@article{pmid40190069,

title = {Management of congenital ichthyoses: guidelines of care: Part two: 2024 update},

author = {Juliette Mazereeuw-Hautier and Amy S Paller and Edel O'Toole and Isabelle Dreyfus and Christine Bodemer and Masashi Akiyama and Andrea Diociaiuti and Maya El Hachem and Judith Fischer and Rogelio Gonzalez-Sarmiento and Carlos Gutiérrez-Cerrajero and Hagen Ott and Cristina Has and Nathalie Jonca and Céline Granier Tournier and Ana Martinez and Heiko Traupe and Carmen Maria Salavastru and Matthias Schmuth and Eli Sprecher and Kathrin Giehl and Mandy Aldwin and Ruth Anton Morales and Saturnino Santos and Marie-Anne Morren and Anne Audouze and Raman Malhotra and Karin Veldman and Joanna Narbutt and Kira Süßmuth and Antoni Gostynski and Angela Hernandez-Martin},

doi = {10.1093/bjd/ljaf077},

issn = {1365-2133},

year  = {2025},

date = {2025-06-01},

urldate = {2025-06-01},

journal = {Br J Dermatol},

volume = {193},

number = {1},

pages = {28--43},

abstract = {In 2019, a group of experts published the first European guidelines for the management of congenital ichthyoses after a multidisciplinary expert meeting held in 2016. An update of these guidelines and literature search was planned every 5 years, given the clinical, molecular and therapeutic advances, including the use of biologic therapies. We present here updated guidelines that have been developed by a reorganized multidisciplinary group of international experts after a systematic review of recent literature, discussions and consensus reached at an expert conference held in June 2023. The guidelines provide summarized evidence and expert-based recommendations that aim to guide clinicians in the management of these rare and often complex diseases. These guidelines consist of two sections. Part one is reported elsewhere. Here, Part two covers the management of complications (eye, ear-nose-throat, pruritus, pain, cutaneous infections, vaccinations, growth failure and nutritional deficiency, hair and nail anomalies, reaction to hot and cold climates, physical limitations, comorbidities) and the particularities of the neonatal period and Netherton syndrome.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid40156154,

title = {Management of congenital ichthyoses: guidelines of care: Part one: 2024 update},

author = {Juliette Mazereeuw-Hautier and Amy S Paller and Isabelle Dreyfus and Eli Sprecher and Edel O'Toole and Christine Bodemer and Masashi Akiyama and Andrea Diociaiuti and Maya El Hachem and Judith Fischer and Rogelio Gonzalez-Sarmiento and Carlos Gutiérrez-Cerrajero and Hagen Ott and Cristina Has and Nathalie Jonca and Céline Granier Tournier and Sarah Milesi and Hélène Texier and Ana Martinez and Heiko Traupe and Carmen Maria Salavastru and Matthias Schmuth and Kathrin Giehl and Mandy Aldwin and Ruth Anton Morales and Saturnino Santos and Marie-Anne Morren and Anne Audouze and Raman Malhotra and Karin Veldman and Joanna Narbutt and Kira Süßmuth and Angela Hernandez-Martin and Antoni Gostynski},

doi = {10.1093/bjd/ljaf076},

issn = {1365-2133},

year  = {2025},

date = {2025-06-01},

urldate = {2025-06-01},

journal = {Br J Dermatol},

volume = {193},

number = {1},

pages = {16--27},

abstract = {In 2019, a group of experts published the first European guidelines for the management of congenital ichthyoses after a multidisciplinary expert meeting held in 2016. An update of these guidelines and literature search was planned every 5 years, given the clinical, molecular and therapeutic advances, including the use of biologic therapies. We present here updated guidelines that have been developed by a reorganized multidisciplinary group of international experts. The evidence is based on a systematic review of recent literature, discussions and consensus reached at an expert conference held in June 2023. The guidelines provide summarized evidence and expert-based recommendations that aim to guide clinicians in the management of these rare and often complex diseases. These guidelines consist of two sections. This Part one covers topical and systemic therapies (including oral retinoids, biologics and Janus kinase inhibitors), future therapeutic approaches, psychosocial management, telemedicine, communicating the diagnosis and genetic counselling, prenatal diagnosis and preimplantation genetic testing.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{hiensch_immunoactinopathies_2025,

