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  1. Article ; Online: Overview of Neutrophilic Biology, Pathophysiology, and Classification of Neutrophilic Dermatoses.

    Delaleu, Jérémie / Bouaziz, Jean-David

    Dermatologic clinics

    2023  Volume 42, Issue 2, Page(s) 147–156

    Abstract: Neutrophilic dermatoses are a group of inflammatory skin conditions characterized by a neutrophilic infiltrate on histopathology with no evidence of infection. These conditions present with a wide range of clinical manifestations, including pustules, ... ...

    Abstract Neutrophilic dermatoses are a group of inflammatory skin conditions characterized by a neutrophilic infiltrate on histopathology with no evidence of infection. These conditions present with a wide range of clinical manifestations, including pustules, bullae, abscesses, papules, nodules, plaques, and ulcers. The classification of neutrophilic dermatoses is based on the localization of neutrophils in the skin. The pathogenic mechanisms of neutrophilic dermatoses involve autoinflammation, neutrophilic dysfunction, clonal somatic mutation and differentiation of the myeloid precursors as encountered in myeloid neoplasm.
    MeSH term(s) Humans ; Dermatitis ; Skin/pathology ; Skin Diseases/pathology ; Biology ; Neutrophils/pathology ; Sweet Syndrome/diagnosis
    Language English
    Publishing date 2023-09-14
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 82798-8
    ISSN 1558-0520 ; 0733-8635
    ISSN (online) 1558-0520
    ISSN 0733-8635
    DOI 10.1016/j.det.2023.08.002
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Immune checkpoint inhibitors unleash pathogenic immune responses against the microbiota.

    Hu, Zishuo Ian / Link, Verena M / Lima-Junior, Djalma S / Delaleu, Jérémie / Bouladoux, Nicolas / Han, Seong-Ji / Collins, Nicholas / Belkaid, Yasmine

    Proceedings of the National Academy of Sciences of the United States of America

    2022  Volume 119, Issue 26, Page(s) e2200348119

    Abstract: Immune checkpoint inhibitors (ICIs) are essential components of the cancer therapeutic armamentarium. While ICIs have demonstrated remarkable clinical responses, they can be accompanied by immune-related adverse events (irAEs). These inflammatory side ... ...

    Abstract Immune checkpoint inhibitors (ICIs) are essential components of the cancer therapeutic armamentarium. While ICIs have demonstrated remarkable clinical responses, they can be accompanied by immune-related adverse events (irAEs). These inflammatory side effects are of unclear etiology and impact virtually all organ systems, with the most common being sites colonized by the microbiota such as the skin and gastrointestinal tract. Here, we establish a mouse model of commensal bacteria-driven skin irAEs and demonstrate that immune checkpoint inhibition unleashes commensal-specific inflammatory T cell responses. These aberrant responses were dependent on production of IL-17 by commensal-specific T cells and induced pathology that recapitulated the cutaneous inflammation seen in patients treated with ICIs. Importantly, aberrant T cell responses unleashed by ICIs were sufficient to perpetuate inflammatory memory responses to the microbiota months following the cessation of treatment. Altogether, we have established a mouse model of skin irAEs and reveal that ICIs unleash aberrant immune responses against skin commensals, with long-lasting inflammatory consequences.
    MeSH term(s) Animals ; Dermatitis/immunology ; Dermatitis/microbiology ; Disease Models, Animal ; Immune Checkpoint Inhibitors/adverse effects ; Immunity/drug effects ; Interleukin-17/metabolism ; Mice ; Microbiota/drug effects ; Microbiota/immunology ; Staphylococcus epidermidis/drug effects ; Staphylococcus epidermidis/immunology ; Symbiosis/drug effects ; T-Lymphocytes/immunology
    Chemical Substances Il17a protein, mouse ; Immune Checkpoint Inhibitors ; Interleukin-17
    Language English
    Publishing date 2022-06-21
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, N.I.H., Intramural
    ZDB-ID 209104-5
    ISSN 1091-6490 ; 0027-8424
    ISSN (online) 1091-6490
    ISSN 0027-8424
    DOI 10.1073/pnas.2200348119
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article: Zoon's plasma cell balanitis associated with male genital lichen sclerosus.

