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A recent study conducted in Beijing, China, explored the potential of using genetically modified macrophages to target and prevent atherosclerosis, a chronic inflammatory disease. The researchers engineered macrophages to overexpress interleukin-10 (IL-10), a protein known for its anti-inflammatory effects. These modified cells were then introduced into mice with atherosclerosis, resulting in a reduction in plaque formation and necrotic core. The study suggests that cell therapy using anti-inflammatory macrophages could be a promising strategy for treating atherosclerosis. [Extracted from the article]

A recent study conducted at the University of Granada in Spain explores the role of macrophages in muscle regeneration and Duchenne Muscular Dystrophy (DMD). Macrophages play a crucial role in muscle repair by regulating inflammation, carrying out phagocytosis, and facilitating tissue repair. In DMD, altered macrophage activity is associated with disease progression and failed regeneration. Understanding the relationship between macrophages and muscle cells is important for developing effective therapies for this muscle disorder. The study provides valuable insights into the functions of macrophages in muscle regeneration and their implications in DMD. [Extracted from the article]

Researchers from Rice University have conducted a study on the behavior of macrophages, innate immune cells that can switch between pro-inflammatory and anti-inflammatory phenotypes. The study focused on the response of macrophages to shear stress, which is a mechanical force. The researchers found that prolonged exposure to shear stress induced a pro-inflammatory phenotype in human macrophages. These findings have implications for medical technology development and understanding disease pathophysiology. The study was supported by the National Institutes of Health. [Extracted from the article]

A recent study conducted by researchers at Case Western Reserve University in Cleveland, Ohio, explores the role of macrophages in tissue repair and regeneration. The study focuses on four main subtypes of macrophages and their effects on fibroblast proliferation and endothelial cell function. The results show that each subtype has distinct effects, such as increased production of tissue inhibitor of metalloproteinases-1 (TIMP-1) and transforming growth factor-beta 1 (TGF-beta 1), as well as elevated vascular endothelial growth factor A (VEGF-A). The findings highlight the need for further characterization and analysis of macrophage subtypes for specific tissue regeneration. The researchers suggest that a higher degree of specificity and control over the initial subtype selection could lead to more consistent long-term outcomes in regenerative medicine. [Extracted from the article]

A recent report from the University of Paris Est Creteil highlights the role of immune cells, specifically macrophages, in bone repair and the treatment of musculoskeletal trauma. The study found that macrophages play a crucial role in the inflammatory response and the modulation of skeletal stem/progenitor cells during bone fracture healing. The researchers also discovered distinct subsets of macrophages with different profiles, including pro-inflammatory, pro-repair, and anti-inflammatory. In a preclinical mouse model, the depletion of macrophages improved bone regeneration, and pharmacological inhibition of macrophages showed promising results in healing. These findings suggest that targeting macrophages could be a potential therapeutic strategy for trauma-associated fibrosis. [Extracted from the article]

A study conducted by researchers at the University of Ottawa in Canada has found that obesity increases the risk of colon cancer by promoting the accumulation of myeloid cells in the colon. The study also showed that exercise can reduce proliferative signaling in colon cancer, potentially preventing its initiation. The researchers used mice fed a high-fat diet and found that those on the diet developed more early markers of colon cancer compared to those on a control diet. However, exercise was found to reduce the number of these markers. The study suggests that exercise may inhibit colon cancer through alternative mechanisms, such as reducing certain signaling pathways. [Extracted from the article]

According to a preprint abstract from biorxiv.org, researchers have found that Mycobacterium tuberculosis (Mtb), the causative agent of tuberculosis (TB), can overcome phosphate starvation by extensively remodeling its lipidome with phosphorus-free lipids. This remodeling allows Mtb to sustain cell division and escape phosphate restriction specifically in the infection of alveolar macrophages, which is one of the earliest steps in establishing pulmonary tuberculosis. The study suggests that the standard culture conditions for Mtb do not reflect the physiological environment during infection, potentially undermining vaccine and drug development for tuberculosis. The discovery of distinct Mtb phosphate-free lipids and the metabolic pathways that generate them could also provide new antibiotic targets. However, it is important to note that this preprint has not been peer-reviewed. [Extracted from the article]