title = {Immunoactinopathies revisited: understanding clinical manifestations and biological pathways},

author = {Fleur Hiensch and Loïc Dupré and Elisabeth Salzer},

doi = {10.1182/blood.2024026763},

issn = {1528-0020},

year  = {2025},

date = {2025-06-01},

urldate = {2025-06-01},

journal = {Blood},

volume = {145},

number = {23},

pages = {2709–2732},

abstract = {Immune cell functionality is highly dependent on the actin cytoskeleton. The actin cytoskeleton is regulated by a complex molecular machinery that involves multiple genes. Mutations in these genes can cause inborn errors of immunity, also termed immunoactinopathies, of which Wiskott-Aldrich syndrome is the best-characterized entity. Currently, mutations in 23 genes can be considered causative of immunoactinopathies. Immunoactinopathies are rare disease entities with complex combinations of clinical manifestations, including immunodeficiency, immune dysregulation, malignancies, atopy, thrombocytopenia and bleeding, skin involvement, or congenital defects. Prompt diagnosis is crucial, because hematopoietic stem cell transplantation in an early phase can offer cure and prevent further complications. This review provides a detailed summary of the clinical experience with immunoactinopathies so far, elaborates on the most distinguishing features of immunoactinopathies by providing a clinical categorization, and links this information to the underlying biological pathways. This information may be of help to clinicians in the diagnosis of patients and to eventually improve patient care.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Coulibaly2025,

title = {Id2 levels determine the development of effector vs. exhausted tissue-resident memory CD8+ T cells during CNS chronic infection},

author = {Aboubacar Sidiki K. Coulibaly and Lucie Nozeran and Céline Thomann and Marine Alis and Emilie Bassot and Ali Hassan and Rémi Porte and Marcy Belloy and Nicolas Blanchard and Frederick Masson},

doi = {10.1016/j.celrep.2025.115861},

issn = {2211-1247},

year  = {2025},

date = {2025-06-00},

journal = {Cell Reports},

volume = {44},

number = {6},

publisher = {Elsevier BV},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid40417978,

title = {The Inactive X Chromosome: A Genetic Driver of Female-Biased Rheumatic Autoimmune Disorders?},

author = {Léa Ferrayé and Mélissa Nieucel and Magali Savignac and Julie Chaumeil and Jean-Charles Guéry},

doi = {10.1002/eji.202451331},

issn = {1521-4141},

year  = {2025},

date = {2025-05-01},

urldate = {2025-05-01},

journal = {Eur J Immunol},

volume = {55},

number = {5},

pages = {e202451331},

abstract = {Females have a better ability to resolve infections compared to males, but also a greater susceptibility to develop autoimmunity. Besides the initial interest in the contribution of sex-steroid hormone signaling, the role of genetic factors linked to the X chromosome has recently received much attention. In humans and mice, the number of X chromosomes, rather than sex-steroid hormones, is associated with a higher risk to develop autoimmunity, particularly rheumatic diseases, such as SLE, Sjögren's syndrome, or systemic sclerosis. In this review, we will summarize the recent advances in the various mechanisms and pathways involving the X chromosome in female sex-biased autoimmune diseases. We will particularly focus on the experimental evidence suggesting that expression of X-linked genes due to dysregulation in X chromosome inactivation maintenance could contribute to the female predisposition for autoautoimmunity.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid39306032,

title = {Superficial Conjunctival Cells from Dupilumab-Treated Patients with Atopic Dermatitis with Ocular Adverse Events Display a Transcriptomic Psoriasis Signature},

author = {Myriam Cassagne and Stéphane Galiacy and Anna Kychygina and Eric Chapotot and Martin Wallaert and Bertrand Vabres and Marie Tauber and Sébastien Barbarot and Carle Paul and Pierre Fournié and Michel Simon},

