PARASITE IMMUNOLOGY寄生虫免疫学
PARASITE IMMUNOLOGY(英文缩写 PARASITE IMMUNOL),ISSN 0141-9838,eISSN 1365-3024,中文译名:寄生虫免疫学 是一本学术期刊。本页汇总该期刊的最新影响因子、分区信息以及最新收录于 PubMed 的文献,帮助您快速了解期刊全貌。
发文量统计区间：2025-10-01 至 2026-09-30，按本站收录文献的发表日期统计。
期刊介绍
历年影响因子趋势
| JCR 数据年份 | 影响因子 | JCR 分区 |
|---|---|---|
| 2021 | 2.206 | Q3 |
| 2022 | 2.200 | Q2 |
| 2023 | 1.400 | Q3 |
| 2024 | 2.100 | Q2 |
| 2025 | 1.200 | Q4 |
PARASITE IMMUNOLOGY 最新收录文献
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1. Vaccination With Trichuris muris Poly-Cysteine and Histidine-Tailed Protein p43 Protects Against Chronic Infection.
PMID:日期:2026-09-30Trichuris trichiura is one of the soil transmitted geohelminths which together currently affect approximately 25% of the global population resulting in considerable morbidity particularly in children and young adults. Recent estimates put infection by T. trichiura at approximately 513 million. De-worming programmes are often not completely effective against T. trichiura and fail to provide resistance to reinfection. Vaccination against these multicellular parasites has proved difficult as they have complex antigenic make-up and the potential to harness the host immune system to their own advantage. Previous vaccination experiments in mice using excretory secretory (ES) material have proved successful although the specific antigens responsible for protection have remained elusive. Here we show that vaccination of mice with native (n)p43, the dominant secreted protein from adult T. muris, formulated with Alum adjuvant can protect against chronic infection. The vaccine candidate generated a strong Type 2 response and host protection was dependent on signalling through IL-4 Rα. Vaccination with a recombinant (r)p43 formulated with alum resulted in stunted worms and reduced worm fecundity but no significant reduction in worm burden. Deglycosylation of np43 significantly abrogated protection against infection suggesting p43 glycans play a role in mediating the protective efficacy of np43. Vaccination using an adenoviral p43 construct generated a robust antibody response to np43 but no protection against challenge infection. Orthologues of p43 are present in other closely related nematodes including T. trichiura and T. suis which infects wild and domestic pigs, suggesting potential for similar vaccine development for both human and veterinary trichiuriasis.
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2. Insights Into Toxocara canis-Induced Liver Fibrosis.
PMID:日期:2026-09-25Toxocara canis larvae migrate through the liver, where persistent tissue injury and immune-mediated inflammation may promote granuloma formation and fibrosis. This review summarizes the histopathological and imaging features, cellular and molecular mechanisms, clinical assessment, and potential reversibility of T. canis-induced liver fibrosis. Experimental evidence indicates that fibrosis is typically focal or multifocal and progresses from eosinophil-rich inflammation and fibrocellular granulomas to collagen-rich lesions, with a later predominance of collagen type I. Fibrogenesis involves hepatic stellate-cell activation within a TGF-β1-, IL-4/IL-13-, and alternatively activated macrophage-associated microenvironment. Toxocara excretory-secretory products, proteases, extracellular vesicles, and regulatory RNAs may further influence NF-κB/MAPK, NOD1/2-RIP2, JAK/STAT, and IL-33/ST2 signaling, although many proposed links remain indirect or unvalidated in the liver. Human evidence is limited mainly to imaging reports and small case series; the epidemiological contribution of toxocariasis to chronic fibrosis and cirrhosis therefore remains unknown. A preliminary murine study suggesting regression of chemically induced fibrosis after infection highlights the context-dependent nature of parasite-host interactions but requires independent confirmation. Standardized human studies and clinically relevant experimental models are needed to define disease burden, validate biomarkers, and identify safe adjunctive antifibrotic strategies.
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3. Egg Deposition-Associated Immune Transition and Tfh-Like Humoral Features During Schistosoma japonicum Infection in Mice.
