The origin and function of CD20 ⁺ T cells are poorly understood. Here, we characterized CD20 ⁺ T cells in mice and humans and investigated how they are affected by anti-CD20 antibody treatment. We report that murine CD20 ⁺ T cells are unable to endogenously express the B cell lineage marker CD20; the development of CD20 ⁺ T cells in rodents requires the presence of CD20-expressing B cells. Our results demonstrated that both murine and human T cells acquire CD20 from B cells via trogocytosis while being activated by an antigen-presenting B cell. In patients with multiple sclerosis (MS) and mice with experimental autoimmune encephalomyelitis (EAE), expression of CD20 on T cells is associated with an up-regulation of activation markers, proinflammatory cytokines, and adhesion molecules, suggesting high pathogenic potential. Supporting this hypothesis, CD20 ⁺ T cells expand during active EAE in rodents; furthermore, adoptive transfer of CD20 ⁺ T cells into EAE-diseased mice worsened histological and clinical severity. Of direct therapeutic relevance, we demonstrate that the exclusive therapeutic elimination of CD20 ⁺ T cells effectively ameliorates EAE, independent of B cells. The results support the hypothesis that CD20 ⁺ T cells arise upon B cell–T cell interaction and that depletion of CD20 ⁺ T cells might contribute to the success of anti-CD20 antibody therapies in MS and other inflammatory disorders.

Metastasis remains the most critical factor limiting patient survival and the most challenging part of cancer-targeted therapy. Identifying the causal drivers of metastasis and characterizing their properties in various key aspects of cancer biology is essential for the development of novel metastasis-targeting approaches. Metastasis-associated in colon cancer 1 (MACC1) is a prognostic and predictive biomarker that is now recognized in more than 20 cancer entities. Although MACC1 can already be linked with many hallmarks of cancer, one key process—the facilitation of immune evasion—remains poorly understood. In this review, we explore the direct and indirect links between MACC1 and the mechanisms of immune escape. Therein, we highlight the signaling pathways and secreted factors influenced by MACC1 as well as their effects on the infiltration and anti-tumor function of immune cells.

In multiple sclerosis (MS), a variety of immunosuppressive treatments are available. While effective, these approaches often lead to sustained impairment of essential components of the immune system, posing long-term safety concerns. Consequently, there is a growing interest in alternative therapeutic approaches that selectively limit pathogenic B-cell functions while preserving their physiologic roles. In this study, we investigated the therapeutic potential of inhibiting the enzyme Bruton tyrosine kinase (BTK), a key signaling molecule in both B-cell and myeloid cell activation. The effects of the BTK inhibitor evobrutinib were evaluated in various experimental in vivo models of CNS demyelination, each representing different aspects of disease pathology as well as a naïve healthy condition. The impact on disease onset and severity was determined, and phenotypical alterations in different cell populations were assessed via flow cytometry. Furthermore, functional changes in both murine and human myeloid cells induced by BTK inhibition under specific Fc receptor-dependent stimulation were analyzed in in vitro settings using flow cytometry. In a naïve, healthy environment, evobrutinib promoted the development of regulatory B-cell properties. In various experimental models of CNS demyelination, BTK inhibition limited the differentiation of proinflammatory B cells while supporting their regulatory properties. Beyond modulating B-cell responses, BTK inhibition also attenuated the activation of myeloid cells after Fc receptor-mediated antigen uptake, a process assumed to be of importance in conditions, such as neuromyelitis optica spectrum disorder and myelin oligodendrocyte glycoprotein-antibody associated disease. In addition, BTK inhibition was shown to suppress the secretion of proinflammatory cytokines and reduce antigen presentation, further dampening pathogenic immune responses. These findings highlight the potential of BTK inhibition as a selective and sustainable immunomodulatory strategy for both B cells and myeloid cells in the context of chronic CNS inflammation. Despite their efficacy, broad-spectrum immunosuppressive therapies often fail to provide targeted immune modulation. By contrast, BTK inhibition promotes regulatory B-cell properties while leaving other B-cell functions intact, providing the basis for its broad use-potentially in combination with established anti-inflammatory agents.

Background/Objectives: Amplitude-modulated radiofrequency (AMRF) fields have emerged as promising non-temperature-induced strategies in oncology. While conventional hyperthermia (HT) relies on thermal stress, the biological impact of AMRF, particularly in combination with radiotherapy (RT), remains insufficiently characterized. Methods: We assessed RF and AMRF, alone or with RT, using phenotypic analyses of proliferation, apoptosis, and necrosis across four cancer cell lines (HT29, SW620, U343, U138). Transcriptomic profiling with Kyoto Encyclopedia of Genes and Genomes (KEGG), GO:BP, and Reactome enrichment was performed in SW620 and U138 cells, selected for their strong phenotypic responses. Results: Across the panel, AMRF was associated with broader cytotoxic responses than RF or HT in most but not all cell lines. AMRF+RT produced the strongest necrotic responses, with cell-line-specific exceptions identified explicitly in the Results (the absence of a significant AMRF+RT apoptotic effect in SW620 and the absence of a significant AMRF+RT necrotic response in U343). In SW620 cells, AMRF was associated with extensive transcriptional reprogramming involving immune modulation, extracellular matrix remodeling, and cell cycle regulation, whereas RF alone showed narrower and delayed effects. In contrast, U138 cells showed elevated apoptosis and necrosis but limited transcriptional changes—a phenotype–transcriptome divergence that points to mechanisms operating downstream of transcription and warrants functional investigation in dedicated follow-up studies. Conclusions: AMRF and AMRF+RT emerge as promising non-temperature-induced anticancer modalities in the cell-line models profiled here, with the pattern of response varying between cell lines. These findings expand the biological impact of RF-based treatments and set the grounds for further investigation in mechanistic and translational studies.