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Article ; Online: Omenn Syndrome in Two Infants with Different Hypomorphic Variants in Janus Kinase 3.

Tsilifis, Christo / Spegarova, Jarmila Stremenova / Good, Ross / Griffin, Helen / Engelhardt, Karin R / Graham, Sophie / Hughes, Stephen / Arkwright, Peter D / Hambleton, Sophie / Gennery, Andrew R

Journal of clinical immunology

2024 Volume 44, Issue 4, Page(s) 98

Abstract: Biallelic null or hypomorphic variants in JAK3 cause SCID and less frequently Omenn syndrome. We investigated homozygous hypomorphic JAK3 mutations in two patients, and expression and function of a novel ... ...

Abstract	Biallelic null or hypomorphic variants in JAK3 cause SCID and less frequently Omenn syndrome. We investigated homozygous hypomorphic JAK3 mutations in two patients, and expression and function of a novel JAK3
MeSH term(s)	Humans ; Infant ; Interleukin-15 ; Interleukin-2 ; Interleukin-7 ; Janus Kinase 3/genetics ; Leukocytes, Mononuclear ; Severe Combined Immunodeficiency/diagnosis ; Severe Combined Immunodeficiency/genetics ; Severe Combined Immunodeficiency/therapy
Chemical Substances	Interleukin-15 ; Interleukin-2 ; Interleukin-7 ; Janus Kinase 3 (EC 2.7.10.2) ; JAK3 protein, human (EC 2.7.10.2)
Language	English
Publishing date	2024-04-10
Publishing country	Netherlands
Document type	Case Reports ; Journal Article
ZDB-ID	779361-3
ISSN	1573-2592 ; 0271-9142
ISSN (online)	1573-2592
ISSN	0271-9142
DOI	10.1007/s10875-024-01699-5
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Article ; Online: Congenital nephrotic syndrome in IL7Rα-SCID: A rare feature of maternofetal graft-versus-host disease.

Tsilifis, Christo / Slatter, Mary / Cordeiro, Ana Isabel / Hambleton, Sophie / Engelhardt, Karin R / Griffin, Helen / Gennery, Andrew R / Neves, João Farela

The journal of allergy and clinical immunology. In practice

2021 Volume 9, Issue 11, Page(s) 4151–4153.e1

MeSH term(s)	Graft vs Host Disease/diagnosis ; Humans ; Nephrotic Syndrome/diagnosis
Language	English
Publishing date	2021-06-18
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2843237-X
ISSN	2213-2201 ; 2213-2198
ISSN (online)	2213-2201
ISSN	2213-2198
DOI	10.1016/j.jaip.2021.05.040
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Article: IL-10 in humans: lessons from the gut, IL-10/IL-10 receptor deficiencies, and IL-10 polymorphisms.

Engelhardt, Karin R / Grimbacher, Bodo

Current topics in microbiology and immunology

2014 Volume 380, Page(s) 1–18

Abstract: Inflammatory bowel disease (IBD) represents a heterogeneous group of gastrointestinal disorders, where commensal gut flora provokes an either (a) insufficient or (b) uncontrolled immune response. This results either in a lack of or in excessive ... ...

Abstract	Inflammatory bowel disease (IBD) represents a heterogeneous group of gastrointestinal disorders, where commensal gut flora provokes an either (a) insufficient or (b) uncontrolled immune response. This results either in a lack of or in excessive inflammation mainly manifesting as Crohn's disease or ulcerative colitis. IBD commonly presents in adolescence and adulthood and often follows a chronic relapsing course. Genetic and/or environmental factors contribute to the failure of gut immune homeostasis. Genome-wide association studies have identified over 160 susceptibility loci associated with IBD, including polymorphisms in interleukin-10 (IL-10). The anti-inflammatory cytokine IL-10 dampens intestinal inflammation and is therefore a good candidate gene for IBD. Polymorphisms in the IL-10 receptor are also associated with ulcerative colitis presenting in early childhood. Moreover, severe infantile enterocolitis resembling Crohn's disease, caused by loss-of-function mutations in IL-10 and IL-10 receptor, is characterised by a very early onset (usually within the first 3 months of life), unresponsiveness to standard treatment including immunosuppressive therapy, and severe perianal disease with abscesses and fistulas. In these patients, inflammation and polymorphic infiltrates are mainly confined to the colon with very little involvement of the small intestine. Ulceration and granulomas, bloody diarrhoea and failure to thrive also occur. Furthermore, patients may suffer from recurrent fever and respiratory infections. Individuals with IL-10 receptor mutations also experience cutaneous folliculitis and arthritis. Hematopoietic stem cell transplantation is currently the only curative therapy.
MeSH term(s)	Animals ; Gastrointestinal Tract/immunology ; Humans ; Inflammatory Bowel Diseases/etiology ; Inflammatory Bowel Diseases/genetics ; Inflammatory Bowel Diseases/therapy ; Interleukin-10/deficiency ; Interleukin-10/genetics ; Interleukin-10/physiology ; Polymorphism, Genetic ; Receptors, Interleukin-10/deficiency ; Receptors, Interleukin-10/genetics ; Receptors, Interleukin-10/physiology
Chemical Substances	Receptors, Interleukin-10 ; Interleukin-10 (130068-27-8)
Language	English
Publishing date	2014
Publishing country	Germany
Document type	Journal Article ; Review
ISSN	0070-217X
ISSN	0070-217X
DOI	10.1007/978-3-662-43492-5_1
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Article ; Online: Immunomodulatory leptin receptor

