Parasite Immunology最新文献

Cystic echinococcosis (CE) is a highly common zoonosis worldwide and Tunisia remains the most endemic country in North Africa. The variability of clinical manifestations of CE depends on predisposing factors related to the interaction between host genetic and immunological factors. This study investigates the association between single nucleotide polymorphism (SNP) of IL-1β (rs16944 and rs1143634), an important pro-inflammatory cytokine in the CE immune response and susceptibility to CE in a Tunisian population. The case group included 152 paediatric patients diagnosed with CE, whereas the control group included 152 healthy individuals. The DNA was extracted via the salting-out method and genotyped via polymerase chain reaction restriction fragment length polymorphism (PCR-RFLP). The -511C/T genotype is more frequent in the control group than in patients (OR = 0,57, p = 0.03, CI = 0.3418-0.96). The haplotype -511C/+3954T was higher in the case group compared to the control group (OR = 2.6, p = 0.00011, CI = 1.62-4.31). The SNP -511C/T in IL-1β gene was associated with CE protection in our paediatric population. The haplotype -511C/+3954T might be considered as the influential factor for resistance to the disease.

Canine visceral leishmaniasis (CanL) is a tropical zoonosis caused by Brazil's protozoan Leishmania (L.) infantum. Disorders in the hypothalamic-pituitary-adrenal (HPA) axis have been reported in human and experimental visceral leishmaniasis, but not yet in canine leishmaniasis. Cortisol is a steroid hormone that regulates several processes, including immune responses. This study investigated HPA axis disorders in dogs with visceral leishmaniasis and their link to clinical and immunological parameters. ELISA quantified serum levels of cortisol and adrenocorticotrophic hormone (ACTH) in 12 healthy dogs and 13 dogs with leishmaniasis. The expression of the enzymes inducible nitric oxide synthase (iNOS) and arginase-1 and programmed cell death protein-1 (PD-1) were evaluated by flow cytometry in peripheral blood mononuclear cells (PBMC). Additionally, serum levels of the cytokines interleukin (IL)-1β, IL-6, IL-10, IL-12, interferon-gamma (IFN-γ), tumour necrosis factor-alpha (TNF-α), and transforming growth factor-beta (TGF-β) were quantified by capture Enzyme-Linked Immunosorbent Assay (ELISA). Parasite load was quantified in peripheral blood and conjunctival swabs by real-time polymerase chain reaction (qPCR). All parameters evaluated were correlated with serum cortisol. We observed an increase in cortisol, while ACTH levels were reduced in dogs with leishmaniasis. The expression of iNOS, arginase-1 and PD-1 was higher in the PBMC of dogs with leishmaniasis. Serum levels of the cytokines IL-10, IL-6, IL-12, and IFN-γ were increased in dogs with leishmaniasis. Cortisol showed a negative correlation with PD-1 and IL-12. Our findings suggest that infection natural with L. infantum in dogs may induce dysregulation of the HPA axis, leading to elevated serum cortisol levels and modulation of the immune response, as it is associated with immunological markers involved in disease pathogenesis. These results contribute to a better understanding of the pathogenic mechanisms of the disease.

Trichuris trichiura infects nearly 500 million people worldwide, causing intestinal inflammation, malnutrition, and growth impairment, particularly in children from low-resource settings. While host immunity is central to parasite clearance, diet and the gut microbiota may also modulate infection. Using the Trichuris muris model, we examined how immune competence and diet interact to influence worm burden, antibody responses, and gut microbiota composition. Wild-type (WT), RAG1-deficient (lacking adaptive immunity), and RAG1/γc-deficient (lacking both adaptive and innate lymphoid immunity) mice were fed either a normal diet (ND) or high-fat diet (HFD) and infected with a low dose of T. muris. WT mice on ND developed chronic infection with strong IgG2a/c responses, consistent with Th1-biased immunity. In contrast, WT mice on HFD achieved near-complete parasite clearance, accompanied by elevated IgG1 and reduced IgG2a/c titres, indicating diet-induced Th2 bias. In RAG1- and RAG1/γc-deficient mice, infection persisted under a normal diet but worm burdens were partially reduced on HFD, indicating that diet enhances parasite control through immune-independent, possibly microbiota-mediated pathways. Microbiota clustered by genotype and diet, with HFD-associated enrichment of Bacteroides, Parabacteroides, and Blautia. These findings demonstrate that diet and immune status jointly shape helminth susceptibility through coordinated effects on host immunity and the gut microbiota.

