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BackgroundIn this exploratory study, the impact of local irradiation on systemic changes in stress and immune parameters was investigated in eight patients treated with intensity-modulated radiation therapy (IMRT) or stereotactic ablative body radiotherapy (SABR) for prostate adenocarcinoma to gain deeper insights into how radiotherapy (RT) modulates the immune system.Patients and methodsRT-qPCR, flow cytometry, metabolomics, and antibody arrays were used to monitor a panel of stress- and immune-related parameters before RT, after the first fraction (SABR) or the first week of treatment (IMRT), after the last fraction, and 3 weeks later in the blood of IMRT (N = 4) or SABR (N = 4) patients. Effect size analysis was used for comparison of results at different timepoints.ResultsSeveral parameters were found to be differentially modulated in IMRT and SABR patients: the expression of TGFB1, IL1B, and CCL3 genes; the expression of HLA-DR on circulating monocytes; the abundance and ratio of phosphatidylcholine and lysophosphatidylcholine metabolites in plasma. More immune modulators in plasma were modulated during IMRT than SABR, with only two common proteins, namely GDF-15 and Tim‑3.ConclusionLocally delivered RT induces systemic modulation of the immune system in prostate adenocarcinoma patients. IMRT and SABR appear to specifically affect distinct immune components.

Febrile infection related epilepsy syndrome (FIRES) is a rare presentation of refractory status epilepticus with immune dysregulation as a potential pathologic mechanism. Despite promising results from second‐line immunomodulators, approximately 30% remain refractory to treatment. We describe two children with FIRES who were unable to wean from anesthetic infusions with immunomodulatory treatment and subsequently received concurrent intrathecal dexamethasone and anakinra/tocilizumab as escalation of therapy. Following the initiation of this combined regimen, anesthetic infusions were decreased while maintaining seizure freedom. These cases demonstrate proof of principle that a multi‐modal approach may be beneficial and should be considered in the treatment of FIRES.

Type 1 diabetes results from autoimmune destruction of insulin-producing cells in the pancreatic islets, leading to deficiency in glucose uptake by the cells of the body. The resulting complications and mortality call into attention the need for therapeutic strategies to treat this disease. While general immunosuppressive treatment and antigen-based therapy have both proven effective in aborting the autoimmune attack on cells, cellular therapy and synergistic combination of agents probably represent the most promising approaches for efficient targeting of autoreactive cells. The underlying challenge is fine tuning of immune therapy to avoid harmful side effects on the immune system or other host-defense functions. This should be rendered possible by identifying the optimal regimen and underlying mechanisms of action.

Gut microbiota alterations have been considered one of the attributes of Systemic Lupus Erythematosus (SLE), and may offer an immunological disorder and even cause the disease. The probiotic administration, especially the Lactobacillus and Bifidobacterium probiotics, is becoming highly utilized for the maintenance of the intestinal barrier’s integrity and immune function, minimizing further the risks of developing some complications such as lupus nephritis, mechanisms that have remained so incompletely defined. This review focuses on the analysis of literature data about the influence of certain probiotic strains on the pathogenesis and course of SLE as immunomodulators and a new therapy strategy that seeks to achieve a synergistic effect with the help of an additional probiotic in combination with dietary supplements gingerols or vitamin D. The current review, therefore, provided the limitations in current trials addressing SLE and therapy optimization. The work is done with the intention of addressing the existing gaps in knowledge, thereby creating more space for new approaches to emerge toward the SLE management and improvement of patients’ outcomes.

Colorectal cancer (CRC) is still one of the most common types of cancer in the world, and the gut microbiome plays an important role in its development. The microbiome is involved in the carcinogenesis, formation and progression of CRC as well as its response to different systemic therapies. The composition of bacterial strains and the influence of geography, race, sex, and diet on the composition of the microbiome serve as important information for screening, early detection and prediction of the treatment outcome of CRC. Microbiome modulation is one of the most prospective new strategies in medicine to improve the health of individuals. Therefore, future research and clinical trials on the gut microbiome in oncology as well as in the treatment of CRC patients are warranted to determine the efficacy of systemic treatments for CRC, minimize adverse effects and increase survival rates.

Granulocyte-macrophage colony-stimulating factor (GM-CSF) was first described as a growth factor that induces the differentiation and proliferation of myeloid progenitors in the bone marrow. GM-CSF also has an important cytokine effect in chronic inflammatory diseases by stimulating the activation and migration of myeloid cells to inflammation sites, promoting survival of target cells and stimulating the renewal of effector granulocytes and macrophages. Because of these pro-cellular effects, an imbalance in GM-CSF production/signaling may lead to harmful inflammatory conditions. In this context, GM-CSF has a pathogenic role in autoimmune diseases that are dependent on cellular immune responses such as multiple sclerosis (MS) and rheumatoid arthritis (RA). Conversely, a protective role has also been described in other autoimmune diseases where humoral responses are detrimental such as myasthenia gravis (MG), Hashimoto's thyroiditis (HT), inflammatory bowel disease (IBD), and systemic lupus erythematosus (SLE). In this review, we aimed for a comprehensive analysis of literature data on the multiple roles of GM-CSF in autoimmue diseases and possible therapeutic strategies that target GM-CSF production.

