Search Results (155)

Background/Objectives: Hepatocellular carcinoma (HCC) is challenging to treat with chemotherapy. Immunotherapy has shown moderate responses in inflammatory and immunosuppressive tumor environments. Hepatic cytochrome P450 monooxygenases (CYPs) play a crucial role in xenobiotic and drug metabolism, as well as lipid and steroid metabolism. We aimed to investigate whether CYP expression and various parameters of the innate and adaptive immune system are prognostic factors for the survival of HCC patients. Methods: HCC biopsies (n = 370) from The Cancer Genome Atlas (TCGA) database were analyzed using Kaplan–Meier statistics and the KMPlotter algorithm. Parameters such as immune cell infiltration, DNA mutation rates, and neoantigen load were selected for survival analysis and subjected to hierarchical cluster analysis. The expression of candidate CYP genes in tumors was compared to that in normal liver tissues. Furthermore, tumor infiltration of innate immune cells (basophilic and eosinophilic granulocytes, natural killer cells), adaptive immune cells (CD4+ memory and CD8+ cytotoxic T cells, regulatory T cells, type 1 and type 2 helper T cells), and mesenchymal stem cells was examined. Results: High expression of CYP19A1 and CYP26B1 was associated with shorter survival, whereas high expression of CYP3A5, CYP3A43, CYP7A1, and CYP27A1 was linked to longer survival. Mutation rates combined with CYP expression showed a correlation with five out of six CYP genes, while a high neoantigen load produced less definitive results. A specific cluster exhibiting high CYP expression and immune cell counts or mutation/neoantigen rates was associated with shorter survival, while another cluster was linked to longer survival. Conclusions: CYPs involved in the metabolic regulation of HCC, including CYP3A5, CYP3A43, CYP7A1, CYP19A1, CYP26B1, and CYP27A1, were found to have prognostic value for patient survival. Combined signatures that include CYP expression, mutational rates, and immune cell infiltration into tumors further enhanced the prognostic value for patient survival. This suggests that CYPs may influence the creation of a tumor-specific metabolic microenvironment that impacts immune functions. These combined signatures could be utilized for patient stratification to personalize tumor treatment and develop novel combination therapies aimed at optimizing treatment outcomes, such as combining transarterial chemoembolization (TACE) with immune checkpoint inhibitors. Full article

Eicosanoids and their receptors act as key regulators of inflammation, calcium homeostasis, mitochondrial function, and cardiomyocyte survival, thereby contributing to the onset and progression of cardiac dysfunction. This review aims to summarize the evidence to underscore the pivotal role of eicosanoids and their receptors in the pathophysiology of cardiomyopathy, analysing the potential protective activity of traditional and natural compounds to counteract cardiovascular disease onset and progression. Among eicosanoid receptors, prostaglandin E2 receptor 3 (EP3), prostaglandin E2 receptor 4 (EP4), chemoattractant receptor expressed on type 2 helper T cells (CRTH2), and thromboxane prostanoid (TP) emerge as critical modulators with distinct and often opposing effects on cardiac physiology. While EP3 and CRTH2 are predominantly associated with detrimental outcomes such as impaired contractility and enhanced apoptosis, EP4 signalling consistently demonstrates cardioprotective properties, including improved calcium handling and preservation of mitochondrial integrity. These findings highlight the therapeutic potential of selectively targeting eicosanoid receptor pathways to mitigate cardiac remodelling and dysfunction. In parallel, increasing attention has been directed toward natural bioactive compounds as complementary strategies for cardioprotection. Polyphenols, flavonoids, carotenoids, and other nutraceuticals exert beneficial effects through antioxidant, anti-inflammatory, and anti-apoptotic mechanisms, often intersecting with eicosanoid signalling pathways. Their ability to modulate oxidative stress and inflammatory responses suggests a promising role in preventing or attenuating cardiomyopathy, particularly in metabolic and drug-induced contexts. Future research should focus on well-designed clinical trials, a deeper characterization of receptor-specific signalling networks, and the development of targeted therapies that combine pharmacological and nutraceutical approaches. Overall, a better understanding of eicosanoid-mediated mechanisms may open new ways for cardiomyopathy prevention and treatment, ultimately improving patient outcomes and reducing the burden of cardiovascular disease. Full article

