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        <title>Experimental Biology and Medicine | Immunology section | New and Recent Articles</title>
        <link>https://www.ebm-journal.org/journals/experimental-biology-and-medicine/sections/immunology</link>
        <description>RSS Feed for Immunology section in the Experimental Biology and Medicine journal | New and Recent Articles</description>
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        <pubDate>2026-04-04T05:43:29.671+00:00</pubDate>
        <ttl>60</ttl>
        <item>
        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2026.10938</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2026.10938</link>
        <title><![CDATA[How can we balance risk and benefit of interleukin-18 armored T cell therapies?]]></title>
        <pubdate>2026-02-06T00:00:00Z</pubdate>
        <category>Mini Review</category>
        <author>Paulina Vicenova</author><author>John Maher</author>
        <description><![CDATA[CD19-specific CAR T cells engineered to secrete a constitutively active form of the pro-inflammatory cytokine, interleukin (IL)-18 have demonstrated impressive efficacy in a recent clinical trial involving subjects who had failed prior CAR T cell therapy. Corroborating these clinical data, preclinical studies of IL-18-armored CAR and T cell receptor-engineered T cells have demonstrated enhanced anti-tumor activity in several xenograft and syngeneic mouse cancer models. Interleukin-18 improves tumor clearance via direct effects on CAR T cells and indirect actions on cells on a variety of host immune cells, including natural killer, macrophage and dendritic cells. Compared to unarmored CAR T cells, IL-18-secreting CAR T cells are less exhausted, expand more efficiently and produce greater quantities of interferon (IFN)-γ. However, upregulated circulating IL-18 and its downstream mediator, IFN-γ, are also associated with systemic toxicities which have proven to be severe on occasions. In light of this, several groups have developed strategies that set out to restrict IL-18 release or biological activity to the tumor microenvironment. Among these, CAR T cells armored with NFAT-inducible IL-18 are now undergoing clinical testing. The evaluation of inducible or tumor-selective IL-18 deployment will show whether it is possible to minimize IL-18 related systemic toxicities while preserving localized amplification of anti-tumor activity.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2026.10869</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2026.10869</link>
        <title><![CDATA[Expression of MicroRNA-155 and its associations with EBV serological markers and inflammatory cytokines in young lymphoma patients with evidence of active EBV infection]]></title>
        <pubdate>2026-02-03T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Lezan Medhat Mohammed</author><author>Payman S. Ali</author><author>Ali Qasim Taha</author><author>Luay M. Mohammad</author>
        <description><![CDATA[The Epstein–Barr virus (EBV) is implicated in several lymphoproliferative disorders, particularly among children and adolescents who frequently experience primary EBV infection. MicroRNA-155 (miR-155), an oncogenic and immunoregulatory molecule, is known to participate in EBV-related immune modulation; however, its expression profile and relationship with EBV serological markers and inflammatory cytokines in young lymphoma patients remain insufficiently characterized. This cross-sectional observational study included 80 participants, comprising 40 young lymphoma patients with serological evidence of active EBV infection and 40 healthy controls. Serum EBV IgM and IgG levels were measured using ELISA, as were IL-18 and IL-32 concentrations, while serum miR-155 levels were quantified using qRT-PCR with an absolute quantification approach. The mean age of participants was 13.19 ± 2.51 years, and 55% were male. Serum miR-155 levels were significantly higher in lymphoma patients compared with controls (median: 1.13 vs. 0.43 ng/mL; p = 0.012). Elevated miR-155 expression was significantly associated with EBV IgM positivity (p < 0.001), IL-18 (p = 0.001), and IL-32 (p < 0.001). In multivariate logistic regression analysis, IL-32 positivity emerged as a strong independent predictor of elevated miR-155 levels (AOR = 19.02, p = 0.001). Receiver operating characteristic curve analysis demonstrated good discriminative performance of miR-155 (AUC = 0.87), with 87% sensitivity and 90% specificity at a cutoff value of ≥1.11 ng/mL. These findings indicate that serum miR-155 is significantly elevated in young lymphoma patients with serological evidence of active EBV infection and is statistically associated with inflammatory cytokines, particularly IL-32. miR-155 may represent a promising non-invasive biomarker reflecting EBV-related immune activation, although tissue-based EBV confirmation and mechanistic studies are required to establish causality.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2025.10687</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2025.10687</link>
        <title><![CDATA[HIV-HPV interactions via extracellular vesicles among tobacco smokers and nonsmokers]]></title>
