{"entity": "journal", "iuid": "a4404ad171d14a838a76d2c81499ba4e", "timestamp": "2026-03-17T00:28:31.602Z", "links": {"self": {"href": "https://publications.scilifelab.se/journal/Clin.%20Immunol..json"}, "display": {"href": "https://publications.scilifelab.se/journal/Clin.%20Immunol."}}, "title": "Clin. Immunol.", "issn": "1521-7035", "issn-l": "1521-6616", "publications_count": 3, "publications": [{"entity": "publication", "iuid": "14f1504c9c7c4920969417300aea155d", "links": {"self": {"href": "https://publications.scilifelab.se/publication/14f1504c9c7c4920969417300aea155d.json"}, "display": {"href": "https://publications.scilifelab.se/publication/14f1504c9c7c4920969417300aea155d"}}, "title": "Diffuse large B cell lymphoma in rheumatoid arthritis patients is associated with elevated B-cell driving factors including CXCL13.", "authors": [{"family": "Euler", "given": "Nora", "initials": "N"}, {"family": "Hellbacher", "given": "Erik", "initials": "E"}, {"family": "Klint", "given": "Erik Af", "initials": "EA"}, {"family": "Hansson", "given": "Monika", "initials": "M"}, {"family": "Larsson", "given": "Anders", "initials": "A"}, {"family": "Enblad", "given": "Gunilla", "initials": "G"}, {"family": "Malmstr\u00f6m", "given": "Vivianne", "initials": "V"}, {"family": "Baecklund", "given": "Eva", "initials": "E"}, {"family": "Gr\u00f6nwall", "given": "Caroline", "initials": "C"}, {"family": "AUTO-LYMPHOMA study group", "given": "", "initials": ""}], "type": "journal article", "published": "2025-06-00", "journal": {"title": "Clin. Immunol.", "issn": "1521-7035", "volume": "275", "pages": "110476", "issn-l": "1521-6616"}, "abstract": "Patients with rheumatoid arthritis (RA) are at increased risk of diffuse large B cell lymphoma (DLBCL) compared to the general population. Here, we explored the inflammatory profiles in the blood of RA patients who had developed DLBCL. RA-DLBCL patients had significantly higher levels of the pro-inflammatory markers TNF, IL-8, CXCL9, APRIL, and particularly CXCL13 (median 796 vs. 206 pg/mL, p = 0.001), compared to RA controls. By including an extensive autoantibody panel of rheumatoid factor, IgG anti-CCP2, anti-citrullinated protein antibodies (ACPA) fine-specificities, and other anti-modified protein antibodies, all RA-DLBCL patients were autoantibody seropositive. Yet, RA-DLBCL patients did not display significantly different autoantibody signatures compared to RA controls. The levels of immunoglobulin free light chains and C-reactive protein were similar in RA-DLBCL patients and RA controls. In conclusion, RA-DLBCL patients exhibit pro-inflammatory signatures with elevated markers that are important for B cells and may contribute to enhanced B-cell activation and promote lymphoma development.", "doi": "10.1016/j.clim.2025.110476", "pmid": "40118130", "labels": {"Affinity Proteomics Stockholm": "Service"}, "xrefs": [{"db": "pii", "key": "S1521-6616(25)00051-8"}], "notes": [], "created": "2025-04-30T12:27:52.440Z", "modified": "2025-04-30T12:27:52.444Z"}, {"entity": "publication", "iuid": "9f5521a2e4ae475c8c0ac6eb8aeff27d", "links": {"self": {"href": "https://publications.scilifelab.se/publication/9f5521a2e4ae475c8c0ac6eb8aeff27d.json"}, "display": {"href": "https://publications.scilifelab.se/publication/9f5521a2e4ae475c8c0ac6eb8aeff27d"}}, "title": "In-depth immune profiling reveals advanced B- and T-cell differentiation to be associated with Th1-driven immune dysregulation in common variable immunodeficiency.", "authors": [{"family": "Hultberg", "given": "Jonas", "initials": "J"}, {"family": "Blixt", "given": "Emelie", "initials": "E"}, {"family": "G\u00f6ransson", "given": "Robin", "initials": "R"}, {"family": "Adolfsson", "given": "J\u00f6rgen", "initials": "J"}, {"family": "Govender", "given": "Melissa", "initials": "M"}, {"family": "Larsson", "given": "Marie", "initials": "M"}, {"family": "Nilsdotter-Augustinsson", "given": "\u00c5sa", "initials": "\u00c5"}, {"family": "Ernerudh", "given": "Jan", "initials": "J"}, {"family": "Nystr\u00f6m", "given": "Sofia", "initials": "S"}], "type": "journal article", "published": "2023-12-00", "journal": {"title": "Clin. Immunol.", "issn": "1521-7035", "volume": "257", "pages": "109816", "issn-l": "1521-6616"}, "abstract": "Common variable immunodeficiency (CVID) is an inborn error of immunity characterized by low levels of antibodies. In addition to infections, many patients also suffer from