{"entity": "journal", "iuid": "a4c3bc448804454197faae79c7c416d3", "timestamp": "2026-08-10T16:34:48.283Z", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/journal/Eur.%20J.%20Immunol..json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/journal/Eur.%20J.%20Immunol."}}, "title": "Eur. J. Immunol.", "issn": "1521-4141", "issn-l": "0014-2980", "publications_count": 8, "publications": [{"entity": "publication", "iuid": "5525e8c2fa2e4a2990e85500f6960d6a", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/publication/5525e8c2fa2e4a2990e85500f6960d6a.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/publication/5525e8c2fa2e4a2990e85500f6960d6a"}}, "title": "Mast Cell Phenotypic Heterogeneity Impacts the Interplay with Pathogenic Salmonella Typhimurium Bacteria.", "authors": [{"family": "von Beek", "given": "Christopher", "initials": "C"}, {"family": "Prensa", "given": "Grisna I", "initials": "GI"}, {"family": "Andersson", "given": "Julia H M", "initials": "JHM"}, {"family": "Pejler", "given": "Gunnar", "initials": "G"}, {"family": "Sellin", "given": "Mikael E", "initials": "ME", "orcid": "0000-0002-8355-0803", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/559c18ec87d64318a0afc6267ea879e2.json"}}], "type": "journal article", "published": "2025-08-00", "journal": {"title": "Eur. J. Immunol.", "issn": "1521-4141", "volume": "55", "issue": "8", "pages": "e70040", "issn-l": "0014-2980"}, "abstract": "Mast cells (MCs) lodge within barrier tissues and respond to infectious microbes. Recent work demonstrated that MCs differentiate their cytokine response to extracellular versus invasive Gram-negative enterobacteria by a two-step activation mechanism that integrates Toll-like-receptor (TLR) sensing with signals elicited by type-III-secretion-system (TTSS) effectors during bacterial invasion. However, multiple MC subtypes exist, and it remains unclear how their phenotypic heterogeneity impacts microbial interactions. We find that murine MCs maintained in IL-3, or differentiated toward a connective-tissue phenotype (CT-MCs), respond potently to the enteropathogen Salmonella enterica Typhimurium (S.Tm) through two-step activation, with the TLR component explained by functional TLR4 and TLR2. By contrast, murine mucosal mast cells (M-MCs) express insignificant levels of these TLRs, therefore being unresponsive to extracellular S.Tm, but still mounting a response to invasive bacteria. Following invasion, MC granule maintenance by serglycin restricts S.Tm vacuolar and cytosolic colonization. Notably, this has no impact on the cytokine release from infected MCs, thus uncoupling S.Tm\u00b4s intracellular life-cycle from the MC cytokine response. Finally, human LUVA MCs employ a variant of two-step activation where TLR2/6 signaling combines with the TTSS-elicited signals. Together, this study explains how MC subtypes can respond differently to S.Tm-infection depending on their TLR expression and granule features.", "doi": "10.1002/eji.70040", "pmid": "40838737", "labels": {"Mikael Sellin": null, "SciLifeLab Fellow": null}, "xrefs": [{"db": "pmc", "key": "PMC12369454"}], "notes": [], "created": "2025-11-17T07:46:00.715Z", "modified": "2025-11-17T07:46:00.753Z"}, {"entity": "publication", "iuid": "0b86433bca284a9ea11c23c315e9501b", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/publication/0b86433bca284a9ea11c23c315e9501b.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/publication/0b86433bca284a9ea11c23c315e9501b"}}, "title": "Infection with a Brazilian isolate of Zika virus generates RIG-I stimulatory RNA and the viral NS5 protein blocks type I IFN induction and signaling.", "authors": [{"family": "Hertzog", "given": "Jonny", "initials": "J"}, {"family": "Dias Junior", "given": "Antonio Gregorio", "initials": "AG"}, {"family": "Rigby", "given": "Rachel E", "initials": "RE"}, {"family": "Donald", "given": "Claire L", "initials": "CL"}, {"family": "Mayer", "given": "Alice", "initials": "A"}, {"family": "Sezgin", "given": "Erdinc", "initials": "E"}, {"family": "Song", "given": "Chaojun", "initials": "C"}, {"family": "Jin", "given": "Boquan", "initials": "B"}, {"family": "Hublitz", "given": "Philip", "initials": "P"}, {"family": "Eggeling", "given": "Christian", "initials": "C"}, {"family": "Kohl", "given": "Alain", "initials": "A"}, {"family": "Rehwinkel", "given": "Jan", "initials": "J"}], "type": "journal