doi = {10.1016/j.jid.2024.08.024},

issn = {1523-1747},

year  = {2025},

date = {2025-05-01},

urldate = {2025-05-01},

journal = {J Invest Dermatol},

volume = {145},

number = {5},

pages = {1050--1059.e6},

abstract = {Dupilumab has demonstrated efficacy in the treatment of atopic dermatitis. However, a subset of patients experiences ocular adverse events (OAEs), including conjunctivitis and dry eye syndrome, the pathological mechanisms of which are still unknown. In a bicentric study, we used DNA microarray analysis to compare the transcriptome of conjunctival cells of patients with atopic dermatitis collected by impression cytology before (M0) and 4 months after (M4) initiating dupilumab treatment. Thirty-six patients were included and divided in 2 groups according to their ophthalmological status at M4: 12 with OAEs (OAE+) and 24 without (OAE-). The analysis revealed 52 differentially expressed genes between OAE+ and OAE- patients at M0 and 113 at M4. Ingenuity Pathway Analysis enrichment revealed a psoriasis signature in OAE+ patients, both before and after OAE outcomes. In addition, we noticed the overexpression of several genes involved in keratinocyte differentiation, particularly encoding cornified envelope components. Among the 16 differentially expressed genes selected for real-time RT-PCR validation, 9 were confirmed as upregulated at M4 in OAE+ versus OAE- patients, validating the psoriasis signature, whereas MUC7 was downregulated. In conclusion, these results suggest that a conjunctival transcriptomic profile predisposes some patients with atopic dermatitis to developing OAEs upon dupilumab treatment.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid40138920,

title = {Biological solutions activated by cold plasma at atmospheric pressure: A new therapeutic approach for skin wound healing},

author = {Solène Roux and Aurélie Marchès and Stéphane Galiacy and Nofel Merbahi and Michel Simon},

doi = {10.1016/j.biopha.2025.118001},

issn = {1950-6007},

year  = {2025},

date = {2025-05-01},

urldate = {2025-05-01},

journal = {Biomed Pharmacother},

volume = {186},

pages = {118001},

abstract = {Chronic wounds are a major public health problem, and nearly 35 % of them do not heal with conventional treatments. The direct application of cold plasmas at atmospheric pressure, partially ionized gases, is an emerging technology with a range of potential biomedical applications, including the improvement of wound healing. A new method that is easier to implement has been developed: the use of biological solutions exposed to cold plasmas at atmospheric pressure, known as plasma-activated media (PAM). Numerous preclinical studies and in vitro models indicate that PAM treatments facilitate wound healing by promoting the migration of cell types such as keratinocytes, fibroblasts and mesenchymal stem/stromal cells, stimulating angiogenesis, and inhibiting bacterial proliferation, all of which are critical to this vital process. PAM treatments modulate the inflammatory response, induce the expression of growth factors and matrix metalloproteinases, reduce cellular adhesion, promote cytoskeletal modifications and activate several biochemical pathways involved in the wound healing process, possibly through the action of plasma-generated reactive oxygen and nitrogen species. Some studies have shown that PAM may have applications in the treatment of other skin conditions either by reducing the production of pro-inflammatory cytokines or by inducing apoptosis of tumor cells. PAM treatments therefore represent a promising new therapy for the management of dermatological conditions, particularly for chronic skin and mucosal wounds.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid40277215,

title = {Epidermolytic ichthyosis: New insights and ongoing challenges},

author = {J Mazereeuw-Hautier},

doi = {10.1111/jdv.20636},

issn = {1468-3083},

year  = {2025},

date = {2025-05-01},

urldate = {2025-05-01},

journal = {J Eur Acad Dermatol Venereol},

volume = {39},

number = {5},

pages = {893--894},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid40399512,

title = {Wastewater Surveillance to Estimate and Characterize Hepatitis E Virus Circulation},

author = {C Dimeglio and O Schlosser and S Laperche and C De Smet and S Demmou and J Latour and N Jeanne and M Tribout and N Bleuez and J Figoni and F Abravanel and S Lhomme and J Izopet},