This article discusses the role of lipid-associated macrophages (LAMs) in maintaining tissue homeostasis and their potential as a therapeutic target in metabolic and chronic inflammatory diseases. The study utilized single-cell RNA sequencing data to profile LAMs in mice and humans across various tissues and inflammatory conditions. The analysis identified both conserved and tissue-specific transcriptional profiles for LAMs, providing insights into their functions in different diseases. The findings may help guide the development of targeted interventions to modulate LAM populations in disease. [Extracted from the article]

A preprint abstract from biorxiv.org discusses the potential benefits of combining PARP14 inhibition and PD-1 blockade therapy in the treatment of relapsed melanoma. The study suggests that while PD-1 blockade is effective in treating melanoma, chronic interferon-gamma signaling in melanoma cells can reduce its efficacy. The researchers found that inhibiting PARP14, a gene associated with interferon-gamma signaling, prolonged responsiveness to PD-1 blockade in preclinical models. However, combining PARP14 inhibition with PD-1 blockade therapy showed initial enhancement of immune responses, but adaptive resistance mechanisms emerged within tumor cells. The study suggests that this combination therapy may leave immune cells primed for further therapeutic intervention, offering a strategy to address resistance development and optimize treatment outcomes. [Extracted from the article]

A recent study conducted by researchers from Zhejiang University explores the relationship between nanomaterials and lipoproteins, focusing on the impact of nanomaterials on lipoprotein structure and lipid metabolism. The study specifically examines the interaction between graphene oxide (GOs) nanosheets and low-density lipoprotein (LDL). The researchers found that the surface properties of GOs influence the binding affinity with LDL and modulate various lipid metabolism pathways. These findings have implications for the design and application of biocompatible nanomaterials and nanomedicines. The study was published in Nature Communications. [Extracted from the article]

A study conducted by Kobe University Graduate School of Medicine investigated the therapeutic effects of the uncultured adipose-derived stromal vascular fraction (SVF) on osteoarthritis (OA) in immunodeficient rats. The SVF, consisting of adipose-derived stromal cells (ADSCs) and M2 macrophages (M2PH), showed slower OA progression, less synovitis, and higher expression of collagen II and SOX9 compared to the control and ADSC groups. The study suggests that the M2PH in the transplanted SVF directly affected recipient tissue, enhancing the secretion of growth factors and chondrocyte-protecting cytokines, making the SVF an effective option for regenerative therapy for OA. [Extracted from the article]

A study conducted by researchers at Ubon Ratchathani University in Thailand has found that brazilin, a compound found in Caesalpinia sappan Linn., has potential therapeutic benefits for chronic diseases. The study focused on the isolation, purification, and evaluation of brazilin, and found that it exhibited antioxidant and anti-inflammatory properties. Brazilin also demonstrated the ability to bind to iron ions, suggesting it could alleviate the harmful effects of iron-induced oxidative stress and inflammatory disorders. This research provides valuable insights into the potential use of brazilin as a protective agent in the treatment of various chronic diseases. [Extracted from the article]

A recent study conducted by researchers at Umea University in Sweden explored the efficacy of natural therapeutic agents in preventing periodontal disease caused by the bacterium Aggregatibacter actinomycetemcomitans. The study focused on the bacterium's high leukotoxin production, which contributes to bone loss and inflammation. The researchers investigated whether extracts from Matcha or Guava leaves could neutralize the bacterium's leukotoxin and prolong the viability of macrophages in cell cultures. The results showed that the extracts moderately neutralized the leukotoxin, leading to increased macrophage viability and decreased inflammation. These findings suggest that Matcha and Guava leaf extracts could be used in future treatment strategies to prevent periodontitis in individuals carrying the bacterium. [Extracted from the article]

A recent study conducted by researchers at Third Military Medical University - Army Medical University has identified a subset of tumor-associated macrophages (TAMs) in glioblastoma that are influenced by hypoxic cues and contribute to the formation of hyperpermeable neovasculature, which hinders drug delivery. These TAMs secrete adrenomedullin, which destabilizes tumor vasculature. However, blocking adrenomedullin can restore vascular integrity, enhance drug delivery, and provide therapeutic benefits. The study highlights the heterogeneity of TAMs in glioblastoma and suggests future directions for studying their dynamics. [Extracted from the article]