article", "published": "2018-07-00", "journal": {"title": "Eur. J. Immunol.", "issn": "1521-4141", "volume": "48", "issue": "7", "pages": "1120-1136", "issn-l": "0014-2980"}, "abstract": "Zika virus (ZIKV) is a major public health concern in the Americas. We report that ZIKV infection and RNA extracted from ZIKV infected cells potently activated the induction of type I interferons (IFNs). This effect was fully dependent on the mitochondrial antiviral signaling protein (MAVS), implicating RIG-I-like receptors (RLRs) as upstream sensors of viral RNA. Indeed, RIG-I and the related RNA sensor MDA5 contributed to type I IFN induction in response to RNA from infected cells. We found that ZIKV NS5 from a recent Brazilian isolate blocked type I IFN induction downstream of RLRs and also inhibited type I IFN receptor (IFNAR) signaling. We defined the ZIKV NS5 nuclear localization signal and report that NS5 nuclear localization was not required for inhibition of signaling downstream of IFNAR. Mechanistically, NS5 blocked IFNAR signaling by both leading to reduced levels of STAT2 and by blocking phosphorylation of STAT1, two transcription factors activated by type I IFNs. Taken together, our observations suggest that ZIKV infection induces a type I IFN response via RLRs and that ZIKV interferes with this response by blocking signaling downstream of RLRs and IFNAR.", "doi": "10.1002/eji.201847483", "pmid": "29572905", "labels": {"Erdinc Sezgin": null, "SciLifeLab Fellow": null}, "xrefs": [{"db": "pmc", "key": "PMC6055886"}], "notes": [], "created": "2020-09-28T08:56:09.011Z", "modified": "2022-11-07T11:31:19.157Z"}, {"entity": "publication", "iuid": "f9cb241ea9fc48f987a734c950f33666", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/publication/f9cb241ea9fc48f987a734c950f33666.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/publication/f9cb241ea9fc48f987a734c950f33666"}}, "title": "EOMES-positive CD4", "authors": [{"family": "Chemin", "given": "Karine", "initials": "K"}, {"family": "Ramsk\u00f6ld", "given": "Daniel", "initials": "D"}, {"family": "Diaz-Gallo", "given": "Lina-Marcela", "initials": "LM"}, {"family": "Herrath", "given": "Jessica", "initials": "J"}, {"family": "Houtman", "given": "Miranda", "initials": "M"}, {"family": "Tandre", "given": "Karolina", "initials": "K"}, {"family": "R\u00f6nnblom", "given": "Lars", "initials": "L"}, {"family": "Catrina", "given": "Anca", "initials": "A"}, {"family": "Malmstr\u00f6m", "given": "Vivianne", "initials": "V"}], "type": "journal article", "published": "2018-04-00", "journal": {"title": "Eur. J. Immunol.", "issn": "1521-4141", "volume": "48", "issue": "4", "pages": "655-669", "issn-l": "0014-2980"}, "abstract": "The presence of the PTPN22 risk allele (1858T) is associated with several autoimmune diseases including rheumatoid arthritis (RA). Despite a number of studies exploring the function of PTPN22 in T\u00a0cells, the exact impact of the PTPN22 risk allele on T-cell function in humans is still unclear. In this study, using RNA sequencing, we show that, upon TCR-activation, na\u00efve human CD4", "doi": "10.1002/eji.201747296", "pmid": "29388193", "labels": {"Affiliated researcher": null}, "xrefs": [], "notes": [], "created": "2018-12-05T12:43:21.798Z", "modified": "2018-12-05T12:43:21.816Z"}, {"entity": "publication", "iuid": "2b393d9a8ac043b5ba659ff41fdcb642", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/publication/2b393d9a8ac043b5ba659ff41fdcb642.