doi = {10.1007/s12560-025-09644-4},

issn = {1867-0342},

year  = {2025},

date = {2025-05-01},

urldate = {2025-05-01},

journal = {Food Environ Virol},

volume = {17},

number = {2},

pages = {30},

abstract = {Hepatitis E virus (HEV) is a cause of enterically transmitted hepatitis around the world. Because of the high frequency of asymptomatic infections, the magnitude of HEV infection is underestimated. Wastewater monitoring could be useful to improve our knowledge on HEV epidemiology. In this study, we analyzed the capacity of wastewater surveillance to give an insight into the circulation and the diversity of HEV in two French cities. HEV RNA was detected and quantified by digital PCR in 115 untreated composite wastewater samples collected weekly at the inlet of wastewater treatment plants (WWTPs), 58 at Toulouse WWTP and 57 at Dunkerque WWTP. Plasma HEV RNA in blood donors was detected by a commercial assay (Roche Cobas) over the same period in the same area. HEV diversity was analyzed using long-read single-molecule real-time sequencing (Pacific Biosciences). HEV RNA was detected in 88% and 95% wastewater samples collected at Toulouse (Occitanie region, Southern France) and Dunkerque (Hauts-de-France region, Northern France) WWTPs, respectively. HEV RNA concentration ranged between 4.1 and 5.7 log copies/L and was almost similar between the two sites. A long orf2 fragment of HEV genome (1030 nucleotides) was obtained and sequenced in 45% and 70% of positive HEV RNA wastewater samples collected at Toulouse site and Dunkerque site, respectively. Out of 31 strains identified in Toulouse wastewater, 24 were HEV-3c (77%), 6 were HEV-3f (19%), and 1 was HEV-3h (3%). Out of 55 strains identified in Dunkerque, 30 were HEV-3c (55%) and 25 were HEV-3f (45%). All HEV RNA-positive samples from blood donors that could be genotyped during the study period contained HEV-3. Subtype distribution in 51 blood donors living in Toulouse did not differ from that in Toulouse wastewater. The HEV-3 subtype distribution in 51 Hauts-de-France region blood donors and in Dunkerque wastewater were different, but the predominant subtype was the same (HEV-3c). Lastly, we explored the link between the measurement of viral loads in wastewater and the extent of infection in the served population. Although a good correlation between the peaks of positive HEV RNA estimated in wastewater samples and that observed in blood donors was observed with a lag of + 3 weeks for Toulouse, the correlation was weaker for Dunkerque. Wastewater surveillance system applied locally could be very useful for assessing the HEV infection status of a population.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{nokey,

title = {Antibody-secreting cell repertoires hold high-affinity anti-rocuronium specificities that can induce anaphylaxis in vivo},

author = {Alice Dejoux and Qianqian Zhu and Adam Woolfe and Ophélie Godon and Sami Ellouze and Guillaume Mottet and Carlos Castrillon and Caitlin Gillis and Cyprien Pecalvel and Christelle Ganneau and Bruno Iannascoli and Frédéric Lemoine and Frederick Saul and Patrick England and Laurent L Reber and Aurélie Gouel-Chéron and Luc de Chaisemartin and Ahmed Haouz and Gaël A Millot and Sylvie Bay and Annabelle Gérard and Friederike Jönsson and Sylvie Chollet-Martin and Pierre Bruhns},

url = {https://pubmed.ncbi.nlm.nih.gov/39892658/},

doi = {10.1016/j.jaci.2025.01.025},

year  = {2025},

date = {2025-05-01},

urldate = {2025-05-01},

journal = {J Allergy Clin Immunol},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid40231463,

title = {SLAMF7 and SLAMF8 receptors shape human plasmacytoid dendritic cell responses to intracellular bacteria},

author = {Joaquín Miguel Pellegrini and Anne Keriel and Laurent Gorvel and Sean Hanniffy and Vilma Arce-Gorvel and Mile Bosilkovski and Javier Solera and Stéphane Méresse and Sylvie Mémet and Jean-Pierre Gorvel},