Malaria pathogenesis is driven by intricate host-parasite interactions that determine immune balance and clinical outcome. The Plasmodium yoelii model, particularly its lethal (17XL) and non-lethal (17XNL) strains, provides a robust framework to investigate these dynamics. This review integrates recent findings demonstrating that 17XL infections trigger excessive pro-inflammatory cytokine release and immune exhaustion, while 17XNL infections sustain regulated Th1/Th2 responses enabling parasite control and survival. Emerging pathways involving MIF, TLR7 signalling, and immune checkpoints (PD-1, LAG-3) underscore the immunological divergence between strains. Evidence converges on a central concept: malaria severity reflects not parasite load but the timing and resolution of host immune responses. Future research using humanised models, single-cell profiling, and immunomodulatory interventions will deepen our understanding of immune regulation and guide novel therapeutic and vaccine strategies against malaria.

Malaria remains a major global health challenge, profoundly influencing host nutritional and immune status. Essential trace elements such as iron, zinc, copper and magnesium play pivotal roles in immune regulation, antioxidant defence, and pathogen control. However, their alterations during malaria infection and implications for disease outcome have been inconsistently reported. This systematic review aimed to synthesise current evidence on serum and plasma concentrations of key trace elements in malaria-infected individuals and experimental models, and to evaluate their relationship with immune responses, disease severity, and treatment outcomes. A systematic search was conducted in various academic databases, including PubMed, Web of Science, Scopus, and Google Scholar for studies published from January 2010 to November 2025. The quality assessment of the studies was done using the Critical Appraisal Skills Programme (CASP) tool. The review followed the Preferred Reporting Items for Systematic Reviews and Meta-Analysis (PRISMA) guidelines to ensure a comprehensive and transparent process. Across human and experimental studies, malaria infection was consistently associated with reduced serum concentrations of iron, zinc, and magnesium, while copper levels showed variable trends, often elevated in acute infection, reflecting an inflammatory response. These alterations were linked to dysregulated cytokine production, particularly increased TNF-α and IL-10, higher parasitemia, and worsened clinical outcomes. Zinc supplementation improved micronutrient status but showed limited impact on malaria incidence. Emerging spectrometric approaches demonstrated utility in trace element profiling for malaria diagnosis and prognosis. Malaria-induced disturbances in trace element homeostasis, notably reduced iron, zinc, and magnesium, and altered copper levels, contribute to immune dysfunction and oxidative stress, aggravating disease severity. Integrating targeted micronutrient interventions with antimalarial therapy may enhance host immune competence and improve treatment outcomes.

Hepatic echinococcosis (HE), a major zoonotic disease, remains endemic in pastoral regions of Western China, where its incidence is closely linked to geographical, livestock and sanitary conditions. The disease presents a significant clinical challenge due to the complexity of host-parasite interactions and a high recurrence rate. To date, the underlying pathogenesis and effective prevention and control strategies remain inadequately studied. Particularly, it is still unclear how innate lymphoid cells (ILCs) affect disease progression and therapeutic intervention. This review focuses on ILCs and their emerging role in the pathogenesis of HE. Through an in-depth analysis of the biological characteristics of ILCs, we revealed their significant role in immune responses and therapeutic mechanisms. Additionally, we also investigated their dynamic involvement in the development of HE. Furthermore, the specific role of gene editing in modulating ILC function was examined. Clinically, we assessed the distribution and functional status of ILCs in patients with HE and analysed their association with hepatic fibrosis and other complications. Finally, we explored novel diagnostic and therapeutic strategies based on ILC functional modulation. In short, this review highlights the critical role of ILCs in shaping the immunological landscape of HE, offering a theoretical basis for the development of ILC-targeted diagnosis and treatment of the disease. Through ILC functional modulation, the intervention of fibrotic progression and immune imbalance holds promise for overcoming current therapeutic limitations and advancing clinical translation.