    Delaleu, Jérémie / Cavelier-Balloy, Bénédicte / Bagot, Martine / Fouéré, Sébastien / Dauendorffer, Jean-Noël

    JAAD case reports

    2020  Volume 6, Issue 7, Page(s) 670–672

    Language English
    Publishing date 2020-05-20
    Publishing country United States
    Document type Case Reports
    ZDB-ID 2834220-3
    ISSN 2352-5126
    ISSN 2352-5126
    DOI 10.1016/j.jdcr.2020.05.018
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  4. Article ; Online: Granular parakeratosis involving the glans of the penis and foreskin.

    Delaleu, Jérémie / Moulonguet, Isabelle / Breton, Anne-Laure / Bagot, Martine / Foueré, Sébastien / Dauendorffer, Jean-Noël

    The Journal of dermatology

    2020  Volume 47, Issue 8, Page(s) e295–e296

    MeSH term(s) Foreskin/surgery ; Humans ; Male ; Parakeratosis/diagnosis ; Penis
    Language English
    Publishing date 2020-06-11
    Publishing country England
    Document type Letter
    ZDB-ID 800103-0
    ISSN 1346-8138 ; 0385-2407
    ISSN (online) 1346-8138
    ISSN 0385-2407
    DOI 10.1111/1346-8138.15403
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  5. Article ; Online: Methotrexate-induced Primary Cutaneous Diffuse Large B-cell Lymphoma in Patients with Erythrodermic Cutaneous T-cell Lymphoma.

    Delaleu, Jérémie / Maubec, Eve / Rodrigues, Francois / Lévy, Annie / Szablewski, Vanessa / Laroche, Lilliane / Dereure, Olivier

    Acta dermato-venereologica

    2020  Volume 100, Issue 15, Page(s) adv00226

    Abstract: is missing (Short communication). ...

    Abstract is missing (Short communication).
    MeSH term(s) Epstein-Barr Virus Infections ; Humans ; Lymphoma, Large B-Cell, Diffuse/chemically induced ; Lymphoma, Large B-Cell, Diffuse/drug therapy ; Lymphoma, T-Cell, Cutaneous/chemically induced ; Lymphoma, T-Cell, Cutaneous/diagnosis ; Lymphoma, T-Cell, Cutaneous/drug therapy ; Methotrexate/adverse effects ; Mycosis Fungoides ; Skin Neoplasms/drug therapy
    Chemical Substances Methotrexate (YL5FZ2Y5U1)
    Language English
    Publishing date 2020-08-17
    Publishing country Sweden
    Document type Journal Article
    ZDB-ID 80007-7
    ISSN 1651-2057 ; 0001-5555
    ISSN (online) 1651-2057
    ISSN 0001-5555
    DOI 10.2340/00015555-3554
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Efficacy of tocilizumab in adult H syndrome: a promising therapeutic option.

    Hamann, Pierre / Moguelet, Philippe / Chasset, François / Delaleu, Jeremie / Barbaud, Annick / Senet, Patricia / Frances, Camille / De Risi-Pugliese, Tullia

    International journal of dermatology

    2021  Volume 60, Issue 10, Page(s) e417–e419

    MeSH term(s) Adult ; Antibodies, Monoclonal, Humanized ; Contracture ; Histiocytosis ; Humans ; Interleukin-6 ; Treatment Outcome
    Chemical Substances Antibodies, Monoclonal, Humanized ; Interleukin-6 ; tocilizumab (I031V2H011)
    Language English
    Publishing date 2021-05-05
    Publishing country England
    Document type Letter
    ZDB-ID 412254-9
    ISSN 1365-4632 ; 0011-9059 ; 1461-1244
    ISSN (online) 1365-4632
    ISSN 0011-9059 ; 1461-1244
    DOI 10.1111/ijd.15649
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  7. Article ; Online: Cutaneous clonal mature plasmacytoid dendritic cell dermatosis in patients with myeloid neoplasms.

    Mahévas, Thibault / Osio, Amélie / Larcher, Lise / Clappier, Emmanuelle / Kempf, Werner / Adès, Lionel / Fenaux, Pierre / Sébert, Marie / Delaleu, Jérémie / Jachiet, Marie / Cordoliani, Florence / Charvet, Estelle / Carpentier, Olivier / Itzykson, Raphaël A / Weinborn, Marie / Mardare, Nicoleta / Marco-Bonnet, Joséfina / de Masson, Adèle / Duployez, Nicolas /
    Huynh, Tony / Bouaziz, Jean-David / Vignon-Pennamen, Marie-Dominique / Battistella, Maxime

    Blood advances

    2024  

    Language English
    Publishing date 2024-04-12
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2915908-8
    ISSN 2473-9537 ; 2473-9529
    ISSN (online) 2473-9537
    ISSN 2473-9529
    DOI 10.1182/bloodadvances.2023012489
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  8. Article ; Online: Glucocorticoids dosing in obese subjects: A systematic review.