Mitophagy clears damaged mitochondria and maintains normal macrophage function. Clarifying the associations between idiopathic pulmonary fibrosis (IPF), macrophages, and mitophagy is crucial for early diagnosis and clinical management. Core macrophage subsets were identified as M2 macrophages via single-cell RNA sequencing and immune infiltration analysis. Differentially expressed genes related to this subset were obtained. Integrated differential expression analysis, weighted gene co-expression network analysis, machine learning, and expression verification were applied to screen biomarkers. CD163 and SPP1 were identified through biomarker screening, both showing significantly increased expression in IPF. Functional enrichment showed that these biomarkers are mainly involved in cell cycle checkpoints and ciliopathies. Immune microenvironment analysis identified 16 immune cell types with significant differences between IPF and control groups, among which T helper 2 cells were strongly positively correlated with CD163. A total of nine drugs were found to be associated with CD163 and SPP1. The expression of these biomarkers changed dynamically during M2 macrophage differentiation. This study integrates single-cell and bulk transcriptomics analysis to reveal the critical roles of CD163 and SPP1 in the IPF macrophage–mitochondrial autophagy axis, a novel framework for understanding the macrophage–mitophagy axis in IPF pathogenesis. Full article

Atopic dermatitis (AD) is a chronic inflammatory skin disorder characterized by epidermal barrier dysfunction and dysregulated immune responses, particularly an imbalance between T helper type 1 (Th1) and type 2 (Th2) cytokines. Natural products with immunomodulatory activity have attracted increasing attention as potential strategies for regulating allergic inflammation. In this study, we investigated the immunomodulatory effects of bioprocessed black rice bran (BRB-F) and bioprocessed balloon flower root (BFR-F). In vitro assays using human B cells, mast cells, and keratinocytes were conducted to evaluate IgE production, mast cell degranulation, and epithelial inflammatory mediator release. The efficacy of the BRB-F:BFR-F mixture was further evaluated in BALB/c mice with 2,4-dinitrochlorobenzene (DNCB)/Dermatophagoides farinae extract (DFE)-induced AD-like dermatitis. BRB-F and BFR-F suppressed IgE production, attenuated mast cell degranulation and thymic stromal lymphopoietin (TSLP) release, and reduced keratinocyte-derived inflammatory mediators (thymus and activation-regulated chemokine (TARC), macrophage-derived chemokine (MDC), and IL-6). In mice, dietary supplementation with the BRB-F:BFR-F mixture (10–80 mg/kg/day) dose-dependently improved clinical skin lesions and histopathological changes, with serum IgE reduced by up to 87.1% at the highest dose. The treatment significantly suppressed Th2 cytokine mRNA expression in ear tissue (IL-4, IL-5, and IL-13) by 37.2%, 32.7%, and 34.0%, respectively, compared with the positive control. In contrast, splenic Th1 cytokine mRNA expression (IL-2, IL-12, and IFN-γ) was partially restored by 37.1%, 22.5%, and 18.7%, respectively. These findings indicate that BRB-F and BFR-F modulate multiple immune pathways and help restore Th1/Th2 immune balance, suggesting their potential as functional materials for regulating immune dysregulation associated with AD. Full article

Adipose-derived stem cells (ASCs) and their secretome have been reported to improve allergic airway inflammation. Eosinophilic chronic rhinosinusitis with nasal polyps (ECRSwNP) is characterized by type 2 helper T (Th2)-diven inflammation, which shares similar mechanisms with allergic airway diseases. We assessed the immunomodulatory effects of ASC secretome on an ECRSwNP mouse model. ECRSwNP was induced by ovalbumin (OVA) and Staphylococcus aureus enterotoxin B (SEB) intranasal challenges in five-week-old BALB/c mice. To evaluate the effect of ASC secretome on eosinophilic nasal inflammation, 10 μg/50 μL of ASC-conditioned media were administered three times a week during the eight weeks. H&E and Sirius red staining were performed to evaluate the formation of nasal polyps (NPs) and the infiltration of eosinophils. The cytokine levels of interleukin (IL)-4, IL-5, IL-13, interferon-γ, IL-8, and eotaxin-1 were measured using ELISA(eBiosciences, San Diego, CA, USA). The expression levels of IL-8 and eotaxin-1 mRNA were determined by quantitative PCR. Eosinophil cationic protein (ECP) and eotaxin-1 expression were assessed by immunohistochemistry. Intranasal administration of ASC secretome significantly decreased NP-like formation and eosinophilic infiltration in the sinonasal mucosa of ECRSwNP mice. The increased IL-4, IL-5, and eotaxin-1 levels after OVA + SEB challenge remarkably decreased by ASC secretome treatment. Furthermore, ASC secretome notably decreased the gene expression of eotaxin-1 by PCR, as well as ECP and eotaxin-1 expression by immunohistochemistry. ASC secretome had immunomodulatory effects in a mouse model of ECRSwNP. Intranasal administration of ASC secretome resulted in a significant reduction in NP formation and eosinophilic inflammation through the suppression of IL-4, IL-5, eotaxin-1, and ECP. Full article