T-helper 1-driven immune dysregulation, which is associated with increased mortality. The aim of this study was to perform in-depth characterization of the T and the B cell compartments in a well-defined cohort of patients affected by CVID and correlate the findings to the level of clinical immune dysregulation. We used mass cytometry, targeted proteomics, flow cytometry and functional assays to delineate the immunological phenotype of 15 CVID-affected patients with different levels of immune dysregulation. Unbiased clustering of T cell mass cytometry data correlated with CVID-related immune dysregulation and plasma protein profiles. Expanded CXCR3+ T-bet-expressing B cells correlated with effector memory CD4+ T cell clusters, and increased plasma levels of CXCR3-ligands. Our findings indicate an interplay between B cells and T cells in CVID-related immune dysregulation and provide a better understanding of the underlying pathological mechanisms.", "doi": "10.1016/j.clim.2023.109816", "pmid": "37918468", "labels": {"Affinity Proteomics Uppsala": "Service", "Cellular Immunomonitoring": "Service"}, "xrefs": [{"db": "pii", "key": "S1521-6616(23)00579-X"}], "notes": [], "created": "2023-11-29T19:26:13.178Z", "modified": "2023-12-21T12:57:37.400Z"}, {"entity": "publication", "iuid": "a8c44f4ced194d43864e892c138660c6", "links": {"self": {"href": "https://publications.scilifelab.se/publication/a8c44f4ced194d43864e892c138660c6.json"}, "display": {"href": "https://publications.scilifelab.se/publication/a8c44f4ced194d43864e892c138660c6"}}, "title": "Susceptibility to infections, without concomitant hyper-IgE, reported in 1976, is caused by hypomorphic mutation in the phosphoglucomutase 3 (PGM3) gene.", "authors": [{"family": "Lundin", "given": "Karin E", "initials": "KE"}, {"family": "Hamasy", "given": "Abdulrahman", "initials": "A"}, {"family": "Backe", "given": "Paul Hoff", "initials": "PH"}, {"family": "Moens", "given": "Lotte N", "initials": "LN"}, {"family": "Falk-S\u00f6rqvist", "given": "Elin", "initials": "E"}, {"family": "Elgst\u00f8en", "given": "Katja B", "initials": "KB"}, {"family": "M\u00f8rkrid", "given": "Lars", "initials": "L"}, {"family": "Bj\u00f8r\u00e5s", "given": "Magnar", "initials": "M"}, {"family": "Granert", "given": "Carl", "initials": "C"}, {"family": "Norlin", "given": "Anna-Carin", "initials": "AC"}, {"family": "Nilsson", "given": "Mats", "initials": "M", "orcid": "0000-0001-9985-0387", "researcher": {"href": "https://publications.scilifelab.se/researcher/197cf8ba83ba430f9712b2f4d94dc3e5.json"}}, {"family": "Christensson", "given": "Birger", "initials": "B"}, {"family": "Stenmark", "given": "Stephan", "initials": "S"}, {"family": "Smith", "given": "C I Edvard", "initials": "CI"}], "type": "case reports", "published": "2015-12-00", "journal": {"volume": "161", "issn": "1521-7035", "issue": "2", "pages": "366-372", "title": "Clin. Immunol.", "issn-l": "1521-6616"}, "abstract": "Phosphoglucomutase 3 (PGM3) is an enzyme converting N-acetyl-glucosamine-6-phosphate to N-acetyl-glucosamine-1-phosphate, a precursor important for glycosylation. Mutations in the PGM3 gene have recently been identified as the cause of novel primary immunodeficiency with a hyper-IgE like syndrome. Here we report the occurrence of a homozygous mutation in the PGM3 gene in a family with immunodeficient children, described already in 1976. DNA from two of the immunodeficient siblings was sequenced and shown to encode the same homozygous missense mutation, causing a destabilized protein with reduced enzymatic capacity. Affected individuals were highly prone to infections, but lack the developmental defects in the nervous and skeletal systems, reported in other families. Moreover, normal IgE levels were found. Thus, belonging to the expanding group of congenital glycosylation defects, PGM3 deficiency is characterized by immunodeficiency, with or without increased IgE levels, and with variable forms of developmental defects affecting other organ systems.", "doi": "10.1016/j.clim.2015.10.002", "pmid": "26482871", "labels": {"Clinical Genomics Uppsala": "Collaborative", "Clinical Genomics": "Collaborative"}, "xrefs": [{"db": "pii", "key": "S1521-6616(15)30049-8"}, {"db": "pmc", "key": "PMC4695917"}], "notes": [], "created": "2017-05-03T13:02:22.866Z", "modified": "2021-07-07T13:54:46.124Z"}], "created": "2017-05-09T09:12:52.173Z", "modified": "2020-11-27T13:14:04.442Z"}