Immunity

2023 Volume 57, Issue 1, Page(s) 141–152.e5

Abstract: Adipose tissues (ATs) are innervated by sympathetic nerves, which drive reduction of fat mass via lipolysis and thermogenesis. Here, we report a population of immunomodulatory leptin receptor-positive ( ... ...

Abstract	Adipose tissues (ATs) are innervated by sympathetic nerves, which drive reduction of fat mass via lipolysis and thermogenesis. Here, we report a population of immunomodulatory leptin receptor-positive (LepR
MeSH term(s)	Animals ; Humans ; Mice ; Adipose Tissue, Brown/innervation ; Adipose Tissue, Brown/metabolism ; Body Weight ; Energy Metabolism/physiology ; Interleukin-33/genetics ; Interleukin-33/metabolism ; Leptin ; Obesity/metabolism ; Receptors, Leptin/genetics ; Receptors, Leptin/metabolism ; Thermogenesis/physiology
Chemical Substances	Interleukin-33 ; Leptin ; Receptors, Leptin ; LEPR protein, human ; leptin receptor, mouse
Language	English
Publishing date	2023-12-12
Publishing country	United States
Document type	Journal Article
ZDB-ID	1217235-2
ISSN	1097-4180 ; 1074-7613
ISSN (online)	1097-4180
ISSN	1074-7613
DOI	10.1016/j.immuni.2023.11.006
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Zs.A 4227: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Mendelian traits causing susceptibility to mucocutaneous fungal infections in human subjects.

Engelhardt, Karin R / Grimbacher, Bodo

The Journal of allergy and clinical immunology

2012 Volume 129, Issue 2, Page(s) 294–305; quiz 306–7

Abstract: Mucocutaneous candidiasis and dermatophyte infections occur either in isolation or alongside other symptoms in patients with various primary immunodeficiency diseases with diverse genetic defects, which result in impaired IL-17 immunity, IL-22 immunity, ... ...

Abstract	Mucocutaneous candidiasis and dermatophyte infections occur either in isolation or alongside other symptoms in patients with various primary immunodeficiency diseases with diverse genetic defects, which result in impaired IL-17 immunity, IL-22 immunity, or both. In patients with chronic mucocutaneous candidiasis, disease-associated polymorphisms in DECTIN1 act on the level of fungal recognition, whereas mutations in caspase recruitment domain-containing protein 9 (CARD9) disturb the subsequent spleen tyrosine kinase 2-CARD9/BCL10/MALT1-driven signaling cascade, impairing nuclear factor κB-mediated maturation of antigen-presenting cells and priming of naive T cells to differentiate into the T(H)17 cell lineage. T(H)17-priming cytokines signal through the transcription factor signal transducer and activator of transcription (STAT) 3, which in turn induces the T(H)17 lineage-determining transcription factor retinoic acid-related orphan receptor γt. Dominant-negative mutations in STAT3 result in reduced numbers of T(H)17 cells, causing localized candidiasis in patients with hyper-IgE syndrome. In patients with chronic mucocutaneous candidiasis, gain-of-function STAT1 mutations shift the cellular response toward T(H)17 cell-inhibiting cytokines. T(H)17 cells secrete IL-17 and IL-22, which are cytokines with potent antifungal properties, including production of antimicrobial peptides and activation and recruitment of neutrophils. Neutrophils mediate microbial killing through phagocytosis, degranulation, and neutrophil extracellular traps. Mutations in IL17F and IL17R in patients with chronic mucocutaneous candidiasis, as well as neutralizing autoantibodies against IL-17 and IL-22 in patients with autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy, directly impair IL-17 and IL-22 immunity.
MeSH term(s)	Animals ; Dermatomycoses/genetics ; Dermatomycoses/immunology ; Genetic Predisposition to Disease ; Humans ; Immunologic Deficiency Syndromes/genetics ; Immunologic Deficiency Syndromes/immunology
Language	English
Publishing date	2012-02
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	121011-7
ISSN	1097-6825 ; 1085-8725 ; 0091-6749
ISSN (online)	1097-6825 ; 1085-8725
ISSN	0091-6749
DOI	10.1016/j.jaci.2011.12.966
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Article: Mendelian traits causing susceptibility to mucocutaneous fungal infections in human subjects