Background and Objectives: MGN-3/Biobran (BRM4, Lentin Plus or Ribraxx) is a natural, rice bran-derived arabinoxylan immunoceutical that modulates the adaptive immune response to viral infections. In response to bacterial infections, basophils act as “first responders” and are also associated with modulation of the adaptive immune response. The maturation of pluripotent CD34⁺ stem cells into basophils is supported by the cytokine interleukin-3 (IL-3). The aim was to test the hypothesis that modulation of the adaptive immune response in bacterial infection by MGN-3/Biobran entails a basophilic response. The tick-related disorder Lyme borreliosis was chosen as the disease model; tick bites are associated with cutaneous IL-3-mediated basophil recruitment. Materials and Methods: A three-month randomised double-blind placebo-controlled trial was conducted in patients with a history of borreliosis who were suffering from symptoms attributable to this disorder. The immunoceutical group received oral Biobran; the dosage for both groups was 1 g thrice daily. Both groups were matched for age, sex, and ethnicity. Results: A higher percentage of basophil count occurred in the immunoceutical group (p = 0.038). The final general linear model included the group (immunoceutical/placebo) and change in fatigue assessed by the 11-item Chalder Fatigue Questionnaire (CFQ) (r² = 0.63; p = 0.0066). The change in basophil count was positively correlated with CFQ change (r_s = 0.633; p = 0.020); only the immunoceutical group showed a positive correlation. Conclusions: These results support the hypothesis being tested. Basophils may modulate the adaptive immune response by acting as immunoregulatory cells. They can regulate the functioning of type 2 T-helper lymphocytes, enhance immunological memory, and present antigens to CD8 T lymphocytes. Further studies are needed to clarify potential mechanistic factors and the timing of this basophilic response. Full article

T helper 2 (Th2)-mediated dermatoses are inflammatory skin diseases driven by CD4⁺ Th2 cells that produce interleukin (IL)-4, IL-5, IL-13, and IL-31, promoting immunoglobulin E (IgE) class switching, eosinophil recruitment, mast cell degranulation, and pruritus. We aimed to place these conditions in context and clarify how Th2 biology informs diagnosis and therapy. We conducted a narrative synthesis of mechanistic, translational, and clinical evidence on Th2 pathways in atopic dermatitis (AD), prurigo nodularis, bullous pemphigoid, chronic spontaneous urticaria, and selected type I/IVb hypersensitivity reactions, with focused appraisal of trials targeting IL-4Rα, IL-13, and IL-31R. Persistent Th2 activation is associated with epidermal barrier dysfunction, immune dysregulation, and pruritogenic neural signaling; AD is the archetype, showing prominent lesional IL-4/IL-13 activity correlated with severity and itch. Across disorders, pathway-directed biologics against IL-4Rα, IL-13, and IL-31R consistently reduce disease activity and pruritus in AD and prurigo nodularis, with emerging signals of benefit in bullous pemphigoid and chronic spontaneous urticaria. The Th2 axis provides a unifying pathogenic framework and actionable therapeutic target across multiple dermatoses. Integrating cytokine profiling with clinical phenotypes may refine patient stratification and optimize the deployment of existing and next-generation Th2-targeting therapies. Full article