Researchers at the French National Institute of Health and Medical Research (INSERM) have published a report on tissue engineering and its role in cutaneous wound repair. The report highlights the importance of macrophages in the healing process and the potential use of adipose tissue-derived stromal cells (ADSCs) and biomaterials in promoting wound healing. Functional biomaterials have shown promising results in pre-clinical reports for accelerating and improving the quality of cutaneous healing. This research provides valuable insights for future applications in skin regeneration. [Extracted from the article]

A recent study conducted by researchers at Centurion University of Technology and Management in Odisha, India, explores the use of bioactive phytochemicals in the treatment of diabetes-related ulcers and slow-healing wounds. The study focuses on the role of these natural compounds in immunomodulation, particularly in relation to macrophages, which play a crucial role in wound healing. The researchers found that phytochemicals and their derivatives have the potential to regulate the immune system and promote the resolution of inflammation in diabetic wounds. This research provides valuable insights into potential therapies for individuals with diabetes who are at risk of developing ulcers and slow-healing wounds. [Extracted from the article]

A recent study conducted by researchers at the University of Florida investigated the role and regulation of GPNMB in progranulin-deficient macrophages. Progranulin is a protein critical for successful aging, and insufficient levels of it are associated with an increased risk of neurodegenerative diseases. The study found that GPNMB expression was increased in peripheral immune cells due to insufficient progranulin, and stimulation-dependent cytokine release was decreased in progranulin-deficient macrophages. These findings suggest that understanding early-stage disease mechanisms in peripheral populations may inform treatment strategies to delay disease progression. [Extracted from the article]

Researchers at the Feil Family Brain and Mind Research Institute in New York City have discovered that border-associated macrophages (BAMs), a type of myeloid cell, play a role in the neurovascular dysfunction associated with Apolipoprotein E4 (ApoE4), a genetic risk factor for Alzheimer's disease. The study found that BAMs are both sources and effectors of ApoE4, mediating neurovascular dysfunction through reactive oxygen species. This new understanding of BAM pathobiology could have therapeutic implications for the treatment of ApoE4-related cognitive impairment. The research has been published in Nature Neuroscience. [Extracted from the article]

Researchers at the University of Messina in Italy have conducted a study on the anti-inflammatory effects and antibiofilm activity of a mannose-rich exopolysaccharide (EPS) produced by Bacillus licheniformis B3-15. The EPS was found to have potential as an antiviral and immunomodulatory agent, as well as the ability to prevent the adhesion of certain pathogenic bacteria. The study showed that the EPS reduced inflammation in macrophage cells and inhibited biofilm formation related to respiratory tract infections. The researchers suggest that the EPS could be used as a nasal spray with anti-inflammatory properties and as a surface-coating agent for medical devices. [Extracted from the article]

A recent study from the University of Illinois explores the toxicity of ambient particulate matter (PM) using in vitro methods. The researchers discuss the challenges of comprehending the results of cell-based methods due to the diversity of cellular endpoints, cell types, and assays, as well as the interference of PM chemical components. The study suggests the use of more physiologically relevant cellular models, such as epithelial cells, for oxidative stress measurement, and encourages the use of co-culture systems to investigate the comprehensive effects of PM. The review also identifies two major groups of toxic PM chemical species, metals and organic compounds, but notes that the relative toxicities of these species are still debated. The researchers conclude that their review will guide future investigations and contribute to a better understanding of the health effects of PM exposure. [Extracted from the article]

A recent study conducted by researchers at the University of Maryland in College Park examined the role of type I interferons (IFNs) in Salmonella enterica serovar Typhimurium (STm) macrophage infections. The study found that STm infection inhibits IFN beta signaling in murine macrophages, but does not affect IFN gamma signaling. This inhibition is Toll-like receptor 4 (TLR4)-dependent and is mediated by reduced host cell surface IFNAR1. The research concluded that macrophages exposed to STm have reduced IFN beta signaling, but this does not affect the cell-autonomous host defense against STm. [Extracted from the article]

A recent study conducted by researchers at Southwest University has shed light on the mechanism behind Streptococcus suis-induced macrophage pyroptosis. Streptococcus suis serotype 2 (SS2) is a zoonotic pathogen that triggers an NLRP3-dependent cytokine storm, leading to inflammation and pyroptosis. The study found that SS2 induces pyroptosis through the activation of the NLRP3-GSDMD pathway, with RACK1 and NEK7 playing important roles in this process. These findings provide new insights into SS2-induced cell death. [Extracted from the article]