Engelhardt, Karin R / Grimbacher, Bodo

The Journal of Allergy and Clinical Immunology. 2012 Feb., v. 129, no. 2

2012

Abstract	Mucocutaneous candidiasis and dermatophyte infections occur either in isolation or alongside other symptoms in patients with various primary immunodeficiency diseases with diverse genetic defects, which result in impaired IL-17 immunity, IL-22 immunity, or both. In patients with chronic mucocutaneous candidiasis, disease-associated polymorphisms in DECTIN1 act on the level of fungal recognition, whereas mutations in caspase recruitment domain–containing protein 9 (CARD9) disturb the subsequent spleen tyrosine kinase 2–CARD9/BCL10/MALT1–driven signaling cascade, impairing nuclear factor κB–mediated maturation of antigen-presenting cells and priming of naive T cells to differentiate into the TH17 cell lineage. TH17-priming cytokines signal through the transcription factor signal transducer and activator of transcription (STAT) 3, which in turn induces the TH17 lineage–determining transcription factor retinoic acid–related orphan receptor γt. Dominant-negative mutations in STAT3 result in reduced numbers of TH17 cells, causing localized candidiasis in patients with hyper-IgE syndrome. In patients with chronic mucocutaneous candidiasis, gain-of-function STAT1 mutations shift the cellular response toward TH17 cell–inhibiting cytokines. TH17 cells secrete IL-17 and IL-22, which are cytokines with potent antifungal properties, including production of antimicrobial peptides and activation and recruitment of neutrophils. Neutrophils mediate microbial killing through phagocytosis, degranulation, and neutrophil extracellular traps. Mutations in IL17F and IL17R in patients with chronic mucocutaneous candidiasis, as well as neutralizing autoantibodies against IL-17 and IL-22 in patients with autoimmune polyendocrinopathy–candidiasis–ectodermal dystrophy, directly impair IL-17 and IL-22 immunity.
Keywords	T-lymphocytes ; antifungal properties ; antigen-presenting cells ; antimicrobial peptides ; autoantibodies ; candidiasis ; caspases ; fungi ; genetic disorders ; human diseases ; immunosuppression (physiological) ; interleukin-17 ; mutation ; neutralization ; neutrophils ; non-specific protein-tyrosine kinase ; patients ; phagocytosis ; signal transduction ; transcription factors
Language	English
Dates of publication	2012-02
Size	p. 294-305.
Publishing place	Mosby, Inc.
Document type	Article
ZDB-ID	121011-7
ISSN	1085-8725 ; 1097-6825 ; 0091-6749
ISSN (online)	1085-8725 ; 1097-6825
ISSN	0091-6749
DOI	10.1016/j.jaci.2011.12.966
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Expanding the PRAAS spectrum: De novo mutations of immunoproteasome subunit β-type 10 in six infants with SCID-Omenn syndrome.

van der Made, Caspar I / Kersten, Simone / Chorin, Odelia / Engelhardt, Karin R / Ramakrishnan, Gayatri / Griffin, Helen / Schim van der Loeff, Ina / Venselaar, Hanka / Rothschild, Annick Raas / Segev, Meirav / Schuurs-Hoeijmakers, Janneke H M / Mantere, Tuomo / Essers, Rick / Esteki, Masoud Zamani / Avital, Amir L / Loo, Peh Sun / Simons, Annet / Pfundt, Rolph / Warris, Adilia /

Seyger, Marieke M / van de Veerdonk, Frank L / Netea, Mihai G / Slatter, Mary A / Flood, Terry / Gennery, Andrew R / Simon, Amos J / Lev, Atar / Frizinsky, Shirley / Barel, Ortal / van der Burg, Mirjam / Somech, Raz / Hambleton, Sophie / Henriet, Stefanie S V / Hoischen, Alexander

American journal of human genetics

2024 Volume 111, Issue 4, Page(s) 791–804

Abstract: Mutations in proteasome β-subunits or their chaperone and regulatory proteins are associated with proteasome-associated autoinflammatory disorders (PRAAS). We studied six unrelated infants with three de novo heterozygous missense variants in PSMB10, ... ...

