European Journal of Immunology

Our medical research library holds 6 studies published in European Journal of Immunology (2011–2026). Each entry links to the study's record on PubMed and, where there is one, to the publisher's page and a free full text. 6 have an abstract, the authors' own summary as PubMed records it: open "Abstract" to read it.

About the journal

• Publisher: Wiley-VCH
• Published: 1971 to the present, Germany
• Language: English
• ISSN: 0014-2980 (print), 1521-4141 (electronic)
• Its record in the NLM Catalog

2020s

• A Multimodal Framework to Guide Solid Tumor Indications for Natural Killer Cell-Based Therapy. L. Chiossone, V. Picant, Q. Barbier, et al. 2026;56(9):e70283. Systematic review PubMed · Publisher · Free full text

  Abstract

  T cell-based immunotherapies have achieved remarkable success in hematological malignancies but remain limited in solid tumors. Natural killer (NK) cells offer a compelling complementary approach, given their ability to recognize and kill tumor cells independently of neoantigen presentation and MHC class I expression. This study integrates multiomic analyses, clinical trial data, and transcriptomic analyses to systematically identify solid tumor indications most likely to benefit from NK cell-based therapies. Immunohistochemical analysis revealed that NK cells infiltrate multiple tumor types, with the highest abundance in kidney tumors. Systematic review of 177 clinical trials identified variable efficacy across solid tumor indications, without a clearly superior tumor type or intervention. Transcriptomic profiling of over 10,000 TCGA samples assessed NK cell infiltration, cytotoxic fitness, and tumor microenvironment composition, highlighting kidney renal cell carcinoma, lung adenocarcinoma and squamous cell carcinoma, cervical and endocervical cancers, and mesothelioma as promising candidates for future clinical evaluation. Together, these findings provide a multimodal framework to prioritize tumor indications and improve the rational design of future NK cell clinical trials.

  © 2026 The Author(s). European Journal of Immunology published by Wiley‐VCH GmbH.

• NAV-003, a bispecific antibody targeting a unique mesothelin epitope and CD3ε with improved cytotoxicity against humoral immunosuppressed tumors. L. Grasso, Q. Jiang, R. Hassan, et al. 2023;53(8):e2250309. PubMed · Publisher · Free full text

  Abstract

  Mesothelin (MSLN) is a cell surface protein overexpressed in a number of cancer types. Several antibody- and cellular-based MSLN targeting agents have been tested in clinical trials where their therapeutic efficacy has been moderate at best. Previous studies using antibody and Chimeric Antigen Receptor-T cells (CAR-T) strategies have shown the importance of particular MSLN epitopes for optimal therapeutic response, while other studies have found that certain MSLN-positive tumors can produce proteins that can bind to subsets of IgG1-type antibodies and suppress their immune effector activities. In an attempt to develop an improved anti-MSLN targeting agent, we engineered a humanized divalent anti-MSLN/anti-CD3ε bispecific antibody that avoids suppressive factors, can target a MSLN epitope proximal to the tumor cell surface, and is capable of effectively binding, activating, and redirecting T cells to the surface of MSLN-positive tumor cells. NAV-003 has shown significantly improved tumor cell killing against lines producing immunosuppressive proteins in vitro and in vivo. Moreover, NAV-003 demonstrated good tolerability in mice and efficacy against patient-derived mesothelioma xenografts co-engrafted with human peripheral blood mononuclear cells. Together these data support the potential for NAV-003 clinical development and human proof-of-concept studies in patients with MSLN-expressing cancers.

  © 2023 Wiley-VCH GmbH.

2010s

• Tumor-infiltrating dendritic cells exhibit defective cross-presentation of tumor antigens, but is reversed by chemotherapy. A.M. McDonnell, W.J. Lesterhuis, A. Khong, et al. 2015;45(1):49-59. PubMed · Publisher

  Abstract

  Cross-presentation defines the unique capacity of an APC to present exogenous Ag via MHC class I molecules to CD8(+) T cells. DCs are specialized cross-presenting cells and as such have a critical role in antitumor immunity. DCs are routinely found within the tumor microenvironment, but their capacity for endogenous or therapeutically enhanced cross-presentation is not well characterized. In this study, we examined the tumor and lymph node DC cross-presentation of a nominal marker tumor Ag, HA, expressed by the murine mesothelioma tumor AB1-HA. We found that tumors were infiltrated by predominantly CD11b(+) DCs with a semimature phenotype that could not cross-present tumor Ag, and therefore, were unable to induce tumor-specific T-cell activation or proliferation. Although tumor-infiltrating DCs were able to take up, process, and cross-present exogenous cell-bound and soluble Ags, this was significantly impaired relative to lymph node DCs. Importantly, however, systemic chemotherapy using gemcitabine reversed the defect in Ag cross-presentation of tumor DCs. These data demonstrate that DC cross-presentation within the tumor microenvironment is defective, but can be reversed by chemotherapy. These results have important implications for anticancer therapy, particularly regarding the use of immunotherapy in conjunction with cytotoxic chemotherapy.