doi = {10.1172/JCI182467},

issn = {1558-8238},

year  = {2025},

date = {2025-04-01},

urldate = {2025-04-01},

journal = {J Clin Invest},

volume = {135},

number = {8},

abstract = {Plasmacytoid dendritic cells (pDCs), professional type I IFN-producing cells, have been implicated in host responses against bacterial infections. However, their role in host defense is debated, and the operating molecular mechanisms are unknown. Certain signaling lymphocyte activation molecule family (SLAMF) members act as microbial sensors and modulate immune functions in response to infection. Here, human blood transcriptomic analyses reveal the involvement of SLAMF7 and SLAMF8 in many infectious diseases, with elevated levels associated with type I IFN responses in salmonellosis and brucellosis patients. We further identify SLAMF7 and SLAMF8 as key regulators of human pDC function. They activate pDC maturation and cytokine production during infection with bacteria that induce acute (Salmonella) or chronic (Brucella) inflammation. SLAMF7 and SLAMF8 signal through NF-κB, IRF7, and STAT-1, and limit mitochondrial ROS accumulation upon Salmonella infection. Remarkably, this SLAMF7/8-dependent control of mitochondrial ROS levels favors bacterial persistence and NF-κB activation. Overall, our results unravel essential shared multifaceted roles of SLAMF7 and SLAMF8 in finely tuning human pDC responses to intracellular bacterial infections with potential for future diagnostic and therapeutic applications.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid39212522,

title = {Large-scale HEV genotype 3 outbreak on New Caledonia Island},

author = {Florence Abravanel and Clémence Vignon and Ambroise Mercier and Jean-Baptiste Gaumery and Antoine Biron and Clément Filisetti and Marie-Amélie Goujart and Julien Colot and Xavier Chamillard and Justine Demortier and Maxime Raz and Catherine Boutet and Laura Dupont and Sylvie Duval and Catherine Castric and Denise Desoutter and Anais Desoutter and Marjorie Verge and Clémentine De Smet and Sofia Demmou and Sébastien Lhomme and Ann-Claire Gourinat and Florence Nicot and Jacques Izopet},

doi = {10.1097/HEP.0000000000001081},

issn = {1527-3350},

year  = {2025},

date = {2025-04-01},

urldate = {2025-04-01},

journal = {Hepatology},

volume = {81},

number = {4},

pages = {1343--1352},

abstract = {BACKGROUND AND AIMS: Several symptomatic cases of HEV infections were reported to the New Caledonia Island Public Health Service between August and December 2023. This prompted epidemiological and virological investigations to identify the source of infection.nnAPPROACH AND RESULTS: HEV RNA was assessed in symptomatic patients, various food items, and pig farms on the Island. HEV strains were characterized by sequencing. A seroprevalence study was also conducted on asymptomatic blood donors before and after the outbreak. One hundred twenty-seven symptomatic cases were reported. Hospitalization was required for 29/127 patients (22.8%). Hospitalized patients presented more frequently with comorbidities, including liver and cardiovascular diseases (80.7% vs. 27%, p < 0.01), and 3 persons died (2.3%). Among the 100 HEV RNA-positive samples received at the French National Reference Centre for HEV, viral sequencing was possible for 76 samples. All strains were identified as HEV genotype 3, and 74/76 strains were grouped together (nucleotide identity: 98%-100%). Full-length sequencing indicated a new HEV-3 subtype within HEV-3 subclade abk. Only genotype 3f strains were detected on the Island's pig farms. No food items tested positive for HEV RNA. The seroprevalence of HEV IgG and IgM in blood donors was 9.2% (9/98) and 0%, respectively, in 2020, rising to 17.3% (17/98) and 2% (2/98) in 2024.nnCONCLUSIONS: Although all previous large-scale epidemics in Asia and Africa were associated with HEV-1 or 2, the New Caledonia outbreak was linked to HEV-3. A high number of symptomatic cases were admitted to the hospital, with a case-fatality rate of 2.3%.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid40086106,

title = {Human placental models for studying viral infections},

author = {Charlène Martin and Mathilde Bergamelli and Hélène Martin and Mélinda Bénard and Charlotte Tscherning and Cécile E Malnou},

