships between lamellar body trafficking and skin barrier dysfunction.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{muhlgrabner_gauging_2025,

title = {Gauging antigen recognition by human primary T-cells featuring orthotopically exchanged TCRs of choice},

author = {Vanessa Mühlgrabner and Angelika Plach and Johannes Holler and Judith Leitner and Peter Steinberger and Loïc Dupré and Janett Göhring and Johannes B. Huppa},

doi = {10.1016/bs.mcb.2024.03.003},

issn = {0091-679X},

year  = {2025},

date = {2025-01-01},

urldate = {2025-01-01},

journal = {Methods in Cell Biology},

volume = {193},

pages = {127–154},

abstract = {Understanding human T-cell antigen recognition in health and disease is becoming increasingly instrumental for monitoring T-cell responses to pathogen challenge and for the rational design of T-cell-based therapies targeting cancer, autoimmunity and organ transplant rejection. Here we showcase a quantitative imaging platform which is based on the use of planar glass-supported lipid bilayers (SLBs). The latter are functionalized with antigen (peptide-loaded HLA) as adhesion and costimulatory molecules (ICAM-1, B7-1) to serve as surrogate antigen presenting cell for antigen recognition by T-cells, which are equipped with T-cell antigen receptors (TCRs) sequenced from antigen-specific patient T-cells. We outline in detail, how the experimental use of SLBs supports recoding and analysis of synaptic antigen engagement and calcium signaling at the single cell level in response to user-defined antigen densities for quantitative comparison.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid39559950,

title = {SNX17 Regulates Antigen Internalisation and Phagosomal Maturation by Dendritic Cells},

author = {Sofía Dinamarca and Cristina Croce and Anna Salvioni and Facundo Garrido and Sandra Estrada Fidalgo and Gonzalo Bigliani and Luis S Mayorga and Nicolas Blanchard and Ignacio Cebrian},

doi = {10.1111/imm.13878},

issn = {1365-2567},

year  = {2025},

date = {2025-01-01},

journal = {Immunology},

volume = {174},

number = {1},

pages = {167--185},

abstract = {Antigen cross-presentation is the process whereby small peptides derived from exogenous antigens are attached to MHC-I molecules triggering CD8+ T lymphocyte activation. The endocytic route of dendritic cells (DCs) is highly specialised for cross-presentation to initiate cytotoxic immune responses against numerous intracellular pathogens and tumours. In this study, we identify the endosomal protein sorting nexin (SNX) 17 as a key regulator of antigen internalisation and cross-presentation by DCs. SNX17 expression in DCs guarantees optimal cross-presentation of soluble, particulate, and Toxoplasma gondii-associated antigens. The silencing of SNX17 expression in DCs significantly affected the internalisation of exogenous antigens by fluid-phase endocytosis, phagocytosis, and more strikingly, T. gondii invasion. We show that SNX17 controls proper integrin recycling, actin cytoskeleton organisation, and phagosomal maturation. Altogether, our findings provide compelling evidence that SNX17 plays a central role in the modulation of the DC endocytic network, which is essential for competent antigen cross-presentation.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid39794349,

title = {Heterochromatic gene silencing controls CD4 T cell susceptibility to regulatory T cell-mediated suppression in a murine allograft model},

author = {Julie Noguerol and Karl Laviolette and Margot Zahm and Adeline Chaubet and Ambrine Sahal and Claire Détraves and Romain Torres and Clothilde Demont and Véronique Adoue and Carine Joffre and Florence Cammas and Joost Pm van Meerwijk and Olivier P Joffre},

doi = {10.1038/s41467-025-55848-4},

issn = {2041-1723},

year  = {2025},

date = {2025-01-01},

urldate = {2025-01-01},

journal = {Nat Commun},

volume = {16},

number = {1},

pages = {566},

abstract = {Protective immune responses require close interactions between conventional (Tconv) and regulatory T cells (Treg). The extracellular mediators and signaling events that regulate the crosstalk between these CD4 T cell subsets have been extensively characterized. However, how Tconv translate Treg-dependent suppressive signals at the chromatin level remains largely unknown. Here we show, using a murine bone marrow allograft model in which graft rejection is coordinated by CD4 T cells and can be inhibited by Treg, that Treg-mediated T cell suppression involves Heterochromatin Protein 1 α (HP1α)-dependent gene silencing. Unexpectedly, our screen also reveals that T cells deficient for HP1γ or the methyltransferase SUV39H1 are better repressed by Treg than their wild-type counterparts. Mechanistically, our transcriptional and epigenetic profiling identifies HP1γ as a negative regulator of a gene network functionally associated with T-cell exhaustion, including those encoding the inhibitory receptors PD-1 and LAG-3. In conclusion, we identify HP1 variants as rheostats that finely tune the balance between tolerance and immunity. While HP1α converts immunosuppressive signals into heterochromatin-dependent gene silencing mechanisms, HP1γ adjusts Tconv sensitivity to inhibitory environmental signals.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{RN28d,

title = {Porcine-derived pancreatic enzyme replacement therapy: a cause of hepatitis E virus transmission?},

author = {N. Kamar and O. Marion and F. Abravanel and L. Esposito and A. Del Bello and J. Izopet},

url = {https://www.ncbi.nlm.nih.gov/pubmed/38960583},

doi = {10.1136/gutjnl-2024-332744},

issn = {1468-3288 (Electronic) 0017-5749 (Linking)},

year  = {2025},

date = {2025-01-01},

urldate = {2025-01-01},

journal = {Gut},

volume = {74},

number = {2},

pages = {331-332},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Martin2025,