Homeostasis must be maintained for the healthy living of an organism. In addition to physiological and anatomical homeostasis, the maintenance of the immune system, called immune homeostasis or immunohomeostasis, is critical for overall well-being and general homeostasis. CD8⁺ cytotoxic T cells/lymphocytes (CTLs) are crucial components of the adaptive immune systems of all vertebrates with a thymus. Hence, the thymus is an essential primary lymphoid organ (PLO) for developing T cell-mediated immunity (TCMI) that comprises CD4⁺ helper T cells (Th) cells and their subtypes, such as Th0 (naïve helper T cells), Th1 (pro-inflammatory Th cells that secrete IFN-γ), Th2 (secrete type 2 cytokines, such as IL-4, IL-5, IL-6, IL-10, and IL-13), Th9 (secrete IL-9), Th17 (secrete IL-17), Th22 (secrete IL-22), follicular Th cells (T_fhs, secrete IL-21), regulatory T cells (T_regs), and CD8⁺CTLs. The current article explores the critical role of CD8⁺CTLs in the maintenance of immune homeostasis. The role of the thymus (PLO) in generating and regulating CD8⁺CTLs, as well as mobilizing them to distant lymph nodes (LNs) and the spleen, which are referred to as secondary lymphoid organs (SLOs) and target organs, is discussed in section two of the article. The subsequent third section discusses the role of CD8⁺CTLs’ cytotoxic and immunoregulatory action to maintain immune homeostasis during infection and other inflammatory conditions. Moreover, they mask themselves to different cell types, like Th cells, such as Tc2s, Tc9s, Tc17s, and Tc22s, to maintain immune homeostasis. CD8⁺CTLs also behave as T_regs to exert their immunoregulatory functions. In addition to conventional CD8⁺CTLs, granzyme K (GzmK)⁺CD8⁺CTLs and CD4⁺CTLs with their cytotoxic action to maintain immune homeostasis have also been discussed. The next section discusses cell–cell (APC–CD8⁺CTL) interactions that not only increase the cytotoxic functions of CD8⁺CTLs but also program APCs to support their cytotoxic functions. These CD8⁺CTLs secrete different cytokines (IFN-γ and IL-10) and cytotoxic molecules (perforin and Gzms), which exert immunoregulatory actions to maintain immune homeostasis. The article concludes with a future perspective and a conclusion section, highlighting the critical need to understand CD8⁺CTLs’ cytotoxic and immunoregulatory functions in maintaining immune homeostasis across various diseases, including those with newly identified roles for CD8⁺CTLs. Full article

Lupus nephritis (LN) is a serious complication of systemic lupus erythematosus that is associated with long-term morbidity and mortality. Pathomorphological findings of LN are broadly divided into proliferative lupus nephritis (PLN) and membranous lupus nephritis (MLN). PLN is characterized by diffuse global or segmental proliferative glomerulonephritis with significant infiltration of inflammatory cells. Type 1 T-helper (Th1) cells, which predominate under inflammatory conditions, and NETosis, as the process of forming neutrophil extracellular traps (NETs), are key factors in the development of PLN. Meanwhile, MLN is characterized by diffuse membranous nephropathy (MN) with global granular subepithelial immune deposits. MLN patients usually experience massive proteinuria, and occasionally show an unfavorable renal prognosis despite aggressive treatment, similar to PLN patients. Intriguingly, in some instances, MLN patients do not show the general immunoserological characteristics of SLE, such as low serum complement and elevated anti-DNA antibody titers. Several reports have indicated an association between Th2 cell dominance and the development of MLN. Moreover, exostosin 1 (EXT1) and exostosin 2 (EXT2) on the glomerular basement membrane have recently been discovered as novel putative antigens for secondary MN, and have been shown to be up-regulated in patients with MLN. To date, many studies have focused on the dissimilarities between PLN and MLN. However, the reason for two polar morphological forms existing within the same disease is not completely clear. The present review addresses published observations on this topic in addition to providing our assertion regarding characteristic NETosis and glomerular EXT1/EXT2 expressions between PLN and MLN. Full article

Mast cells (MC) are key effector cells in allergic diseases and are increasingly recognized for their roles in the immunopathogenesis of tuberculosis (TB). In allergic conditions, MCs are hyperactivated, driving T-helper Type 2 (Th2)-skewed immune responses that may antagonize the T-helper Type 1 (Th1)-mediated immunity essential for controlling Mycobacterium tuberculosis (Mtb) infection. This immunological imbalance may contribute to increased TB susceptibility, altered granuloma dynamics, and accelerated fibrotic remodeling. Histopathological and in vivo studies have revealed that MCs are recruited to TB lesions, where they release a spectrum of mediators, including histamine, IL-17A, TNF-α, TGF-β, tryptase, and chymase. These mediators can either support initial immune defense or promote chronic inflammation and tissue damage, depending on context and regulation. Moreover, individuals with chronic allergic diseases such as asthma and allergic rhinitis may experience worse TB outcomes due to their baseline immune dysregulation. Environmental exposures (e.g., air pollution, smoking), genetic polymorphisms (e.g., IL-4 −589C/T, IL-13 R130Q), and gut-lung axis disturbances further modulate MC activity and TB pathogenesis. This review synthesizes current findings on MC involvement in TB, particularly in allergic settings, and highlights the need for epidemiological studies and mechanistic research. It also explores the promise of host-directed therapies (HDTs) that target MCs or their mediators, such as antihistamines, MC stabilizers, leukotriene inhibitors, and cytokine modulators, as novel adjuncts to standard TB treatment. Personalized approaches that consider immune profiles, genetic risk, and comorbid allergies may improve TB outcomes and inform future clinical guidelines. Full article