Abstract	Mutations in proteasome β-subunits or their chaperone and regulatory proteins are associated with proteasome-associated autoinflammatory disorders (PRAAS). We studied six unrelated infants with three de novo heterozygous missense variants in PSMB10, encoding the proteasome β2i-subunit. Individuals presented with T-B-NK± severe combined immunodeficiency (SCID) and clinical features suggestive of Omenn syndrome, including diarrhea, alopecia, and desquamating erythematous rash. Remaining T cells had limited T cell receptor repertoires, a skewed memory phenotype, and an elevated CD4/CD8 ratio. Bone marrow examination indicated severely impaired B cell maturation with limited V(D)J recombination. All infants received an allogeneic stem cell transplant and exhibited a variety of severe inflammatory complications thereafter, with 2 peri-transplant and 2 delayed deaths. The single long-term transplant survivor showed evidence for genetic rescue through revertant mosaicism overlapping the affected PSMB10 locus. The identified variants (c.166G>C [p.Asp56His] and c.601G>A/c.601G>C [p.Gly201Arg]) were predicted in silico to profoundly disrupt 20S immunoproteasome structure through impaired β-ring/β-ring interaction. Our identification of PSMB10 mutations as a cause of SCID-Omenn syndrome reinforces the connection between PRAAS-related diseases and SCID.
MeSH term(s)	Infant ; Humans ; Severe Combined Immunodeficiency/genetics ; Severe Combined Immunodeficiency/metabolism ; Proteasome Endopeptidase Complex/genetics ; Proteasome Endopeptidase Complex/metabolism ; Mutation/genetics ; T-Lymphocytes/metabolism ; Mutation, Missense/genetics
Chemical Substances	Proteasome Endopeptidase Complex (EC 3.4.25.1)
Language	English
Publishing date	2024-03-18
Publishing country	United States
Document type	Journal Article
ZDB-ID	219384-x
ISSN	1537-6605 ; 0002-9297
ISSN (online)	1537-6605
ISSN	0002-9297
DOI	10.1016/j.ajhg.2024.02.013
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Article ; Online: Defective neutrophil development and specific granule deficiency caused by a homozygous splice-site mutation in SMARCD2.

Schim van der Loeff, Ina / Sprenkeler, Evelien G G / Tool, Anton T J / Abinun, Mario / Grainger, Angela / Engelhardt, Karin R / van Houdt, Michel / Janssen, Hans / Kuijpers, Taco W / Hambleton, Sophie

The Journal of allergy and clinical immunology

2020 Volume 147, Issue 6, Page(s) 2381–2385.e2

Abstract: Background: SMARCD2 (SWI/SNF-related, matrix-associated, actin-dependent regulator of chromatin, subfamily D, member 2) has recently been shown to have a critical role in granulopoiesis in humans, mice, and zebrafish. Our patient presented with delayed ... ...

Abstract	Background: SMARCD2 (SWI/SNF-related, matrix-associated, actin-dependent regulator of chromatin, subfamily D, member 2) has recently been shown to have a critical role in granulopoiesis in humans, mice, and zebrafish. Our patient presented with delayed cord separation, failure to thrive, and sepsis. Retrospective whole-exome sequencing confirmed a homozygous splice-site mutation in SMARCD2. Objective: We sought to provide the second description of human SMARCD2 deficiency and the first functional analysis of human primary SMARCD2-deficient cells. Methods: Heparinized venous blood and bone marrow were collected from the patient after obtaining informed consent. Patient leukocytes and CD34 Results: Circulating neutrophils appeared phenotypically immature, lacking multilobed nuclei, and neutrophil granules lacked lactoferrin but showed normal levels of myeloperoxidase. Neutrophil oxidative burst was preserved in response to phorbol 12-myristate 13-acetate. Patient bone marrow-derived neutrophils and white blood cells showed a severely impaired chemotactic response. Furthermore, white blood cells showed defective in vitro killing of Staphylococcus aureus, consistent with a specific granule deficiency. Finally, patient bone marrow-derived CD34 Conclusions: This report highlights an important role for SMARCD2 in human myelopoiesis and the curative effect of hematopoietic stem cell transplantation for the hematopoietic features of SMARCD2 deficiency.
MeSH term(s)	Biomarkers ; Cell Differentiation/genetics ; Cell Differentiation/immunology ; Chemotaxis, Leukocyte/genetics ; Chemotaxis, Leukocyte/immunology ; Chromosomal Proteins, Non-Histone/genetics ; Cytotoxicity, Immunologic ; Female ; Genetic Predisposition to Disease ; Homozygote ; Humans ; Immunophenotyping ; Infant, Newborn ; Lactoferrin/deficiency ; Leukocyte Disorders/diagnosis ; Leukocyte Disorders/etiology ; Mutation ; NADPH Oxidases/metabolism ; Neutrophils/metabolism ; Neutrophils/pathology ; Neutrophils/ultrastructure ; Pedigree ; Phenotype ; RNA Splice Sites ; Respiratory Burst/genetics ; Respiratory Burst/immunology
Chemical Substances	Biomarkers ; Chromosomal Proteins, Non-Histone ; RNA Splice Sites ; SMARCD2 protein, human ; NADPH Oxidases (EC 1.6.3.-) ; Lactoferrin (EC 3.4.21.-)
Language	English
Publishing date	2020-12-03
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	121011-7
ISSN	1097-6825 ; 1085-8725 ; 0091-6749
ISSN (online)	1097-6825 ; 1085-8725
ISSN	0091-6749
DOI	10.1016/j.jaci.2020.11.025
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Article ; Online: Signal transducer and activator of transcription 5B deficiency due to a novel missense mutation in the coiled-coil domain.