A recent study conducted by the University of East Anglia in Norwich, United Kingdom, has found that a low protein diet can protect the liver from Salmonella Typhimurium-induced injury by modulating the mTOR/autophagy axis in macrophages. The research suggests that Western diets, which are high in protein, may contribute to metabolic and liver diseases, and reducing protein consumption could have a positive impact on innate immunity. The study used mice and observed reduced inflammation and upregulation of autophagy-related genes in myeloid cells in mice fed with a low protein diet after Salmonella infection. These findings support the idea that dietary components play a role in the fitness of the immune system. [Extracted from the article]

A recent report from Southern Medical University discusses research findings on idiopathic pulmonary fibrosis (IPF), a complex and incurable lung disease. The study aimed to identify new immune patterns and biomarkers in IPF patients. The researchers identified two distinct immune subtypes in IPF patients, one characterized by immune activation and inflammation, and the other by immune suppression. They also developed a prognostic model called the immune-related risk score (IRS) that can predict the immune status and prognosis of IPF patients. The study identified PLA2G7, derived from macrophages, as a potential biomarker for IPF patients. Celecoxib, a drug, was found to effectively bind with PLA2G7. This research provides valuable insights into the diagnosis and prognosis of IPF and may contribute to improved outcomes for patients. [Extracted from the article]

A recent study conducted in Jiangsu, China explored the relationship between immune cell traits and schizophrenia. The researchers used a bidirectional two-sample Mendelian randomization approach and public GWAS data to investigate the causal relationship. The study found that schizophrenia may lead to an increase in immune cells and identified four immune cell traits that may increase the risk of schizophrenia. However, no significant causal effects of schizophrenia on immune cell traits were detected. The findings contribute to a better understanding of the role of immune regulation in schizophrenia and may offer new insights for diagnosis and treatment options. [Extracted from the article]

A patent application has been submitted for a new invention called "Human Ipsc-Derived Macrophage." This invention involves the use of human pluripotent stem cells to create macrophages, which are a type of immune cell that can infiltrate tumors and stimulate immune responses. The invention also includes the use of chimeric antigen receptor (CAR) technology to enhance the macrophages' ability to target and kill cancer cells. The inventors believe that this approach could be effective in treating solid tumors, such as ovarian cancer. The patent application provides methods for manufacturing the macrophages and administering them to patients, along with additional treatments such as antibodies and immune-stimulating agents. [Extracted from the article]

A recent study conducted at the University of Adelaide explores the role of breastmilk in the interactions between breast cancer cells and macrophages in postpartum breast cancer. The research found that breastmilk can both promote breast cancer proliferation and reduce breast cancer progression. It increases the proliferation and viability of breast cancer cells, reduces cell migration, and regulates macrophage polarization. These findings suggest that breastmilk has the potential to shape the tumor microenvironment in postpartum breast cancer. [Extracted from the article]

A study conducted by researchers at Shandong University in Yantai, China, explores the use of a nanoplatform for the treatment of ovarian cancer. The researchers focused on the immunosuppressive tumor microenvironment (TME) in ovarian cancer and developed a nanoplatform that combines sonodynamic therapy (SDT) with immunotherapy. The nanoplatform, called SIM@TR-NP, enhances macrophage function and triggers the polarization of tumor-associated macrophages (TAMs) towards the M1 phenotype, improving the immunosuppressive TME. The study suggests that this emerging therapeutic regimen has the potential to improve the treatment of ovarian cancer by synergizing TAM-based immunotherapy and SDT. [Extracted from the article]

New research from Keio University explores the role of heat shock protein 90 (HSP90) in the differentiation of monocytes into tumor-associated macrophages (TAMs) in triple-negative breast cancer (TNBC). The study found that an HSP90 inhibitor blocked TNBC-induced monocyte-to-TAM differentiation and suppressed tumor growth in a mouse model. The researchers suggest that HSP90 could be a potential target for TNBC immunotherapy due to its regulatory role in TAM differentiation. This information may be useful for individuals conducting research on breast cancer and immunotherapy. [Extracted from the article]