        <pubdate>2026-01-21T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Namita Sinha</author><author>Laree Hiser</author><author>Sandip Godse</author><author>Lina Zhou</author><author>Zhanserik Shynykul</author><author>Carolann Risley</author><author>Theodore Cory</author><author>Santosh Kumar</author>
        <description><![CDATA[Human Immunodeficiency Virus (HIV) and Human Papillomavirus (HPV) co-infections are significantly prevalent, especially among African Americans (AA), a situation further compounded by the prevalence of tobacco smoking. Extracellular vesicles (EVs) are integral to the mechanisms of viral pathogenesis, as they are pivotal in the modulation of immune responses and the inflammatory process. This research study examines the varying concentrations of EVs, their associated biomarkers, and the cytokine/chemokine profiles present in plasma obtained from individuals infected with HIV and those coinfected with HIV and HPV, with particular emphasis on the ramifications of smoking behavior. Our findings revealed that HIV infection markedly elevates EV formation and modifies their protein composition, whereas HPV co-infection does not significantly augment EV levels but does influence the specific cytokine packaging. Notably, monocyte chemoattractant protein-1 (MCP-1 or CCL2) and Regulated upon Activation, Normal T cell Expressed and presumably Secreted (RANTES or CCL5) exhibited substantial enrichment in EVs derived from individuals coinfected with HIV and HPV, implying a potential role of EVs in immune modulation related to viral persistence. Importantly, smoking was found to affect EV characteristics, resulting in an increase in EV size and the packaging of inflammatory mediators, such as MCP-1 and interleukin-18 (IL-18), from plasma into EVs in HIV- and/or HIV+HPV-infected samples. This observation suggests that oxidative stress induced by smoking may intensify immune dysregulation through modifications in EV-mediated cytokine signaling pathways. Nevertheless, smoking did not exhibit a significant impact on the expression of EV marker proteins or the overall levels of EVs. These outcomes underscore the intricate interactions between HIV, HPV, and/or smoking in influencing the immune milieu via EVs. Further comprehensive understanding of the role of EVs in the context of these viral infections could yield valuable insights into potential biomarkers for disease progression and new therapeutic strategies.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2026.10876</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2026.10876</link>
        <title><![CDATA[The gut-eye axis in age-related macular degeneration: from microbial dysbiosis to targeted intervention strategies]]></title>
        <pubdate>2026-01-20T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Nan Wang</author><author>Lin Luo</author><author>Xiaolan Yang</author>
        <description><![CDATA[Age-related macular degeneration (AMD) represents a leading cause of irreversible blindness among the older persons. Characterized by a complex pathogenesis and multiple risk factors, AMD poses substantial challenges for treatment and has emerged as a significant public health concern. The gut microbiota constitutes a vast and dynamically evolving ecosystem, with a healthy microbial community playing an essential role in maintaining host homeostasis through its involvement in digestion and immune defense. However, alterations in microbial composition or function can compromise intestinal barrier integrity, trigger systemic inflammation, and contribute to disease pathogenesis. Evidence now underscores the influence of gut microbiota on the development and progression of AMD. This review examines the mechanisms by which gut microbes may contribute to AMD pathogenesis and evaluates the therapeutic potential of interventions targeting the gut microbiome—including dietary modifications, Pharmacological and Biological Agents, probiotics, prebiotics, and fecal microbiota transplantation—for AMD management.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2025.10849</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2025.10849</link>
        <title><![CDATA[The correlation between pro- and anti-inflammatory cytokines and anti-spike IgG antibody responses induced by the SARS-CoV-2 coronavirus vaccine]]></title>
        <pubdate>2026-01-14T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Mustafa Abdulkareem Salman</author><author>Thowiba Yousif Jameel</author><author>Abdurrahman Ayvaz</author><author>Ahmed Rushdi Abdullah</author>