Background/Objectives: We previously demonstrated that dendritic cell (DC) expression of CXCR5 is required for T_H2 priming in mice infected with the helminth Heligmosomoides polygyrus (Hp). In this manuscript we examined how CXCR5 controls DC mediated CD4 T helper 2 cell (T_H2) development. Methods: We used in vitro T_H2 priming assays, RNA-seq analyses and in vivo Hp infection mouse models to identify roles for the CXCR5-expressing DCs in T_H2 development. Results: We showed that migratory conventional type 2 dendritic cells (cDC2) express CXCR5 and that deletion of Cxcr5 prevents migratory DC priming of T_H2 cells in vitro while overexpression of CXCR5 enhances migratory DC priming of T_H2 cells in vitro. To understand how CXCR5 facilitates the T_H2 priming capabilities of migratory cDC2 cells, we performed RNAseq analysis on wildtype and Cxcr5^−/− DC subsets isolated from msLN of Hp-infected mice. We observed that CXCR5 expression specifically by the migratory cDC2 subset promoted a pro-proliferative transcriptional program in cDC2 cells and was required for cDC2 cell accumulation in the msLN following Hp infection. We demonstrated that CXCR5 expression specifically by cDC2 cells was necessary for upregulation of Chitinase 3-like-1 (Chi3l1), which encodes a secreted protein (Chi3l1) that regulates allergic T_H2 responses. We showed that addition of recombinant Chi3l1 protein to in vitro T_H2 priming cultures enhanced T_H2 development and that deletion of Chi3l1 specifically in DCs resulted in fewer cDC2 cells and decreased T_H2 development in vivo following Hp infection. Conclusions: CXCR5 expressed by cDC2 cells is required for induction of Chi3l1, which in turn promotes the T_H2 priming capacity of these DCs. These findings provide insight into the actions of CXCR5 and Chi3l1 in helminth infection. Full article

Respiratory syncytial virus (RSV) remains a leading cause of acute lower respiratory tract infections globally, particularly affecting infants, older adults, and immunocompromised individuals. While recent advances in prophylaxis, such as long-acting monoclonal antibodies and maternal immunization, offer promise for prevention, therapeutic options for active infection remain limited. Severe RSV disease is often driven not solely by viral replication but by dysregulated host immune responses, including excessive cytokine production, T helper type 2 (Th2) and T helper type 17 (Th17) cell polarization, and impaired interferon signaling. RSV has evolved sophisticated immune evasion strategies, such as inhibition of dendritic cell maturation, degradation of signal transducer and activator of transcription 2 (STAT2) via nonstructural proteins 1 and 2 (NS1/NS2), and interference with pattern recognition receptor signaling, particularly Toll-like receptors (TLRs) and retinoic acid-inducible gene I (RIG-I)-like receptors. These mechanisms result in attenuated innate immune responses and defective adaptive immunity, contributing to viral persistence, immunopathology, and recurrent infections. Moreover, age-dependent vulnerabilities, such as immune immaturity in infants and immunosenescence in older adults, exacerbate disease severity. Excessive immune activation leads to bronchiolitis, airway remodeling, and long-term sequelae including wheezing and asthma. Emerging immunomodulatory therapies aim to restore immune balance, targeting cytokines (e.g., interleukin-6 [IL-6], interleukin-1 beta [IL-1β]), the Janus kinase–signal transducer and activator of the transcription (JAK-STAT) pathway, or inflammasome activity. Host-directed therapies and direct-acting antivirals are also under investigation. A better understanding of RSV–host immune interactions is critical for optimizing therapeutic strategies and designing effective vaccines. This review synthesizes current knowledge on RSV immunopathogenesis and highlights immunomodulation as a promising frontier for therapeutic intervention. Full article