PMID:日期:2026-09Schistosoma japonicum infection causes egg-induced hepatic granulomatous inflammation together with extensive remodelling of host immunity. Although infection is known to progress from early Th1-associated immunity to egg-driven type 2 responses, the temporal relationships among egg-induced pathology, CD4+ T-cell polarization, T follicular helper (Tfh)-like phenotypes and parasite-specific humoral immunity remain incompletely defined. We therefore infected BALB/c mice with S. japonicum and examined them at serial time points after infection, assessing hepatic histopathology, serum ALT and AST activities, T-cell frequencies, cytokine-producing CD4+ T cells, helper-lineage transcription factors, PD-1 and ICOS expression on T cells, PD-L1 and ICOSL expression on B cells, CXCR5+ICOS+ phenotypic Tfh-like cells and serum SEA-specific IgG, with five biologically independent mice at each time point. Egg-associated hepatic granulomas first became apparent at week 5, enlarged during the middle stage of infection and regressed at later time points. Early infection was characterized by increased IFN-γ-producing CD4+ T cells and elevated Tbx21 expression; following egg deposition, IL-4-, IL-17A- and IL-21-producing CD4+ T cells and Gata3, Rorc and Bcl6 expression increased, and PD-1 and ICOS on CD4+ T cells together with PD-L1 and ICOSL on B cells changed dynamically over the course of infection. By week 8, CXCR5+ICOS+ Tfh-like cells were increased in the spleen, mesenteric lymph nodes and peripheral blood, and SEA-specific IgG had risen markedly after egg deposition and correlated positively with the frequency of splenic CXCR5+ICOS+ CD4+ T cells (r = 0.3979, p < 0.001). Egg deposition thus represents a temporal immunological transition point in S. japonicum infection: the onset of egg-induced hepatic pathology coincides with the shift from early Th1-associated features to Th2-, Th17-, Tfh-like and SEA-specific humoral responses.
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4. Impact of Prior Exposure to Anisakis simplex Antigens on Immune Response During SARS-CoV-2 Vaccination.
PMID:日期:2026-09Parasitic infections can induce immunomodulatory effects that may influence host responses to vaccination. Chronic exposure to Anisakis antigens could modify T-cell and antibody profiles, potentially affecting SARS-CoV-2 vaccine effectiveness in endemic populations. We aimed to determine whether prior exposure to Anisakis alters SARS-CoV-2 vaccine-induced immunity. Forty healthy volunteers were evaluated at five time points before and after receiving either the Pfizer-BioNTech or Oxford-AstraZeneca COVID-19 vaccines. Serum levels of anti-Anisakis and anti-SARS-CoV-2 antibodies were quantified by ELISA, whereas T- and B-cell subsets and apoptosis rates were analysed by flow cytometry. SARS-CoV-2 vaccination induced significant changes in anti-Anisakis antibody levels, particularly IgG and IgA, which increased after the second dose and persisted throughout follow-up. Individuals seropositive for anti-Anisakis antibodies exhibited higher post-vaccination anti-SARS-CoV-2 IgG levels, and anti-Anisakis IgA positivity correlated with stronger anti-SARS-CoV-2 IgA responses at specific time points. Positive associations were also observed between anti-Anisakis antibody levels and circulating T- and B-cell subsets. Prior sensitization to Anisakis antigens appears to influence both the magnitude and quality of the adaptive immune response elicited by SARS-CoV-2 vaccination, affecting antibody profiles and lymphocyte subset dynamics. Conversely, COVID-19 vaccination can alter humoral reactivity to Anisakis antigens, indicating bidirectional immunomodulation between parasite exposure and vaccine-induced immunity.
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5. Hepatic Granulomatous Inflammation and Angiogenesis Upregulation Provoked by Acanthamoeba polyphaga Infection and Role of Quercetin-Conjugated Silver Nanoparticles.