A report from the First Affiliated Hospital of Harbin Medical University discusses the use of adipose-derived stem cells (ASCs) to improve the retention rate of transplanted fat. The researchers found that ASCs can regulate lipid metabolism in macrophages, leading to increased retention of fat grafts. In both in vivo and in vitro experiments, ASCs were shown to upregulate mitochondrial fatty acid oxidation (FAO) in macrophages, promote the transformation of macrophages into M2 phenotype, and reduce lipid deposition. The findings suggest that ASCs have the potential to enhance the success of fat transplantation procedures. [Extracted from the article]

According to a preprint abstract, researchers have investigated the potential of targeting 12-lipoxygenase (12-LOX), an enzyme involved in inflammatory pathways, to delay the onset of autoimmune diabetes. They used a mouse model with a human ALOX12 gene replacement and found that a 12-LOX inhibitor called VLX-1005 effectively delayed the onset of autoimmune diabetes. The treatment resulted in reductions in infiltrating immune cells and macrophages, as well as alterations in cytokine-responsive pathways. This research provides a platform for evaluating LOX inhibitors and supports VLX-1005 as a potential treatment for delaying autoimmune diabetes. [Extracted from the article]

A study conducted by researchers at Hangzhou Medical College in China explores the role of Src homology 2-containing protein tyrosine phosphatase 2 (SHP2) in macrophages and its association with diabetic nephropathy (DN). The researchers found that SHP2 is upregulated in macrophages in both diabetic patients and a mouse model. Macrophage-specific SHP2-knockout mice showed significant improvements in renal function, collagen deposition, fibrosis, and inflammatory response. The study suggests that SHP2 inhibition may be a potential therapeutic option for patients with DN. [Extracted from the article]

A recent study conducted by researchers at Vanderbilt University School of Medicine has found that excessive iron accumulation in metabolic organs, such as adipose tissue, liver, and skeletal muscle, is associated with an increased risk of diabetes. The study focused on the role of the scavenger receptor CD163, which is present on tissue-resident macrophages and plays a significant role in iron homeostasis. The researchers discovered that the absence of CD163 worsened glucose intolerance and insulin resistance in obese male mice. This study highlights the importance of CD163 in anti-inflammatory and hemoglobin scavenging roles, and its absence can impair systemic insulin action in an obese setting. [Extracted from the article]

A recent preprint abstract discusses the development of a human tendon-on-a-chip model that aims to study the cellular interactions in the injured tendon microenvironment. The model lacked physiological flow in the vascular compartment, so the researchers added a fluidic component to enable the study of circulating immune cell and vascular crosstalk in a tendon injury model. The study found that under physiological shear stress, there was an increase in the activation marker of endothelial leukocytes, as well as enhanced adhesion and transmigration of circulating monocytes across the endothelial barrier. The addition of tissue macrophages further increased the infiltration of circulating monocytes into the tissue matrix. The findings highlight the importance of incorporating physiological flow in tissue inflammation and disease models. [Extracted from the article]

A preprint abstract suggests that metabolic stress may worsen knee pain in patients with early-stage osteoarthritis (OA). The study conducted on rats found that the combination of biomechanical and metabolic stresses led to increased knee pain, cartilage damage, and synovial inflammation compared to biomechanical stress alone. The researchers also identified metabolic shifts, dysregulated communication, and increased expression of Htra1, a pathogenic protease in OA, when metabolic and biomechanical stresses were combined. These findings may provide potential therapeutic targets for patients with metabolic syndrome and OA. However, it is important to note that this preprint has not yet undergone peer review. [Extracted from the article]

A preprint abstract from biorxiv.org discusses the potential use of pexidartinib, a dual inhibitor of FLT3 and CSF1R, in combination with FLT3-directed chimeric antigen receptor-engineered macrophages (FLT3L-CAR-Macrophage) for the treatment of FLT3-ITD-mutated acute myeloid leukemia (AML). The study found that conditioned medium from FLT3-ITD+ AML cells impaired the phagocytic activities of M2-like leukemia-associated macrophages (M2-LAM) and protected AML cells from FLT3 inhibitor treatment. However, treatment with pexidartinib effectively suppressed M2-LAM, reduced leukemic burden, and prolonged the survival of mice with FLT3-ITD+ AML. Additionally, FLT3L-CAR-Macrophages enhanced phagocytic activities and reduced leukemic burden in vitro and in mice. The study suggests that pexidartinib plus FLT3L-CAR-Macrophage could be a promising therapeutic strategy for FLT3-ITD+ AML, but further investigation is needed. [Extracted from the article]