doi = {10.1016/j.coviro.2025.101454},

issn = {1879-6265},

year  = {2025},

date = {2025-04-01},

urldate = {2025-04-01},

journal = {Curr Opin Virol},

volume = {71},

pages = {101454},

abstract = {Viral infections during pregnancy represent a major threat to maternal, fetal, and neonatal health outcome, with a high risk of vertical transmission. It is therefore crucial to understand the mechanisms underlying the interaction between viruses and placenta, which ensures communication between maternal and fetal compartments throughout pregnancy. Human placental models, both in vitro and ex vivo, enable to dissect in detail these interactions. By studying in detail viral entry, replication, and immune responses within the placenta, they represent ideal tools for analyzing the effects of various viruses on pregnancy outcomes. In addition, these models serve as platforms for evaluating diagnostic and therapeutic approaches to protect pregnant women and their babies from viral infections. This review examines recent advances, the main advantages and limitations of different human placental models and discusses their potential to improve our understanding of virus-placenta interactions, thereby contributing to improved maternal and fetal health.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid40300021,

title = {Toxoplasma gondii chronic infection decreases visceral nociception through peripheral opioid receptor signaling},

author = {Alexis Audibert and Xavier Mas-Orea and Léa Rey and Marcy Belloy and Emilie Bassot and Louise Battut and Gilles Marodon and Frederick Masson and Matteo Serino and Nicolas Cenac and Gilles Dietrich and Chrystelle Bonnart and Nicolas Blanchard},

doi = {10.1371/journal.ppat.1013106},

issn = {1553-7374},

year  = {2025},

date = {2025-04-01},

journal = {PLoS Pathog},

volume = {21},

number = {4},

pages = {e1013106},

abstract = {By eliciting immune activation in the digestive tract, intestinal pathogens may perturb gut homeostasis. Some gastrointestinal infections can indeed increase the risk of developing post-infectious irritable bowel syndrome (PI-IBS). Intriguingly, the prevalent foodborne parasite Toxoplasma gondii has not been linked to the development of PI-IBS and the impact of this infection on colon homeostasis remains ill-defined. We show in a mouse model that latent T. gondii decreases visceral nociceptive responses in an opioid signaling-dependent manner. Despite the accumulation of Th1 and cytotoxic T cells in the colon of latently infected mice, the selective invalidation of enkephalin gene in T cells ruled out the involvement of T cell-derived enkephalins in hypoalgesia. These findings provide clues about how this widespread infection durably shapes the gut immune landscape and modifies intestinal physiological parameters. They suggest that in contrast to other gut microbes, T. gondii infection could be negatively associated with abdominal pain.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid39954680,

title = {Mammary intraepithelial lymphocytes promote lactogenesis and offspring fitness},

author = {Dan Corral and Eduard Ansaldo and Jérémie Delaleu and Andrea C Pichler and Juraj Kabat and Cihan Oguz and Ana Teijeiro and Daniel Yong and Mahnoor Abid and Claudia A Rivera and Verena M Link and Katharine Yang and Liang Chi and Jia Nie and Olena Kamenyeva and Yiping Fan and Jerry Kok Yen Chan and Florent Ginhoux and Rémy Bosselut and Yasmine Belkaid},

doi = {10.1016/j.cell.2025.01.028},

issn = {1097-4172},

year  = {2025},

date = {2025-03-01},

urldate = {2025-03-01},

journal = {Cell},

volume = {188},

number = {6},

pages = {1662--1680.e24},

abstract = {Breastfeeding is an obligatory requirement of mammalian survival. This fundamental process is associated with the adaptation of maternal physiology, including the transformation of the mammary gland into a milk-secreting organ. How maternal immunity contributes to mammary gland remodeling and function remains largely unknown. Here, we show that maternal adaptive immunity plays a critical role in shaping lactogenesis. Specifically, physiological adaptation during pregnancy is associated with thymic involution and a paradoxical enrichment in intraepithelial lymphocyte (IEL) precursors that no longer migrate to the gut but instead preferentially accumulate within the mammary gland. IEL precursors differentiate into T-bet-expressing unconventional CD8αα lymphocytes in an IL-15-dependent manner. Mammary IELs control milk production by favoring the differentiation and maturation of contractile and milk-secreting cells, thereby promoting offspring fitness. Altogether, this work uncovers a contribution of the maternal adaptive immune system in organismal remodeling during pregnancy that is associated with mammary gland development and function.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid39670995,