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/publication/2b393d9a8ac043b5ba659ff41fdcb642"}}, "title": "Dendritic cell regulation of NK-cell responses involves lymphotoxin-\u03b1, IL-12, and TGF-\u03b2.", "authors": [{"family": "Sarhan", "given": "Dhifaf", "initials": "D"}, {"family": "Palma", "given": "Marzia", "initials": "M"}, {"family": "Mao", "given": "Yumeng", "initials": "Y"}, {"family": "Adamson", "given": "Lars", "initials": "L"}, {"family": "Kiessling", "given": "Rolf", "initials": "R"}, {"family": "Mellstedt", "given": "H\u00e5kan", "initials": "H"}, {"family": "\u00d6sterborg", "given": "Anders", "initials": "A"}, {"family": "Lundqvist", "given": "Andreas", "initials": "A"}], "type": "journal article", "published": "2015-06-00", "journal": {"title": "Eur. J. Immunol.", "issn": "1521-4141", "volume": "45", "issue": "6", "pages": "1783-1793", "issn-l": "0014-2980"}, "abstract": "Dendritic cell (DC) vaccines induce T-cell responses in cancer patients. However, there is a paucity of data regarding the role of DC vaccines in shaping natural killer (NK) cell responses. Here, we observe that NK cells are less activated following DC vaccination. In vitro, DC-mediated inhibition of NK cells did not require cell-to-cell contact, but required increased Signal transducer and activator of transcription 3 (STAT3) phosphorylation (pSTAT3) in DCs. When phosphorylation of STAT3 was inhibited in DCs, we found that DCs did not suppress NK cells, and observed an increase in the production of lymphotoxin-alpha (LT\u03b1) and interleukin-12 (IL-12) as well as reduced release of transforming growth factor beta (TGF-\u03b2). The addition of recombinant LT\u03b1 or IL-12 to the DC-NK-cell cocultures restored NK-cell activity, and neutralization of TGF-\u03b2 resulted in elevated production of LT\u03b1 and IL-12 from DCs. Compared with LPS, DCs matured with a cocktail of R848, poly I:C, and IFN-\u03b3 showed reduced levels of pSTAT3 and higher levels of LT\u03b1 and IL-12 and did not inhibit NK-cell activity. These results show that LT\u03b1, IL-12, and TGF-\u03b2 are involved in the cross-talk between NK cells and DCs. Our findings have important implications for the development of DC-based vaccination strategies to potentiate NK-cell responses in patients with cancer.", "doi": "10.1002/eji.201444885", "pmid": "25773885", "labels": {"SciLifeLab Fellow": null, "Yumeng Mao": null}, "xrefs": [], "notes": [], "created": "2023-05-12T11:56:36.592Z", "modified": "2023-05-12T12:00:05.099Z"}, {"entity": "publication", "iuid": "ab2b1c67df634f0f8ae340fa81b555eb", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/publication/ab2b1c67df634f0f8ae340fa81b555eb.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/publication/ab2b1c67df634f0f8ae340fa81b555eb"}}, "title": "Treg-cell depletion promotes chemokine production and accumulation of CXCR3(+) conventional T cells in intestinal tumors.", "authors": [{"family": "Akeus", "given": "Paulina", "initials": "P"}, {"family": "Langenes", "given": "Veronica", "initials": "V"}, {"family": "Kristensen", "given": "Jonas", "initials": "J"}, {"family": "von Mentzer", "given": "Astrid", "initials": "A"}, {"family": "Sparwasser", "given": "Tim", "initials": "T"}, {"family": "Raghavan", "given": "Sukanya", "initials": "S"}, {"family": "Quiding-J\u00e4rbrink", "given": "Marianne", "initials": "M"}], "type": "journal article", "published": "2015-06-00", "journal": {"title": "Eur. J. Immunol.", "issn": "1521-4141", "volume": "45", "issue": "6", "pages": "1654-1666", "issn-l": "0014-2980"}, "abstract": "Colorectal cancer (CRC) is one of the most prevalent tumor types worldwide and tumor-infiltrating T cells are crucial for anti-tumor immunity. We previously demonstrated that Treg cells from CRC patients inhibit transendothelial migration of conventional T cells. However, it remains unclear if local Treg cells affect lymphocyte migration into colonic tumors. By breeding APC(Min/+) mice with depletion of regulatory T cells mice, expressing the diphtheria toxin receptor under the control of the FoxP3 promoter, we were able to selectively deplete Treg cells in tumor-bearing mice, and investigate the impact of these cells on the infiltration of conventional T cells into intestinal tumors. Short-term Treg-cell depletion led to a substantial increase in the frequencies of T cells in the tumors, attributed by both increased infiltration and proliferation of T cells in the Treg-cell-depleted tumors. We also demonstrate a selective increase of the chemokines CXCL9 and CXCL10 in Treg-cell-depleted tumors, which were accompanied by accumulation of CXCR3(+) T cells, and increased IFN-\u03b3 mRNA expression. In conclusion, Treg-cell depletion increases the accumulation of conventional T cells in intestinal tumors, and targeting Treg cells could be a possible anti-tumor immunotherapy, which not only affects T-cell effector functions, but also their recruitment to tumors.", "doi": "10.1002/eji.201445058", "pmid": "25754875", "labels": {"Astrid von Mentzer": null, "DDLS Fellow": null}, "xrefs": [], "notes": [], "created": "2025-12-02T15:51:18.144Z", "modified": "2025-12-02T15:51:18.147Z"}, {"entity": "publication", "iuid": "679c539d03164fcab2b452d51e531b5b", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/publication/679c539d03164fcab2b452d51e531b5b.