PMID:日期:2026-09Disseminated acanthamoebiasis is a rare but severe opportunistic infection that can involve multiple organs, including the liver, causing fatal outcomes. This study provides new insights into hepatic pathogenesis and possible relationship with angiogenesis activity and the therapeutic role of quercetin conjugated silver nanoparticles (Q-AgNPs). Sixty BALB/c mice were divided into four groups: uninfected control, uninfected treated with Q-AgNPs, infected group and infected treated with Q-AgNPs. The Q-AgNPs were synthesised and characterised by spectrophotometry, electron microscope, zeta potential and dynamic light scattering. Hepatic tissues were examined histopathologically for granulomas (classified as caseating/non-caseating and immature/mature) and vascular changes. Hypoglycaemia and expression of angiogenic markers (CD31, CD34 and MMP9) were assessed. Acanthamoeba polyphaga infection induced significant hepatic granulomatous inflammation, hypoglycaemia, vascular remodelling and upregulation of CD31, CD34 and MMP9, indicating active angiogenesis. Granulomas exhibited necrotic cores in some cases and progressed from immature to mature stages. Q-AgNPs treatment markedly attenuated granuloma numbers, suppressing angiogenic marker expression, mitigating inflammation, capillary permeability and liver lesions. This study provides novel evidence linking Acanthamoeba infection to hepatic granuloma formation and angiogenesis-driven pathology which may serve as useful biomarkers for extracerebral acanthamoebiasis. Further studies are needed to evaluate long-term outcomes and host-parasite interaction.
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6. {"_":"Cytotoxic CD4 T Cells in Visceral Leishmaniasis Patients.","sup":["+"]}
PMID:日期:2026-08Visceral leishmaniasis (VL), a parasitic disease caused by Leishmania donovani, requires a robust CD4 T-cells response to control parasite replication by interferon-gamma (IFN-γ) production and activation of macrophages. However, in VL patients, the anti-parasitic CD4 T-cell responses are ineffective for reasons that are still unclear. Our recent study reporting a transcriptional signature of CD4 T-cell isolated from the peripheral blood of active VL patients showed enhanced expression of genes related to cytotoxicity. This study investigates the cytotoxic potential of CD4 T-cells in VL patients, focusing on the expression of the key cytotoxic molecules granzyme B (GZMB), granulysin (GNLY), perforin (PRF), natural killer cell granule protein 7 (NKG7) and the degranulation capacity of CD4 T-cells during infection. We observed significant upregulation of these cytotoxic markers in CD4⁺ T-cells from VL patients, particularly prior to anti-parasitic drug treatment (D0), suggesting activation of these cells. However, the degranulation capacity, as indicated by CD107a expression, was comparable between VL patients and endemic controls (ECs), suggesting potential functional impairment in the cytotoxic response. Yet, antigen-specific GZMB secretion in whole blood cultures and intracellular GZMB production in CD4 T-cell subsets (notably Th1, Th9 and Th17/22 cells) were enhanced in VL patients, indicating a robust antigen-specific response, though this did not translate into effective parasite control. These findings highlight a paradox whereby CD4 T-cells from VL patients have heightened production of cytotoxic molecules, but lack translocation of CD107a to the cell surface, which is associated with an inability to eliminate parasites. This study provides new insights into the immune dysfunction in VL, highlighting a potential role for the cytotoxic phenotype that develops in parasite-specific CD4 T-cells. Targeting these pathways may offer novel therapeutic strategies to enhance immune responses and improve clinical outcomes in VL.
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7. Attenuation of Tau Hyperphosphorylation by Chronic Toxoplasma gondii Infection in a Mouse Model of Alzheimer's Disease.
PMID:日期:2026-08Alzheimer's disease (AD) is characterized by amyloid-β (Aβ) peptide accumulation and tau protein-mediated neurodegeneration, and neuroinflammation is increasingly recognized as a major process associated with tau pathology. Chronic Toxoplasma gondii infection reduces amyloid accumulation in AD models through immune modulation, but its stage-specific associations with tau-related pathology remain unclear. Here, we investigated how chronic T. gondii infection is associated with tau-related molecular and neuropathological changes in the 5XFAD AD mouse model. At 40 weeks post-infection, we profiled transcriptomic changes and evaluated Aβ-associated (21 genes), Aβ/tau-shared (22 genes), and tau-associated (21 genes) pathological programs together with p-tau immunoreactivity in brain sections. Chronic infection was associated with selective modulation of molecular networks linked to neuroimmune signalling and tau-related pathways rather than broad suppression of AD-related gene expression. Among tau-related pathological stages, the neuroinflammation-related amplification module linking Aβ and tau exhibited the most prominent transcriptomic change in T. gondii-infected AD mice, whereas upstream kinase-related initiation pathways and downstream toxin conversion or accumulation-related processes changed relatively minimally. These transcriptomic changes were accompanied by a marked reduction in phosphorylated tau load at the tissue level. Collectively, these findings suggest that chronic T. gondii infection is associated with selective modulation of tau-related pathogenic programs and reduced p-tau burden in the 5XFAD brain.