Systemic lupus erythematosus (SLE) is an autoimmune disorder that leads to immune dysregulation and increased infection risk, especially with immunosuppressive therapies and surgical interventions like splenectomy. Immune monitoring in these patients is important. This case report aims to describe the immune changes in an SLE patient, who had received splenectomy, with infective endocarditis (IE) undergoing valve replacement surgery, focusing on immune cell dynamics and exhaustion markers. A 42-year-old Taiwanese man with SLE and recent splenectomy was diagnosed with IE caused by Staphylococcus aureus, requiring mitral valve replacement surgery. Immune profiling between infection and recover phase showed immune regulation and reconstruction with increased exhaustion markers (killer cell lectin-like receptor subfamily G member 1 (KLRG1), T-cell immunoglobulin and mucin-domain containing-3 (Tim-3), programmed cell death protein 1 (PD-1)) in T cells, expanded regulatory T cells, increased plasmablasts, and decreased regulatory B cells. SLE leads to significant immune dysregulation, making patients more susceptible to infections, especially when combined with immunosuppressive therapy. This case demonstrates dynamic changes in immune markers, such as KLRG1, Tim-3, and PD-1, following infection and surgery, highlighting the necessary for monitoring of immune function in SLE patients. Changes in T and B cell component emphasize the importance of tailored treatment strategies to keep immune imbalances in these patients. Ongoing research into immune tolerance and exhaustion mechanisms will be crucial for improving therapeutic outcomes in SLE.

Aging is the primary risk factor for many neuromuscular (NM) diseases that impair motor and cognitive function. Transplantation of young muscle‐derived stem/progenitor cells (MDSPCs) has shown remarkable therapeutic potential across a range of age‐related diseases, primarily through paracrine mechanisms. In this study, secretome profiling of young MDSPCs revealed a unique enrichment of pro‐angiogenic and immunomodulatory proteins compared to their aged counterparts. Our systemic transplantation experiments also demonstrate that young MDSPCs activate biological pathways linked to these secreted factors, providing strong mechanistic evidence of their contribution to the reversal of age‐associated NM decline at molecular, structural, and functional levels. Systemic transplantation of young MDSPCs into naturally aged mice enhanced motor function and reduced anxiety‐like behavior. Structural improvements in aged NM tissues were partially mediated by phosphorylating protein sites involved in muscle neovascularization and regulation of blood–brain barrier integrity in the motor cortex. Paracrine signaling from young MDSPCs enhanced the endogenous regenerative capacity of aged tissues, with effects sustained for up to 2 months post‐transplantation. Overall, this study elucidates the molecular basis of MDSPC‐mediated NM rejuvenation and provides a foundation for developing novel protein–based therapies to combat age‐related functional decline. Young multipotent muscle‐derived stem/progenitor cells (MDSPCs) secrete a unique profile of pro‐angiogenic and immunomodulatory proteins that are diminished with age. Systemic transplantation of young MDSPCs into naturally aged mice activates pathways in neuromuscular tissues, enhancing health and driving molecular, structural, and functional rejuvenation. Diagram was created with BioRender.com.

Pulmonary arterial hypertension (PAH) is a severe complication of systemic lupus erythematosus (SLE), marked by vascular remodeling, immune dysregulation, and progressive right heart failure. Molecular hydrogen therapy, a selective antioxidant and anti-inflammatory agent, has the capacity to modulate immune responses in these autoimmune disease patients. This case report details the clinical improvement in an SLE patient with PAH after starting adjunctive hydrogen capsule therapy, highlighting its potential as a novel approach for this challenging complication. A 45-year-old Taiwanese woman with SLE-PAH who received hydrogen capsule therapy, during which serial immunophenotyping revealed dynamic changes in T cell exhaustion markers, regulatory T cell (Treg) subsets, and regulatory B cells (Breg). Notably, KLRG1+ T cells and CD39+Helios- Tregs were suppressed during therapy but rebounded after cessation, suggesting transient immune suppressing followed by regulatory rebalancing. Bregs also showed a similar pattern, declining during therapy and recovering after discontinuation. These findings suggest a biphasic immunomodulatory effect of hydrogen therapy, that is, initially dampening immune activation, followed by a regulatory rebound after hydrogen therapy.

Pulmonary arterial hypertension (PAH) is a significant and challenging complication for patients with systemic lupus erythematosus (SLE). It is thought to arise from immune dysregulation and vascular remodeling, ultimately leading to progressive right heart failure. Molecular hydrogen therapy, a selective antioxidant and anti-inflammatory agent, may modulate the immune responses seen in autoimmune diseases. This case report details the use of adjuvant hydrogen capsule therapy in a patient with SLE with PAH, suggesting its potential as a novel approach for this difficult clinical condition. A 42-year-old Taiwanese woman with SLE-PAH received hydrogen capsule therapy, during which serial immunophenotyping revealed dynamic changes in suppressive markers including programmed cell death protein 1 (PD1) and Fas cell surface death receptor (FAS), as well as regulatory T- and B-cell subsets. Notably, the populations of double negative and class-switched memory B-cells decreased during therapy, suggesting durable immune suppression. These results support the effect of hydrogen capsule therapy in achieving immune tolerance and inflammation modulation. This case study suggests that molecular hydrogen therapy may be a promising treatment for patients with SLE-PAH, particularly due to its immunomodulatory effects.