A preprint abstract from biorxiv.org discusses the role of MALT1 protease in glioblastoma (GBM)-associated macrophages. The study shows that MALT1 plays a key role in promoting immunosuppression in GBM by inducing a signaling axis within macrophages. Inactivation of MALT1 protease reduces migration and restores a macrophage M1-like phenotype, leading to increased immuno-reactivity and reduced tumor growth. The addition of a MALT1 inhibitor to standard chemotherapy may enhance its efficacy. This research suggests that MALT1 protease inhibition could be a promising immunotherapeutic strategy for GBM treatment. [Extracted from the article]

A study conducted by researchers at Stanford University explores the mechanisms of immune evasion in hepatocellular carcinoma (HCC), a type of liver cancer. The study identifies a spatial neighborhood where PD-L1+ M2-like macrophages interact with stem-like tumor cells, leading to CD8+ T cell exhaustion and poor survival. The researchers also demonstrate that blocking PD-L1 and TGF beta can eliminate immunosuppressive macrophages, recruit activated CD8+ T cells, and eliminate residual stem-like tumor cells in mouse models. This research suggests that targeting the interaction between macrophages and tumor cells may prevent HCC recurrence. [Extracted from the article]

A recent study conducted by researchers at Tabriz University of Medical Sciences in Iran explored the effects of melatonin-treated RAW macrophage cells on A-375 human melanoma cell lines. The study found that melatonin inhibited the growth of melanoma cells in a dose-dependent manner, particularly at concentrations of 150 mM and 200 mM. The researchers concluded that melatonin could potentially be used as a treatment for melanoma at these concentrations. Further research is needed to examine the long-term effects of melatonin on melanoma cells. [Extracted from the article]

This article discusses a preprint abstract that explores the calcium dynamics of skin-resident macrophages, specifically Langerhans cells, during homeostasis and tissue injury. The study found that Langerhans cells in the skin exhibit spontaneous and transient changes in calcium activity, primarily in the cell body and rarely in the dendrites. Triggering somatosensory axon degeneration increased the frequency of calcium activity in Langerhans cell dendrites. Additionally, the study showed that Langerhans cells have a sustained increase in intracellular calcium following the engulfment of damaged keratinocytes, which affects their efficiency in clearing cellular debris. The research highlights the importance of calcium signaling in skin immune cells and suggests that the skin can serve as a useful model for studying calcium dynamics in tissue-resident macrophages. [Extracted from the article]

According to a preprint abstract, phagocytosis is an important process in the human innate immune response. Macrophages, a type of immune cell, play a crucial role in phagocytosis by engulfing and neutralizing pathogens and cell debris. They also release cytokines and lipid mediators to modulate inflammation. The link between oxylipins (lipid mediators) and phagocytosis in different macrophage phenotypes is not well understood. In this study, researchers investigated the relationship between phagocytosis and the arachidonic acid (ARA) cascade in primary human macrophages. They found that M1-like macrophages, which are inflammatory, had higher levels of cyclooxygenase (COX)-2 and its products after stimulation with LPS (lipopolysaccharide) compared to M2-like macrophages, which are anti-inflammatory. LPS increased phagocytosis in M2-like macrophages but not in M1-like macrophages. The researchers also discovered that the COX product PGE2 modulates the effects of LPS on phagocytosis through the EP4 receptor. This finding suggests that blocking COX, such as with NSAIDs, could increase phagocytosis in inflammatory M1-like macrophages and potentially shift their phenotype towards a more pro-resolving state. However, it is important to note that this preprint has not yet [Extracted from the article]

A preprint abstract from biorxiv.org discusses the crosstalk between Toll-like receptor (TLR)4 and Fc gamma receptor (FcγR) in modulating the inflammatory responses of innate immune cells. The study used imaging techniques to examine the molecular organization of these receptors on macrophage cell surfaces and found that their co-activation enhances pro-inflammatory responses and tyrosine phosphorylation. The researchers also discovered that TLR4 and FcγR form discrete nanoclusters after ligand stimulation, and their synergistic co-activation increases the size and spatial overlap of these nanoclusters, leading to amplified immune signaling. These findings suggest that nanocluster interactions play a critical role in modulating innate immune responses. [Extracted from the article]