{"title":"IL-1β and IL-6 synergistically drive murine TFH cell differentiation and maintenance in vitro","authors":"Juliana Restrepo Munera, S Rameeza Allie","doi":"10.1111/imcb.70104","DOIUrl":"10.1111/imcb.70104","url":null,"abstract":"<p>T follicular helper (TFH) cells are critical in supporting B-cell responses, which ultimately establish long-term protective immunity against infection and some cancers by producing protective B cells, including antibody-secreting cells and memory cells. However, this same GC output can also promote autoimmune pathology. Therefore, TFH cells are at the core of humoral immunity, underscoring TFH cells as targets for long-term protective and/or pathologic immune responses. Here we define conditions that promote physiologically relevant TFH cell differentiation <i>in vitro</i>. We demonstrate that in addition to T-cell receptor (TCR) signaling, IL-6 and IL-1β individually and jointly promote TFH cell differentiation. These findings highlight key requirements for generating functional TFH cells, providing a model to study therapeutic impacts on TFH cells across diverse disease settings.</p>","PeriodicalId":179,"journal":{"name":"Immunology & Cell Biology","volume":"104 5","pages":"457-472"},"PeriodicalIF":3.0,"publicationDate":"2026-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13155040/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147588961","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Elena Berenice Martínez-Shio, Leobardo Emmanuel Álvarez-de León, Silvia Guadalupe Ramírez-Segovia, Ricardo Ramírez-Torres, Rogelio Martínez-Wagner, Claudia Guadalupe Castillo-Martín del Campo, Othir Gidalti Galicia-Cruz, Adriana Elizabeth Monsiváis-Urenda
{"title":"Identification of metabolically activated macrophages in human adipose tissue and their possible role in preadipocyte differentiation","authors":"Elena Berenice Martínez-Shio, Leobardo Emmanuel Álvarez-de León, Silvia Guadalupe Ramírez-Segovia, Ricardo Ramírez-Torres, Rogelio Martínez-Wagner, Claudia Guadalupe Castillo-Martín del Campo, Othir Gidalti Galicia-Cruz, Adriana Elizabeth Monsiváis-Urenda","doi":"10.1111/imcb.70115","DOIUrl":"10.1111/imcb.70115","url":null,"abstract":"<p>Dyslipidemia can modify the function and phenotype of adipose tissue macrophages. Accumulated evidence suggests that metabolically activated (MMe) macrophages perform both detrimental and beneficial functions in adipose tissue. However, no studies evaluating their role in adipogenesis have been performed. Here, we combine <i>in vitro</i> assays with flow cytometry to characterize the adipose tissue macrophage populations of 32 specimens from patients with dyslipidemia and control subjects, and determine the role of MMe macrophages in the differentiation of primary human preadipocytes. We observed that the increase of MMe macrophages from adipose tissue is influenced by dyslipidemia, but the frequency of M1 and M2 macrophages did not differ when comparing both study groups. We found that MMe macrophages from dyslipidemic patients promote more adipogenic differentiation of preadipocytes compared with those from control subjects; this effect can be attributed to a mechanism governed by soluble factors and cell contact. We also observed that CD38 is expressed on CD14<sup>+</sup>CD80<sup>+</sup>CD68<sup>+</sup> (M1), CD14<sup>+</sup>CD206<sup>+</sup>CD163<sup>+</sup> (M2) and MMe macrophages from adipose tissue, but a higher frequency of CD38<sup>+</sup> macrophages with MMe phenotype was found compared with M2. In addition, we observed a positive trend between the frequency of CD38<sup>+</sup> MMe macrophages and age of dyslipidemic patients. This study demonstrates that MMe macrophages promote the differentiation of preadipocytes and this effect is favored in dyslipidemia conditions.</p>","PeriodicalId":179,"journal":{"name":"Immunology & Cell Biology","volume":"104 5","pages":"532-544"},"PeriodicalIF":3.0,"publicationDate":"2026-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147758384","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Neuroinflammation as a result of non-neurotropic herpesvirus infection","authors":"Christian Münz","doi":"10.1111/imcb.70108","DOIUrl":"10.1111/imcb.70108","url":null,"abstract":"<p>The non-neurotropic Epstein Barr virus (EBV) has been suggested to initiate the prodromal phase of multiple sclerosis (MS), often years before the first clinical symptoms. This review discusses mechanisms by which EBV might cause neuroinflammatory B-cell migration to the central nervous system (CNS), as observed during primary CNS lymphomas and MS. Furthermore, mechanisms of molecular mimicry and autoreactive B-cell expansion by EBV will also be summarized. Finally, approaches to target EBV-mediated neuroinflammation for therapeutic interventions in people with MS (pwMS) will be explored. The recently provided information on EBV's association with MS gives exciting insights into the initiation of this autoimmune disease. Successful therapeutic interventions on the basis of this knowledge might provide evidence that EBV contributes also to the clinical phase of this autoimmune disease.</p>","PeriodicalId":179,"journal":{"name":"Immunology & Cell Biology","volume":"104 5","pages":"443-451"},"PeriodicalIF":3.0,"publicationDate":"2026-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13155061/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147579930","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Kevin Sek, Kah Min Yap, Woon Xuan Hong, Phillip K. Darcy
{"title":"Cytokine armored CAR T cells for cancer immunotherapy","authors":"Kevin Sek, Kah Min Yap, Woon Xuan Hong, Phillip K. Darcy","doi":"10.1111/imcb.70112","DOIUrl":"10.1111/imcb.70112","url":null,"abstract":"<p>Cytokine armoring of CAR T cells for enhancing the immunotherapy of cancer. Reprogramming of CAR T-cell phenotypes through <b>(a)</b> IL-15<sup>8</sup> or <b>(b)</b> IL-9Rα<sup>9</sup> engineering. Reprogramming of the tumor microenvironment and recruitment of host antitumor immunity through <b>(c)</b> IL-36γ<sup>10</sup> or <b>(d)</b> IL-12<sup>11,12</sup> engineering. <b>(e)</b> Tumor-inducible cytokine expression utilizing synthetic NFAT or endogenous <i>NR4A2</i> promoter systems to restrict systemic expression of potent cytokines for improved safety.\u0000 <figure>\u0000 <div><picture>\u0000 <source></source></picture><p></p>\u0000 </div>\u0000 </figure></p>","PeriodicalId":179,"journal":{"name":"Immunology & Cell Biology","volume":"104 5","pages":"485-489"},"PeriodicalIF":3.0,"publicationDate":"2026-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/imcb.70112","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147621281","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Luca Vinnell, Kate Hitpass Romero, Taylor J Stevenson, Justin Rustenhoven
{"title":"Vascular gatekeepers of central nervous system immunity","authors":"Luca Vinnell, Kate Hitpass Romero, Taylor J Stevenson, Justin Rustenhoven","doi":"10.1111/imcb.70116","DOIUrl":"10.1111/imcb.70116","url":null,"abstract":"<p>In this article for the Highlights of 2025 series, we review recent advances in the vascular biology of CNS border tissues. These studies reveal how blood and lymphatic networks at the meninges, nasal regions, and skull coordinate fluid flow and immune surveillance, uncovering new opportunities for therapeutic intervention in neurological disease.\u0000 <figure>\u0000 <div><picture>\u0000 <source></source></picture><p></p>\u0000 </div>\u0000 </figure></p>","PeriodicalId":179,"journal":{"name":"Immunology & Cell Biology","volume":"104 5","pages":"519-523"},"PeriodicalIF":3.0,"publicationDate":"2026-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/imcb.70116","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147715369","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}