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8. Disruption of the CD47-SIRPα Axis Causes Profound Reduction of Parasitaemia in Mice Infected With Babesia microti.
PMID:日期:2026-08Human babesiosis is an emerging disease in North America caused by the red blood cell (RBC)-infecting parasite Babesia microti. Despite a rise in clinical cases in recent years, the pathogenesis and host immune response to B. microti infection remain unclear. CD47 is a 'marker of self' transmembrane glycoprotein expressed on cell membranes that inhibits phagocytosis through interactions with macrophage signal-regulatory protein alpha (SIRPα). We posit that disruption of CD47-SIRPα signalling will induce macrophage uptake of Babesia-infected RBCs and reduce parasitaemia in susceptible hosts. To evaluate this, we compared the in vivo clearance of B. microti in CD47 knockout (CD47) mice and wild-type C57BL/6J mice. Our results showed pronounced differences in infection kinetics between the two mouse strains. C57BL/6J mice showed steadily increasing parasitaemia that peaked at an average of 12%, whereas CD47 mice exhibited parasitaemia that never exceeded 1.5% throughout infection. Parasitaemia became undetectable by Day 21 in C57BL/6J and by Day 16 in CD47 mice, indicating resolution of infection. These results imply that, in the absence of CD47, growth of B. microti is diminished due to more efficient phagocytosis of infected RBCs by macrophages. We propose that CD47-SIRPα signalling plays a key role in the innate response to Babesia and suggest CD47 modulation as a new therapeutic target for the treatment of babesiosis.
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9. An Immunoinformatic Approach for a Multi-Epitope Vaccine Against Toxoplasma gondii.
PMID:日期:2026-07Infection with the intracellular apicomplexan parasite Toxoplasma gondii causes severe and often fatal clinical outcomes worldwide, especially in patients with immunodeficiency, diabetes and in pregnant women and infants. Despite approximately one-third of the global population being infected with T. gondii, there is currently no effective vaccine available for humans. The objective was to develop a potential vaccine candidate for T. gondii, which would incorporate the B- and T-lymphocyte epitopes derived from three immunogenic antigens of the parasite. Initially, the immunodominant epitopes present in the SAG1, GRA6 and GRA7 proteins of T. gondii were identified. Following this, a multi-epitope vaccine was developed by integrating B-cell epitopes, CTL epitopes and HTL epitopes, with the addition of the 50S ribosomal protein L7/L12 serving as an adjuvant to enhance the immunogenic properties of the vaccine. All identified epitopes demonstrated characteristics of being antigenic, nonallergenic, nontoxic and lacking human homologues. Furthermore, the candidate vaccine exhibited immunogenicity, non-allergenicity and stability. Molecular docking studies indicated robust interactions between the vaccine construct and the TLR-4 immune receptor. Additionally, the stability of the formulated vaccine was confirmed through molecular dynamic simulations. In silico analyses suggested that the vaccine construct could effectively initiate primary immune responses; however, further laboratory evaluations are required to verify its efficacy and safety.
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10. No Simple Fluke: Schistosomiasis as an Emerging Regulator of Haematopoiesis.
PMID:日期:2026-07Schistosomiasis, or bilharzia, is a highly prevalent water-borne helminth infection that accounts for an estimated 1.5-1.7 billion disability-adjusted life years lost annually. Pathology driven by adult worms and eggs is accompanied by robust immunomodulation in the human host. Protective responses may promote worm elimination, limit bystander tissue injury caused by parasite migration and contain eggs within granulomatous lesions. However, evidence also suggests that schistosomes can actively or indirectly influence haematopoiesis, thereby reshaping downstream mature immune cell responses. This perspective reviews current literature on schistosome-dependent and host-derived regulation of haematopoiesis, the importance of preclinical modelling and the emerging relevance of controlled human challenge models. It also discusses bone marrow organoid models and their utility for recapitulating complex infection dynamics, with the aim of informing clinically relevant studies and therapeutic strategies.