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/publication/679c539d03164fcab2b452d51e531b5b"}}, "title": "Innate immune receptor NOD2 promotes vascular inflammation and formation of lipid-rich necrotic cores in hypercholesterolemic mice.", "authors": [{"family": "Johansson", "given": "Maria E", "initials": "ME"}, {"family": "Zhang", "given": "Xiao-Ying", "initials": "XY"}, {"family": "Edfeldt", "given": "Kristina", "initials": "K"}, {"family": "Lundberg", "given": "Anna M", "initials": "AM"}, {"family": "Levin", "given": "Malin C", "initials": "MC"}, {"family": "Bor\u00e9n", "given": "Jan", "initials": "J"}, {"family": "Li", "given": "Wei", "initials": "W"}, {"family": "Yuan", "given": "Xi-Ming", "initials": "XM"}, {"family": "Folkersen", "given": "Lasse", "initials": "L"}, {"family": "Eriksson", "given": "Per", "initials": "P"}, {"family": "Hedin", "given": "Ulf", "initials": "U"}, {"family": "Low", "given": "Hann", "initials": "H"}, {"family": "Sviridov", "given": "Dmitri", "initials": "D"}, {"family": "Rios", "given": "Francisco J", "initials": "FJ"}, {"family": "Hansson", "given": "G\u00f6ran K", "initials": "GK"}, {"family": "Yan", "given": "Zhong-Qun", "initials": "ZQ"}], "type": "journal article", "published": "2014-10-00", "journal": {"title": "Eur. J. Immunol.", "issn": "1521-4141", "volume": "44", "issue": "10", "pages": "3081-3092", "issn-l": "0014-2980"}, "abstract": "Atherosclerosis is an inflammatory disease associated with the activation of innate immune TLRs and nucleotide-binding oligomerization domain-containing protein (NOD)-like receptor pathways. However, the function of most innate immune receptors in atherosclerosis remains unclear. Here, we show that NOD2 is a crucial innate immune receptor influencing vascular inflammation and atherosclerosis severity. 10-week stimulation with muramyl dipeptide (MDP), the NOD2 cognate ligand, aggravated atherosclerosis, as indicated by the augmented lesion burden, increased vascular inflammation and enlarged lipid-rich necrotic cores in Ldlr(-/-) mice. Myeloid-specific ablation of NOD2, but not its downstream kinase, receptor-interacting serine/threonine-protein kinase 2, restrained the expansion of the lipid-rich necrotic core in Ldlr(-/-) chimeric mice. In vitro stimulation of macrophages with MDP enhanced the uptake of oxidized low-density lipoprotein and impaired cholesterol efflux in concordance with upregulation of scavenger receptor A1/2 and downregulation of ATP-binding cassette transporter A1. Ex vivo stimulation of human carotid plaques with MDP led to increased activation of inflammatory signaling pathways p38 MAPK and NF-\u03baB-mediated release of proinflammatory cytokines. Altogether, this study suggests that NOD2 contributes to the expansion of the lipid-rich necrotic core and promotes vascular inflammation in atherosclerosis. ", "doi": "10.1002/eji.201444755", "pmid": "25042478", "labels": {"Affiliated researcher": null}, "xrefs": [], "notes": [], "created": "2018-12-05T10:14:26.874Z", "modified": "2018-12-05T10:14:26.893Z"}, {"entity": "publication", "iuid": "abad8e84c6704b2fb6e4700ed991ae17", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/publication/abad8e84c6704b2fb6e4700ed991ae17.