  © 2014 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.

• NK cells from malignant pleural effusions are not anergic but produce cytokines and display strong antitumor activity on short-term IL-2 activation. P. Vacca, S. Martini, V. Garelli, et al. 2013;43(2):550-61. PubMed · Publisher

  Abstract

  NK cells are a major component of innate immunity and exert a potent antitumor effect both in vitro and in vivo. However, NK cells infiltrating solid tumors have been shown to display severely impaired functional capabilities. In this study, we analyzed NK cells present in pleural effusions (PEs) of patients with primary or metastatic tumors of different origin, including mesothelioma and lung, breast, colon, gastric, bladder, and uterus carcinoma. In all instances, freshly isolated PE-NK cells displayed a CD56(bright) phenotype and expressed normal levels of both activating receptors and HLA class I-specific inhibitory receptors. In addition, they rapidly released large amounts of IFN-γ and TNF-α after stimulation. Upon culture in IL-2, they acquired a potent cytolytic activity against both allogeneic and autologous tumor cells. Tumor cell lysis was primarily mediated by NKG2D and NKp30 and partially by NKp46 and DNAM-1, in agreement with the expression of the corresponding ligands on tumor cells. The finding that PE-NK cells are not functionally impaired and that they can efficiently kill tumor cells upon short-term IL-2 activation may offer important clues for the development of novel approaches in tumor immunotherapy.

  © 2013 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.

• Downregulation of MUC1 expression and its recognition by CD8⁺ T cells on the surface of malignant pleural mesothelioma cells treated with HDACi. D. Roulois, C. Blanquart, C. Panterne, et al. 2012;42(3):783-9. PubMed · Publisher

  Abstract

  Research into new treatments against malignant pleural mesothelioma (MPM) is of great interest, as this aggressive cancer is often resistant to conventional therapies. One potential strategy is the use of epigenetic drugs, such as 5-aza-2'-deoxycytidine (5-azaCdR), a DNA-hypomethylating drug, and valproate (VPA), a histone deacetylase inhibitor (HDACi). Indeed, these drugs not only trigger MPM cell death, but also induce the expression of cancer testis antigens recognized by CD8(+) T cells, such as New York-esophageal cancer-1 (NY-ESO-1). The objective of this study was to assess effects of these drugs on the expression and recognition by CD8(+) T cells of Mucin1 (MUC1), a tumor-associated antigen that is overexpressed by MPM. MPM tumor cell lines were treated with epigenetic drugs, alone or in combination. MUC1 expression by MPM cells, and its recognition by a MUC1-specific CD8(+) T-cell clone, was downregulated by HDACi when used alone or in combination with 5-azaCdR. This effect was not due to a blocking of the HLA class I presentation pathway in treated MPM cells, as NY-ESO-1 induced by 5-azaCdR alone, or with VPA, was recognized by a NY-ESO-1-specific T-cell clone. This study suggests that the choice of tumor antigens could be critical for strategies combining epigenetic drugs with immunotherapy.

  Copyright © 2012 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.

• IL4I1: an inhibitor of the CD8⁺ antitumor T-cell response in vivo. F. Lasoudris, C. Cousin, A. Prevost-Blondel, et al. 2011;41(6):1629-38. PubMed · Publisher · Free full text

  Abstract

  The L-phenylalanine oxidase IL4I1 inhibits T-cell proliferation in vitro through H(2) O(2) production, and is highly expressed in tumor-associated macrophages. IL4I1 is also detected by immunohistochemistry in neoplastic cells from several B-cell lymphomas and some non-lymphoid tumors. To evaluate IL4I1's effect on tumor growth, we developed a mouse melanoma model constitutively coexpressing IL4I1 and the GP33 epitope. After GP33 vaccination, tumors developed more frequently in mice injected with IL4I1-expressing cells in comparison with mice receiving control cells. Tumor escape was preceded by a rapid diminution of IFN-γ-producing cytotoxic antitumor CD8(+) T cells. Moreover, tumor incidence was already increased when only 20% of the injected cells expressed IL4I1. The minimal IL4I1 activities leading to tumor escape were close to those detected in human melanoma and mesothelioma. Thus, we demonstrate the immunosuppressive functions of IL4I1 in vivo and suggest that IL4I1 facilitates human tumor growth by inhibiting the CD8(+) antitumor T-cell response.

  Copyright © 2011 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.

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