title = {\emph{Ex vivo} Culture of Human Placental Explants for the Study of Viral Transmission Across the Maternal-Fetal Interface},

author = {Hélène Martin and Charlène Martin and Loïc Guimbaud and Delphine Duchanois and Paul Guerby and Cécile E. Malnou},

doi = {10.3791/69525},

issn = {1940-087X},

year  = {2025},

date = {2025-00-00},

urldate = {2025-00-00},

journal = {JoVE},

number = {226},

publisher = {MyJove Corporation},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid39444662,

title = {Extrafollicular CD19CXCR5CD11c double negative 3 (DN3) B cells are significantly associated with disease activity in females with systemic lupus erythematosus},

author = {Carlo Chizzolini and Jean-Charles Guery and Fanny Noulet and Lyssia Gruaz and Claire Cenac and Loredana Frasca and David Spoerl and Lionel Arlettaz and Alice Horisberger and Camillo Ribi and Stéphanie Hugues},

doi = {10.1016/j.jtauto.2024.100252},

issn = {2589-9090},

year  = {2024},

date = {2024-12-01},

urldate = {2024-12-01},

journal = {J Transl Autoimmun},

volume = {9},

pages = {100252},

abstract = {OBJECTIVE: B cells play a major role in the development and maintenance of systemic lupus erythematosus (SLE). Double negative (DN) B cells defined by the lack of surface expression of IgD and CD27 have attracted recent interest for their sensitivity to Toll-like receptor 7 (TLR7) ligands and their potential role in the production of autoantibodies. Here we aimed at investigating the possible association of DN B cells and their subsets with SLE disease activity specifically in female patients, in which TLR7 gene has been reported to escape X chromosome inactivation.nnMETHODS: Peripheral blood mononuclear cells were purified from woman participating to the clinically well-characterized Swiss SLE Cohort Study (SSCS). PBMC from age-matched healthy females were used as controls. PBMC were stained for cell surface markers, intracellular Tbet and analyzed by multicolor cytofluorimetry. Single nucleotide TLR7 polymorphisms were assessed by polymerase chain reaction.nnRESULTS: The median SLE disease activity index of the 86 females was 2, IQR [0-6], all but 8 were under chronic SLE treatment. B cells co-expressing CD11c and Tbet were increased, the mean fluorescence intensity (MFI) of CD19 was considerably reduced and we observed a large increase in CD11c + CXCR5-and CD11c-CXCR5-concomitantly with a reduction of CD11c-CXCR5+ B cells in SLE compared to 40 healthy donors (HD). When focusing on the DN B cell subset, we found a reduction of DN1 (CD11c-CXCR5+) and an increase of DN2 (CD11c + CXCR5-) and most impressively of DN3 (CD11c-CXCR5-) cells. The DN subset, particularly DN3, showed the lowest level of CD19 expression. Both DN1 and DN3 percentages as well as the CD19 MFI of DN cells were associated with SLE disease activity. The use of glucocorticoids, immunosuppressants, and antimalarials impacted differentially on the frequencies of DN B cell subsets. CD19 MFI in B cells and the percentage of DN3 were the strongest biomarkers of disease activity. The TLR7 snp3858384 G allele was associated with increased percentages of B cells and CD19CD11c-CXCR5+ and decreased CD19CD11c-CXCR5-.nnCONCLUSIONS: DN3 B cells are strongly associated with SLE clinical activity pointing to their potential involvement in disease pathogenesis, and CD19 expression level performs accurately as disease activity biomarker.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{maire_fine-tuning_2024,

title = {Fine-tuning levels of filamins a and b as a specific mechanism sustaining Th2 lymphocyte functions},

author = {Kilian Maire and Léa Chamy and Samira Ghazali and Manon Carratala-Lasserre and Margot Zahm and Clément Bouisset and Arnaud Métais and Lucie Combes-Soia and Lidia Fuente-Vizuete and Hussein Trad and Adeline Chaubet and Magali Savignac and Anne Gonzalez de Peredo and Arun Subramaniam and Olivier Joffre and Pierre G. Lutz and Isabelle Lamsoul},

doi = {10.1038/s41467-024-53768-3},

issn = {2041-1723},

year  = {2024},

date = {2024-12-01},

urldate = {2024-12-01},

journal = {Nature Communications},

volume = {15},

number = {1},

pages = {10574},

abstract = {Augmenting the portfolio of therapeutics for type 2-driven diseases is crucial to address unmet clinical needs and to design personalized treatment schemes. An attractive therapy for such diseases would consist in targeting the recruitment of T helper 2 (Th2) lymphocytes to inflammatory sites. Herein, we show the degradation of filamins (FLN) a and b by the ASB2α E3 ubiquitin ligase as a mechanism sustaining Th2 lymphocyte functions. Low levels of FLNa and FLNb confer an elongated shape to Th2 lymphocytes associated with efficient αVβ3 integrin-dependent cell migration. Genes encoding the αVβ3 integrin and ASB2α belong to the core of Th2-specific genes. Using genetically modified mice, we find that increasing the levels of FLNa and FLNb in Th2 lymphocytes reduces airway inflammation through diminished Th2 lymphocyte recruitment in inflamed lungs. Collectively, our results highlight ASB2α and its substrates FLNa and FLNb to alter Th2 lymphocyte-mediated responses.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}