    Delaleu, Jérémie / Destere, Alexandre / Hachon, Lorry / Declèves, Xavier / Lloret-Linares, Célia

    Therapie

    2019  Volume 74, Issue 4, Page(s) 451–458

    Abstract: Glucocorticoids (GCs) are amongst the most widely used and effective treatments to control inflammatory and autoimmune diseases. In obese subjects, drug dosing adjusted by body weight is problematic, all the more so as patients are at higher risk of GC ... ...

    Abstract Glucocorticoids (GCs) are amongst the most widely used and effective treatments to control inflammatory and autoimmune diseases. In obese subjects, drug dosing adjusted by body weight is problematic, all the more so as patients are at higher risk of GC metabolic side effects. We propose here to describe the determinants of drug pharmacokinetics (PK) in obese subjects and GC pharmacology, and to identify the existing PK studies that may help discussing the best size descriptor for GC dosing in obese subjects. A clinician and a pharmacist screened PubMed using the MeSH Terms: "glucocorticoids" OR "steroidal agents" AND "pharmacokinetics" AND "obesity" OR "overweight". The search was limited to the publications written in English language and to those performed in humans. A systematic search using the MeSH terms was performed until August 31st, 2017. Only three such PK studies have been published so far that compare dexamethasone, prednisolone and methylprednisolone in obese and normal weight subjects. The studies concur that GC partially distribute in the excess of body weight and that adjustment by total body weight (TBW) or by body weight (BW) excess would increase the initial plasma GC concentration after a loading dose and would thus be inappropriate. Contradictory results are observed regarding GC exposure or clearance according to the GC studied. Behind this overwhelming lack of conclusive evidence for adjusting GC by body weight, further PK studies are clearly needed for guiding their dosing. Furthermore, studies demonstrated an increased sensibility to GC, even when GC exposure was reduced, suggesting that adjustment by body weight may not only be unnecessary but also dangerous.
    MeSH term(s) Body Mass Index ; Body Weight/physiology ; Dose-Response Relationship, Drug ; Drug Dosage Calculations ; Glucocorticoids/administration & dosage ; Glucocorticoids/adverse effects ; Glucocorticoids/pharmacokinetics ; Humans ; Obesity/complications ; Obesity/drug therapy ; Obesity/epidemiology ; Obesity/metabolism
    Chemical Substances Glucocorticoids
    Language English
    Publishing date 2019-02-14
    Publishing country France
    Document type Journal Article ; Systematic Review
    ZDB-ID 603474-3
    ISSN 1958-5578 ; 0040-5957
    ISSN (online) 1958-5578
    ISSN 0040-5957
    DOI 10.1016/j.therap.2018.11.016
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  9. Article ; Online: Suppurative keloids: a complication of severe keloid disease.

    Delaleu, Jeremie / Duverger, Lucie / Shourick, Jason / Tirgan, Michael H / Algain, Maysoon / Tounkara, Thierno / Kourouma, Sarah / Bagot, Martine / Petit, Antoine

    International journal of dermatology

    2021  Volume 60, Issue 11, Page(s) 1392–1396

    Abstract: Background: Some keloids show cystic cavities that give rise to acute inflammatory flares and oozing. These suppurative keloids (SK) have rarely been systematically studied. We conducted a retrospective cohort study to evaluate SK frequency and its risk ...