Toxocariasis is a global zoonotic parasitic disease caused by Toxocara canis that poses significant public health challenges. The development of a vaccine would provide a promising method to control toxocariasis. This study aimed to evaluate the protective efficacy of gamma- and UV-irradiated embryonated T. canis eggs in mice. Seventy Swiss albino mice were classified into four groups: Group (I) the normal control; Group (II) was subdivided into a positive control once (IIA) and positive control twice (IIB); Group (III) was subdivided into a gamma-vaccinated control (IIIA) and gamma-vaccinated challenged (IIIB); and Group (IV) was subdivided into a UV-vaccinated control (IVA) and UV-vaccinated challenged (IVB). On the 28th day post-infection (dpi), scanning electron microscopy, parasitological, histopathological, immunohistochemical and biochemical analyses were performed. Larval counts in the brains and livers of vaccinated mice were significantly decreased. Compared to the positive control groups, vaccinated groups exhibited fewer histopathological alterations, a reduced immunohistochemical expression of IL-1β in the brain and CD68 in the liver, and lower IL-4, IL-10 and IgE levels in both the gamma- and UV-vaccinated challenged groups. Among the two approaches, the UV-irradiated vaccine demonstrated superior protective effects. These findings suggest that vaccination with irradiated T. canis eggs, particularly with UV treatment, is a safe, efficient and cost-effective method for immunoprophylaxis against human toxocariasis.

Leishmania amazonensis is one of the etiological agents of cutaneous leishmaniasis in its localised form. Moreover, this parasite can cause more severe disease conditions, such as diffuse and disseminated cutaneous leishmaniasis. The development of more severe clinical manifestations is associated with the parasite's ability to establish a chronic infection and disseminate to cutaneous tissues distal to the site of primary infection. This ability is dependent on host immune factors but is also influenced by intrinsic factors of the parasite related to pathogenicity and evasion of the immune system. This review discusses immunological and parasitological factors associated with the latency and dissemination of L. amazonensis infection and the consequent development of severe forms of cutaneous disease.

CD154 (CD40L) is of central importance in effector responses mediated by classically activated macrophages. However, there is limited information on the impact of CD154 on macrophage responses in type 2 contexts, characterised by IL-4-induced polarisation and proliferation. CD154 restricts the polarisation and proliferation of peritoneal cavity macrophages in response to exogenous IL-4. Here we address the impact of CD154 on peritoneal macrophages during infection of mice with the intestinal helminth Heligmosomoides polygyrus. This strictly enteric nematode causes recruitment of Th2 cells and macrophages to the peritoneal cavity alongside type 2 polarisation and proliferation of recruited and resident macrophages. Nine days post-infection, there was an increase in the expression of cell-surface CD154 in CD4⁺ T cells together with increased IL-13 levels in the cavity, suggestive of local antigen presentation. Blocking CD154 enhanced the proliferation of resident but not of recently recruited macrophages. CD154 blocking additionally potentiated the expression of type 2 marker Ym1 (Chil3) in resident and recruited macrophages. Unexpectedly, CD154 blocking caused increases in the numbers of recently recruited macrophages and the appearance of cells with characteristics of both differentiating recruited macrophages (expression of folate receptor β and MHCII) and resident macrophages (high-level expression of F4/80 and CD102). Together, these observations suggest that CD154 promotes the acquisition of tissue residence by recruited macrophages. Thus, our results indicate that in a helminth infection CD154 restricts certain aspects of the polarisation and proliferation of macrophages in response to type 2 cytokines while promoting the acquisition of resident phenotype by the recruited macrophages.

Helminth parasites are complex metazoans belonging to diverse taxonomic families, each exhibiting distinct host tissue tropisms as their larval stages migrate through various tissues to complete their life cycles. Migrating larvae through the host trigger tissue disruption/damage, leading to the release of damage-associated molecular patterns (DAMPs). In addition, helminth larvae and adults release excretory/secretory factors, including proteins, lipids, nucleic acids or carry bacterial symbionts, that act as pathogen-associated molecular patterns (PAMPs), which similar to DAMPs, are sensed by innate receptors [pattern recognition receptors (PRRs), and G protein-coupled receptors (GPCRs) and others] in the skin, liver, lungs, intestines, brain, or smooth muscles, triggering localised innate inflammatory responses. The host's innate immunity plays a central role in controlling the infection and/or inducing pathogenesis. This review provides a comprehensive examination of how innate immune receptors and their host- or helminth-derived ligands regulate the control and immunopathogenesis of helminth infections, thereby advancing our understanding of the early host signalling pathways and parasite-derived factors that initiate innate immune responses.