title = {Altered X-chromosome inactivation of the TLR7/8 locus and heterogeneity of pDCs in systemic sclerosis},

author = {Yong Du and Bérénice Faz-Lopez and Marie Dominique Ah Kioon and Claire Cenac and Michael Pierides and Kimberly S Lakin and Robert F Spiera and Julie Chaumeil and Marie-Elise Truchetet and Jessica K Gordon and Jean-Charles Guéry and Franck J Barrat},

doi = {10.1084/jem.20231809},

issn = {1540-9538},

year  = {2025},

date = {2025-03-01},

urldate = {2025-03-01},

journal = {J Exp Med},

volume = {222},

number = {3},

abstract = {Systemic sclerosis (SSc) is an autoimmune disease that has a strong female predominance. Both the X-linked TLR7 and TLR8 can induce type I IFN (IFN-I) by plasmacytoid DCs (pDCs), which can promote fibrosis. We identified five subclusters of pDCs, including ISGhigh clusters that were over-represented in SSc patients. We observed that both TLR7 and TLR8 genes escape from X chromosome inactivation (XCI) at higher frequency in pDCs of SSc patients, which was associated with changes in TLR7 protein profile. Combined DNA/RNA FISH analysis revealed that the TLR7/8 locus is preferentially located outside of the inactive X (Xi) territory when TLR7 is expressed, suggesting that higher-order loop formation is linked to TLR7/8 expression from the Xi. Furthermore, the expression levels of XIST and the transcriptional repressor SPEN were reduced in SSc pDCs. Hence, our data revealed the heterogeneity of pDCs in SSc and suggested that altered XCI at the TLR7/8 locus may contribute to the chronic IFN-I activity of pDCs in female SSc patients.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid40123225,

title = {Meibomian gland atrophy in Keratoconus: A case-control study},

author = {Camille Morice and Valentine Saunier and Maeva Kyheng and Pierre Fournie and David Touboul},

doi = {10.1177/11206721251327651},

issn = {1724-6016},

year  = {2025},

date = {2025-03-01},

urldate = {2025-03-01},

journal = {Eur J Ophthalmol},

pages = {11206721251327651},

abstract = {PurposeTo assess the Meibomian Gland Atrophy (MGA) in keratoconus patients by comparison to healthy controls.SettingFrench Keratoconus national reference center, Bordeaux, France.DesignObservational, monocentric, comparative case control study.MethodsEighty-eight keratoconic eyes free of any surgical treatment (KC group) and 88 healthy eyes (NKC group) matched for age and gender, included from December 2018 to May 2019, underwent infrared meibography providing a meiboscore of MGA (primary outcome measure), scaled from 0 to 6. Secondary outcomes including Lipid Layer Thickness (LLT) assessment using interferometry, Tear Break-Up Time (T-BUT) evaluated by a slit lamp examination, corneal OCT-based topography, and two dry eye questionnaires (OSDI and SPEED) filled by the patients during the consultation.ResultsA significant difference in distribution of meiboscore scores between groups ( < 0.0001 for total, superior and inferior meiboscore) was found, with lower scores in controls compared to eyes with keratoconus. Using a cut-off value of ≥2 as abnormal meiboscore, 64.8% of eyes of cases had abnormal meiboscore by comparison to only 27.3% of controls (OR, 4.91; 95%CI, 2.56 to 9.38). Patients with keratoconus had higher OSDI (mean difference 15.3, 95%CI 1.8 to 1.7) and SPEED (mean difference 2.5, 95%CI 2.5 to 4.5) results. No significant difference was found in T-BUT whereas keratitis was more common in cases.ConclusionKeratoconus was associated with higher meibomian gland atrophy in this study.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid39811760,

title = {Reconstructed Epidermis Produced with Atopic Dog Keratinocytes Only Exhibit Skin Barrier Defects after the Addition of Proinflammatory and Allergic Cytokines},