Atopic dermatitis (AD) is a common chronic inflammatory skin disorder characterized by immune dysregulation and skin barrier impairment. This study evaluated the anti-inflammatory and immunomodulatory effects of Camellia japonica extract in a 2,4-dinitrochlorobenzene (DNCB)-induced AD mouse model using SKH-1 hairless mice. Topical application of Camellia japonica extract for four weeks significantly alleviated AD-like symptoms by reducing epidermal thickness, mast cell infiltration, and overall skin inflammation. Hematological analysis revealed a marked decrease in total white blood cell (WBC) and neutrophil counts. Furthermore, the Camellia japonica extract significantly decreased oxidative stress, as evidenced by reduced serum reactive oxygen species (ROS) and nitric oxide (NO) levels, while enhancing the activity of antioxidant enzymes such as catalase. Importantly, allergic response markers including serum immunoglobulin E (IgE), histamine, and thymic stromal lymphopoietin (TSLP), were also downregulated. At the molecular level, Camellia japonica extract suppressed the expression of key pro-inflammatory cytokines, including tumor necrosis factor-alpha (TNF-α), interleukin (IL)-1β, and T helper 2 (Th2)-type cytokines such as IL-4 and IL-5, while slightly upregulating the anti-inflammatory cytokine IL-10. Collectively, these findings suggest that Camellia japonica extract effectively modulates immune responses, suppresses allergic responses, attenuates oxidative stress, and promotes skin barrier recovery. Therefore, application of Camellia japonica extract holds the promising effect as a natural therapeutic agent for the prevention and treatment of AD-like skin conditions. Full article

Background: Alopecia areata (AA), an autoimmune condition causing non-scarring hair loss, often coexists with atopic dermatitis (AD) due to shared T-helper cell type 2 (Th2)-mediated pathways. Dupilumab, a monoclonal antibody inhibiting IL-4 and IL-13 signaling, is a cornerstone treatment for AD but has conflicting reports regarding its impact on AA, with some suggesting therapeutic benefits and others indicating AA induction. Methods: This retrospective study, utilizing the TriNetX Research Network’s de-identified data from over 300 million patient records, investigates the association between dupilumab use and AA risk in AD patients. Results: After propensity score matching, 23,782 dupilumab users were compared with an equal number of controls. Results revealed a statistically significant increased AA risk in dupilumab users (odds ratio: 1.436, 95% CI: 1.066–1.935, p = 0.0167) after 16 weeks. Cases occurring within 16 weeks were excluded. Conclusions: Potential mechanisms include immune rebalancing, with Th2 suppression possibly upregulating Th1/Th17 pathways or unmasking latent AA in predisposed individuals. These findings challenge dupilumab’s potential as an AA treatment and highlight the need for vigilant monitoring, including routine scalp examinations and patient education. Future research should focus on mechanistic pathways, risk stratification, and comparative studies with other biologics to optimize personalized treatment strategies for AD and AA. Full article

Fasciola gigantica (F. gigantica) is a vital parasite that causes fasciolosis. Liver fluke infections affect livestock animals, and the Fasciola species (Fasciola spp.) vaccine has been tested for many types of these diseases. Currently, computer-based vaccine design represents an attractive alternative for constructing vaccines. Thus, this study aimed to design the epitopes of linear B-cells (BCL) and helper T lymphocytes (HTL) using an immunoinformatic approach and to investigate in silico and the mice’s immune response. A non-conserved host region, overlapping F. gigantica cathepsin B proteins (FgCatB), and the highest conserved residue percentages were the criteria used to construct epitopes. The GPGPG linker was used to link epitopes in the multi-epitope Fasciola gigantica cathepsin B (MeFgCatB) peptide. The MeFgCatB peptide has high antigenicity, non-allergenicity, non-toxicity, good solubility, and a high-quality structure. The molecular docking between the MeFgCatB peptide and Toll-like receptor 2 (TLR-2) was evaluated. The IgM, IgG1, and IgG2 levels were elevated in silico. In mice, the MeFgCatB peptide was synthesized and administered as an injection. The MeFgCatB-specific IgG1 and IgG2a levels were elevated after week 2, showing a predominance of IgG1. The rFgCatB1, rFgCatB2, and rFgCatB3 were detected using the MeFgCatB peptide-immunized sera. The MeFgCatB peptide-immunized sera were detected at approximately 28–34 kDa in the whole body. In addition, the MeFgCatB immunized sera can positively signal at the caecal epithelium in the NEJ, 4WKJ, and adult stages. In summary, the MeFgCatB peptide is able to induce mixed Th1/Th2 immune responses with Th2 dominating and to detect the native protein of F. gigantica. The MeFgCatB peptide should help against F. gigantica in future experiments. Full article