    Abstract Background: Some keloids show cystic cavities that give rise to acute inflammatory flares and oozing. These suppurative keloids (SK) have rarely been systematically studied. We conducted a retrospective cohort study to evaluate SK frequency and its risk factors. We also reviewed microbiological analyses as well as the histological features of removed SKs.
    Methods: Between July 1, 2015, and September 30, 2016, all adult patients attending a specialized keloid clinic were asked to participate. Clinical information and microbiological results were extracted from each patient's file. Histological features were observed and interpreted.
    Results: In this study, we observed an SK rate of 26% for a mean keloid history of 17.2 years. Male gender, African ancestry, and a family history of keloids were significantly associated with suppuration. Microbiological examination revealed commensal skin flora 7/9 (77.8%), Staphylococcus aureus 1/9 (11.1%), and Enterococcus faecalis 1/9 (11.1%).
    Conclusion: Suppuration is a common complication of keloids occurring in patients with severe keloid disease and may arise from pilosebaceous occlusion and aseptic inflammation.
    MeSH term(s) Adult ; Humans ; Keloid/epidemiology ; Keloid/etiology ; Keloid/pathology ; Male ; Medical History Taking ; Retrospective Studies ; Skin/pathology ; Suppuration/pathology
    Language English
    Publishing date 2021-05-11
    Publishing country England
    Document type Journal Article
    ZDB-ID 412254-9
    ISSN 1365-4632 ; 0011-9059 ; 1461-1244
    ISSN (online) 1365-4632
    ISSN 0011-9059 ; 1461-1244
    DOI 10.1111/ijd.15641
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  10. Article ; Online: Mosaic variants in TNFRSF1A: an emerging cause of tumour necrosis factor receptor-associated periodic syndrome.

    Assrawi, Eman / Louvrier, Camille / El Khouri, Elma / Delaleu, Jérémie / Copin, Bruno / Dastot-Le Moal, Florence / Piterboth, William / Legendre, Marie / Karabina, Sonia A / Grateau, Gilles / Amselem, Serge / Giurgea, Irina

    Rheumatology (Oxford, England)

    2022  Volume 62, Issue 1, Page(s) 473–479

    Abstract: Objective: To identify the molecular basis of a systemic autoinflammatory disorder (SAID) evocative of TNF receptor-associated periodic syndrome (TRAPS).: Methods: (i) Deep next generation sequencing (NGS) through a SAID gene panel; (ii) variant ... ...

    Abstract Objective: To identify the molecular basis of a systemic autoinflammatory disorder (SAID) evocative of TNF receptor-associated periodic syndrome (TRAPS).
    Methods: (i) Deep next generation sequencing (NGS) through a SAID gene panel; (ii) variant allele distribution in peripheral blood subpopulations; (iii) in silico analyses of mosaic variants using TNF receptor superfamily 1A (TNFRSF1A) crystal structure; (iv) review of the very rare TNFRSF1A mosaic variants reported previously.
    Results: In a 36-year-old man suffering from recurrent fever for 12 years, high-depth NGS revealed a TNFRSF1A mosaic variant, c.176G>A p.(Cys59Tyr), which Sanger sequencing failed to detect. This mosaic variant displayed a variant allele fraction of 14% in whole blood; it affects both myeloid and lymphoid lineages. p.(Cys59Tyr), a recurrent germline pathogenic variant, affects a crucial cysteine located in the first cysteine-rich domain (CRD1) and involved in a disulphide bridge. Introduction of a tyrosine at this position is expected to disrupt the CRD1 structure. Review of the three previously reported TNFRSF1A mosaic variants revealed that they are all located in a small region of CRD2 and that germinal cells can be affected.
    Conclusion: This study expands the localization of TNFRSF1A mosaic variants to the CRD1 domain. Noticeably, residues involved in germline TNFRSF1A mutational hot spots can also be involved in post-zygotic mutational events. Including our study, only four patients have been thus far reported with TNFRSF1A mosaicism, highlighting the need for a high-depth NGS-based approach to avoid the misdiagnosis of TRAPS. Genetic counselling has to consider the potential occurrence of TNFRSF1A mosaic variants in germinal cells.
    MeSH term(s) Male ; Humans ; Adult ; Cysteine/genetics ; Receptors, Tumor Necrosis Factor, Type I/genetics ; Fever/genetics ; Hereditary Autoinflammatory Diseases/genetics ; Hereditary Autoinflammatory Diseases/diagnosis ; Mutation
    Chemical Substances Cysteine (K848JZ4886) ; Receptors, Tumor Necrosis Factor, Type I ; TNFRSF1A protein, human
    Language English
    Publishing date 2022-06-01
    Publishing country England
    Document type Case Reports ; Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1464822-2
    ISSN 1462-0332 ; 1462-0324
    ISSN (online) 1462-0332
    ISSN 1462-0324
    DOI 10.1093/rheumatology/keac274
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