author = {Daniel Combarros and Rahma Brahmi and Emma Musaefendic and Alizée Heit and Jevgenija Kondratjeva and Fabien Moog and Charline Pressanti and Line A Lecru and Sabine Arbouille and Catherine Laffort and Dominique Goudounèche and Jessie Brun and Michel Simon and Marie-Christine Cadiergues},

doi = {10.1016/j.xjidi.2024.100330},

issn = {2667-0267},

year  = {2025},

date = {2025-03-01},

urldate = {2025-03-01},

journal = {JID Innov},

volume = {5},

number = {2},

pages = {100330},

abstract = {Our objectives were to explore epidermal barrier defects in dogs with atopic dermatitis and to determine whether the defects are genetically determined or secondary to skin inflammation. First, the expression of filaggrin, corneodesmosin, and claudin1, analyzed using indirect immunofluorescence in skin biopsies collected from 32 healthy and 32 dogs with atopic dermatitis, was weaker in the atopic skin ( .003). Second, primary keratinocytes of atopic dogs and healthy dogs were used to produce 3-dimensional reconstructed canine epidermis. The expression of the same proteins was analyzed using indirect immunofluorescence, immunoblotting, and RT-qPCR, whereas reconstructed canine epidermis morphology was investigated by transmission electron microscopy, and the barrier was investigated by functional assays. Next, inflammatory cytokines (IL-4, IL-13, IL-31, and TNFα) were added to the culture medium. The morphology, protein expression, and barrier function of the reconstructed canine epidermis were similar whether produced with keratinocytes from healthy dogs or dogs with atopy. Addition of inflammatory cytokines impaired the protein expression and epidermal barrier of the 2 types of reconstructed canine epidermis equally. To conclude, the reduced expression of epidermal barrier proteins observed in vivo was not reproduced in vitro unless cytokines were used, suggesting that it is induced by the inflammatory milieu.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{nokey,

title = {LuLIPLEX: A Fast, Highly Sensitive, and Multiplexed Method for the Detection of IgE Against Major Allergens},

author = {Edouard Leveque and Cyprien Pecalvel and Natacha Casanovas and Sophie Goyard and Yves L Janin and Thierry Rose and Benjamin Trouche-Estival and Pol André Apoil and Marine Michelet and Laurent Guilleminault and Laurent L Reber},

url = {https://pubmed.ncbi.nlm.nih.gov/39601619/},

doi = {10.1111/all.16403},

year  = {2025},

date = {2025-03-01},

urldate = {2025-03-01},

journal = {Allergy},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{inacio_signature_2025,

title = {Signature cytokine-associated transcriptome analysis of effector γδ T cells identifies subset-specific regulators of peripheral activation},

author = {Daniel Inácio and Tiago Amado and Ana Pamplona and Daniel Sobral and Carolina Cunha and Rita F. Santos and Liliana Oliveira and Nelly Rouquié and Alexandre M. Carmo and Renaud Lesourne and Anita Q. Gomes and Bruno Silva-Santos},

doi = {10.1038/s41590-024-02073-8},

issn = {1529-2916},

year  = {2025},

date = {2025-03-01},

urldate = {2025-03-01},

journal = {Nature Immunology},

volume = {26},

number = {3},

pages = {497–510},

abstract = {γδ T cells producing either interleukin-17A (γδ17 cells) or interferon-γ (γδIFN cells) are generated in the mouse thymus, but the molecular regulators of their peripheral functions are not fully characterized. Here we established an Il17a-GFP:Ifng-YFP double-reporter mouse strain to analyze at unprecedented depth the transcriptomes of pure γδ17 cell versus γδIFN cell populations from peripheral lymph nodes. Within a very high fraction of differentially expressed genes, we identify a panel of 20 new signature genes in steady-state γδ17 cells versus γδIFN cells, which we further validate in models of experimental autoimmune encephalomyelitis and cerebral malaria, respectively. Among the signature genes, we show that the co-receptor CD6 and the signaling protein Themis promote the activation and proliferation of peripheral γδIFN cells in response to T cell antigen receptor stimulation in vitro and to Plasmodium infection in vivo. This resource can help to understand the distinct activities of effector γδ T cell subsets in pathophysiology.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}