        <description><![CDATA[Even with the development of the Pfizer-BioNTech BNT162b2 vaccine, which provides protection against COVID-19 and demonstrates high efficacy in generating immune responses, the complexities of the dynamics linking pro- and anti-inflammatory cytokine profiles with anti-spike IgG production remain unclear. The study aims to elucidate these immune dynamics after vaccination. This prospective cohort research was done at the University of Diyala from January 2022 to January 2023, evaluating the immunological response to the Pfizer-BNT162b2 mRNA vaccine in 180 healthy students. Pro- and anti-inflammatory cytokines and anti-spike IgG antibodies were measured before vaccination, 1 month after the second dose, and 4 months after the second dose. Biomarkers were analyzed via ELISA and CRP assays. The study involved 180 healthy participants (80 males, 100 females; median age, 21 years; BMI, 25.7 kg/m2). After the first Pfizer-BNT162b2 vaccine dose, the level of anti-spike IgG increased by 330-fold, and the levels of pro- and anti-inflammatory markers, such as IL-1β, IL-10, and CRP, increased significantly. Four months after the second dose, anti-spike IgG levels were 136-fold above baseline. Significant correlations emerged between cytokine and IgG levels, with anti-spike IgG/IL-10 ratios elevated and sustained over the long term. Pfizer-BNT162b2 vaccine elicits a significant immune response associated with changes in pro-inflammatory cytokines, and the interaction between these cytokines and anti-spike IgG suggests a potential role for immune regulation in enhancing humoral immunity. Based on these findings, the IgG/IL-17 ratio may serve as a viable exploratory biomarker for assessing short- and medium-term vaccination efficacy.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2025.10781</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2025.10781</link>
        <title><![CDATA[Neutrophil extracellular traps: emerging drivers and therapeutic targets in abdominal aortic aneurysm pathogenesis]]></title>
        <pubdate>2026-01-07T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Xinyi Lyu</author><author>Qi Liu</author><author>Jiahao Shi</author><author>Yajun Chen</author><author>Xianpeng Dai</author>
        <description><![CDATA[Abdominal aortic aneurysm (AAA) is a life-threatening condition with no effective pharmacological treatments, underscoring the critical need to identify novel therapeutic targets. Emerging translational and clinical evidence implicates neutrophil extracellular traps (NETs) as potential drivers of AAA pathogenesis. This review systematically delineates the mechanisms by which NETs contribute to aortic wall degradation, focusing on their direct cytotoxicity to vascular smooth muscle cells (VSMCs), induction of VSMC phenotypic switching and ferroptosis, amplification of inflammatory cascades, and propagation of thromboinflammation. Key mediators include PAD4, IL-1β, PI3Kγ, neutrophil elastase, myeloperoxidase, and mitochondrial DNA. NET components (citrullinated histone H3, cell-free DNA, neutrophil elastase) serve as promising diagnostic and prognostic biomarkers. Preclinical studies highlight the efficacy of NET-targeting strategies, including inhibiting NET formation, degrading existing NETs, neutralizing cytotoxic components, and modulating downstream pathways (e.g., with ferroptosis inhibitors). Nanotechnology platforms enhance site-specific delivery of these agents. By integrating the research background with its practical implications, we conclude that targeting NETs represents a promising paradigm shift. Despite translational challenges, this approach offers a rational framework for developing the first pharmacotherapies aimed at stabilizing AAA and addressing a major unmet clinical need.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2025.10841</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2025.10841</link>
        <title><![CDATA[Chimeric antigen receptor natural killer cell therapy for solid tumors: mechanisms, clinical progress, and strategies to overcome the tumor microenvironment]]></title>
        <pubdate>2025-12-19T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Yu Xiang</author><author>Jiayi Dong</author><author>Lijuan Shao</author><author>Size Chen</author>
        <description><![CDATA[Natural killer (NK) cells represent a fundamental component of the innate immune system, endowed with the ability to identify and eradicate virus-infected and malignant cells. The advent of chimeric antigen receptor (CAR) technology has introduced innovative strategies for augmenting the antitumor potential of natural killer (NK) cells. Chimeric antigen receptor natural killer (CAR-NK) cells exert dual cytotoxic effects against tumor cells through CAR-mediated antigen-specific recognition in concert with the nonspecific cytolytic activity mediated by intrinsic NK receptors. This review critically evaluates the clinical progression of CAR-NK cells specifically against solid tumors, focusing on mechanisms to overcome the immunosuppressive tumor microenvironment (TME), the complexity of allogeneic manufacturing, and the latest engineering strategies for enhanced homing and persistence. Specifically, we emphasize the urgent need for robust Phase II/III clinical data and standardized Good Manufacturing Practice (GMP) protocols to realize the full potential of off-the-shelf allogeneic CAR-NK therapies. Additionally, we examine technological advancements and emerging directions addressing persistent challenges in this domain to offer theoretical underpinnings and research perspectives for the clinical deployment of CAR-NK cell therapy in solid tumor management.]]></description>
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