Acres, Meghan J / Gothe, Florian / Grainger, Angela / Skelton, Andrew J / Swan, David J / Willet, Joseph D P / Leech, Suzy / Galcheva, Sonya / Iotova, Violeta / Hambleton, Sophie / Engelhardt, Karin R

The Journal of allergy and clinical immunology

2018 Volume 143, Issue 1, Page(s) 413–416.e4

MeSH term(s)	Adolescent ; Humans ; Male ; Mutation, Missense ; Protein Domains ; STAT5 Transcription Factor/deficiency ; STAT5 Transcription Factor/immunology
Chemical Substances	STAT5 Transcription Factor ; STAT5B protein, human
Language	English
Publishing date	2018-09-08
Publishing country	United States
Document type	Case Reports ; Letter ; Research Support, Non-U.S. Gov't
ZDB-ID	121011-7
ISSN	1097-6825 ; 1085-8725 ; 0091-6749
ISSN (online)	1097-6825 ; 1085-8725
ISSN	0091-6749
DOI	10.1016/j.jaci.2018.08.032
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Article: Membrane domains in lymphocytes - from lipid rafts to protein scaffolds.

Harder, Thomas / Engelhardt, Karin R

Traffic (Copenhagen, Denmark)

2004 Volume 5, Issue 4, Page(s) 265–275

Abstract: Lateral compartmentalization of the plasma membrane into domains is a key feature of immune cell activation and subsequent immune effector functions. Here, we will review the high diversity of membrane domains, ranging from elementary lipid rafts, ... ...

Abstract	Lateral compartmentalization of the plasma membrane into domains is a key feature of immune cell activation and subsequent immune effector functions. Here, we will review the high diversity of membrane domains, ranging from elementary lipid rafts, envisioned as dynamic and small domains (in the tens of nm), to relatively stable microm-scale membrane domains, which form the immunologic synapse of T lymphocytes. We will discuss the relationship between these different types of plasma membrane domains and how raft lipid- and protein-controlled interactions and cell biological processes cooperate to generate functional domains that mediate lymphocyte activity.
MeSH term(s)	Animals ; Carrier Proteins/physiology ; Humans ; Immune System/cytology ; Immune System/immunology ; Leukocyte Common Antigens/physiology ; Lymphocyte Specific Protein Tyrosine Kinase p56(lck)/physiology ; Lymphocytes/physiology ; Membrane Lipids/physiology ; Membrane Microdomains/physiology ; Membrane Proteins/immunology ; Membrane Proteins/physiology ; Models, Biological ; Signal Transduction/immunology ; Signal Transduction/physiology
Chemical Substances	Carrier Proteins ; Membrane Lipids ; Membrane Proteins ; citrate-binding transport protein ; Lymphocyte Specific Protein Tyrosine Kinase p56(lck) (EC 2.7.10.2) ; Leukocyte Common Antigens (EC 3.1.3.48)
Language	English
Publishing date	2004-04
Publishing country	England
Document type	Clinical Trial ; Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1483852-7
ISSN	1600-0854 ; 1398-9219
ISSN (online)	1600-0854
ISSN	1398-9219
DOI	10.1111/j.1600-0854.2003.00163.x
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