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/publication/abad8e84c6704b2fb6e4700ed991ae17"}}, "title": "Proline substitution independently enhances H-2D(b) complex stabilization and TCR recognition of melanoma-associated peptides.", "authors": [{"family": "Uchtenhagen", "given": "Hannes", "initials": "H"}, {"family": "Abualrous", "given": "Esam T", "initials": "ET"}, {"family": "Stahl", "given": "Evi", "initials": "E"}, {"family": "Allerbring", "given": "Eva B", "initials": "EB"}, {"family": "Sluijter", "given": "Marjolein", "initials": "M"}, {"family": "Zacharias", "given": "Martin", "initials": "M"}, {"family": "Sandalova", "given": "Tatyana", "initials": "T"}, {"family": "van Hall", "given": "Thorbald", "initials": "T"}, {"family": "Springer", "given": "Sebastian", "initials": "S"}, {"family": "Nygren", "given": "Per-\u00c5ke", "initials": "P\u00c5"}, {"family": "Achour", "given": "Adnane", "initials": "A"}], "type": "journal article", "published": "2013-11-00", "journal": {"title": "Eur. J. Immunol.", "issn": "1521-4141", "volume": "43", "issue": "11", "pages": "3051-3060", "issn-l": "0014-2980"}, "abstract": "The immunogenicity of H-2D(b) (D(b)) restricted epitopes can be significantly increased by substituting peptide position 3 to a proline (p3P). The p3P modification enhances MHC stability without altering the conformation of the modified epitope allowing for T-cell cross-reactivity with the native peptide. The present study reveals how specific interactions between p3P and the highly conserved MHC heavy chain residue Y159 increase the stability of D(b) in complex with an optimized version of the melanoma-associated epitope gp10025-33 . Furthermore, the p3P modification directly increased the affinity of the D(b)/gp10025-33 -specific T-cell receptor (TCR) pMel. Surprisingly, the enhanced TCR binding was independent from the observed increased stability of the optimized D(b)/gp10025-33 complex and from the interactions formed between p3P and Y159, indicating a direct effect of the p3P modification on TCR recognition.", "doi": "10.1002/eji.201343456", "pmid": "23939911", "labels": {"Affiliated researcher": null}, "xrefs": [], "notes": [], "created": "2018-12-05T11:02:54.957Z", "modified": "2018-12-05T11:02:54.976Z"}, {"entity": "publication", "iuid": "be84079bc31b46ffb9d5d477f04cd92e", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/publication/be84079bc31b46ffb9d5d477f04cd92e.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/publication/be84079bc31b46ffb9d5d477f04cd92e"}}, "title": "Cis association of leukocyte Ig-like receptor 1 with MHC class I modulates accessibility to antibodies and HCMV UL18.", "authors": [{"family": "Li", "given": "Nicholas L", "initials": "NL"}, {"family": "Fu", "given": "Li", "initials": "L"}, {"family": "Uchtenhagen", "given": "Hannes", "initials": "H"}, {"family": "Achour", "given": "Adnane", "initials": "A"}, {"family": "Burshtyn", "given": "Deborah N", "initials": "DN"}], "type": "journal article", "published": "2013-04-00", "journal": {"title": "Eur. J. Immunol.", "issn": "1521-4141", "volume": "43", "issue": "4", "pages": "1042-1052", "issn-l": "0014-2980"}, "abstract": "Leukocyte Ig-like receptor (LIR) 1 (CD85j/ILT2/LILRB1) is an inhibitory receptor with broad specificity for MHC class I (MHC-I) and the human CMV MHC-I homologue UL18. LIR-1 can inhibit NK cells through the conventional interaction with MHC-I expressed on a target cell (in trans) but the nature and the effects of LIR-1 interactions with MHC-I in cis are not well understood. Here we show that MHC-I expressed in cis has an impact on the detection of LIR-1 with various antibodies. We found the cis interaction alters recognition by only one of two antibodies known to block functional trans recognition by LIR-1 on NK cells. Specifically, we observed an enhancement of recognition with GHI/75 in the presence of various MHC-I alleles on 721.221 cells. We found that blocking the LIR-1 contact site with anti-MHC-I antibodies decreased detection of LIR-1 with GHI/75. We also observed a decrease in GHI/75 following acid denaturation of MHC-I. Finally, disruption of LIR-1 cis interactions with MHC-I significantly enhanced UL18-Fc binding to NK92 cells and enhanced the relative inhibition of NK92 cells by HLA-G. These results have implications for LIR-1 function in scenarios such as infection when MHC-I levels on effector cells may be increased by IFNs.", "doi": "10.1002/eji.201242607", "pmid": "23348966", "labels": {"Affiliated researcher": null}, "xrefs": [], "notes": [], "created": "2018-12-05T09:55:40.393Z", "modified": "2018-12-05T09:55:40.425Z"}], "created": "2018-12-05T09:55:40.406Z", "modified": "2020-11-27T13:12:54.807Z"}