Search Results (89)

The development of FGFR1-driven stem cell leukemia and lymphoma syndrome (SCLL) in mouse models is accompanied by an increase in highly heterogenous myeloid derived suppressor cells (MDSCs), which promote immune evasion. To dissect this heterogeneity, we used a combination of CyTOF and scRNA-Seq to define the phenotypes and genotypes of these MDSCs. CyTOF demonstrated increased levels of circulating macrophages in the peripheral blood of leukemic mice, and flow cytometry demonstrated that these macrophages were derived from Ly6C^Hi M-MDSC as well as the Ly6C^Int and Ly6C^Low monocytic populations. Consistently, scRNA-Seq analysis demonstrated the accumulation of non-classical monocytes (ncMono) during leukemia progression, which also express macrophage markers. These leukemia-induced macrophages show continuous transcriptional reprogramming during leukemia progression, with the upregulation of cellular stress response genes Hspa1a and Hspa1b and inflammation-related gene Nfkbia. Trajectory analysis revealed a transition from classical monocytes (cMono) to ncMono, and potential genes orchestrating this transition process have been identified. Furthermore, T-cell suppression assays demonstrated the immune suppressive abilities of leukemia-induced circulatory macrophages. Targeting these macrophages with the GW2580 CSF1R inhibitor leads to restored immune surveillance and improved survival. Overall, we demonstrate that circulating macrophages are responsible, at least in part, for the immune suppression in SCLL leukemia models, and targeting macrophages in this system improves the survival of leukemic mice. Full article

Background/Objectives: Acne vulgaris can be non-inflammatory lesions, i.e., closed comedones, open comedones, inflammatory lesions, i.e., papules, pustules, cysts, and post-acne lesions. This study aimed to evaluate the expression of TLR2 and TLR4 receptors on classical, intermediate, and non-classical monocyte subpopulations in 38 women with acne vulgaris and to correlate the results with clinical features of the disease and selected skin parameters. Methods: The skin parameters were assessed: level of oiliness, hydration, pH, skin pigmentation (phototype, erythema) using a special diagnostic device (Scientific multi-probe system MPA 6, Courage + Khazaka) with simultaneous determination of monocyte subpopulations in peripheral blood expressing TLR2 and TLR4 using a CytoflexLX flow cytometer (Beckman Coulter). Results: In the study group, the percentage of non-classical monocytes expressing TLR2 was statistically significantly lower than the classical and intermediate monocytes expressing TLR2 (p < 0.001). However, the level of TLR2 receptor expression (MFI) was significantly higher on intermediate monocytes compared to the level of TLR2 expression on classical and non-classical monocytes. In the group of patients with post-acne lesions, a statistically significantly higher percentage of non-classical monocytes with TLR4 expression was observed compared to patients without post-acne lesions (p = 0.009). A statistically significant negative correlation was also observed between the percentage of intermediate and non-classical monocytes with TLR4 expression and the results of the mexameter measurements. Acne has a significant impact on the percentage of monocyte subpopulations expressing TLR2 and TLR4. A higher percentage of non-classical monocytes TLR4+ in the blood is associated with a higher incidence of post-acne lesions. Conclusions: The positive correlation between the degree of skin hydration and the level of TLR2 expression on classical monocytes suggests that these cells play an important role in skin homeostasis and defense against C. acnes. Proper acne care is not only important for aesthetic aspects, but may also have a positive impact on immunological phenomena. Full article

Chikungunya fever (CF), caused by the Chikungunya virus (CHIKV), is characterized by disabling symptoms such as joint pain that can last for months. Monocytes play a central role in immune modulation and viral replication during infection. This study evaluated the clinical and immunological profiles of patients with laboratory-confirmed CF. Fever and joint pain were the most frequently reported symptoms, whereas edema was more common in women. CHIKV-infect individuals exhibited increased TLR4 expression in non-classical monocytes (CD14+CD16++). Additionally, intermediate (CD14+CD16+) and non-classical (CD14+CD16++) monocytes expressing TLR7 were enriched during the acute phase and in some chronic patients, thereby suggest prolonged TLR7 pathway activation. Levels of soluble CD163 (sCD163)—a marker of monocyte/macrophage activation—were elevated as well, indicating sustained immune activation. Coagulation-related mediators—including Tissue factor (TF) and Tissue factor pathway inhibitor (TFPI)—also increased, despite the rarity of hemorrhagic events or thrombocytopenia. Patients with arthritis demonstrated higher frequencies of TLR7+ intermediate monocytes and elevated Epidermal growth factor (EGF) levels, whereas those with edema exhibit increased Vascular endothelial growth factor (VEGF) levels. Overall, these findings highlighted the differential activation of CD16+ monocytes and suggested that sCD163 is a marker of monocyte/macrophage activation during CHIKV infection. Full article

Objective: Anifrolumab is approved for systemic lupus erythematosus (SLE). Its off-label use in non-systemic cutaneous lupus erythematosus (NSCLE) remains poorly characterized. We aimed to assess its effectiveness and safety in refractory NSCLE, supported by a literature review and exploratory immunologic analysis. Methods: This multicenter observational study included patients with NSCLE treated with anifrolumab. Skin disease was assessed using the Cutaneous Lupus Erythematosus Disease Area and Severity Index (CLASI). CLASI scores at baseline were compared to months 1, 3, and 6. A narrative literature review was also conducted. In a subset of three patients, peripheral blood immunophenotyping was performed before and after treatment to explore immunologic surrogate markers associated with clinical response. Results: Fifteen patients (11 women; mean age 52.1 ± 11.7 years) were included. All had received topical corticosteroids and hydroxychloroquine. Most of them had failed multiple systemic therapies. Anifrolumab (300 mg IV every 4 weeks) was used in combination (n = 12) or as monotherapy (n = 3). All patients improved. Median CLASI-A decreased from 16 to 1 (p < 0.001); CLASI-D decreased from 5 to 4 (p < 0.001). The literature review identified 6 publications reporting 14 additional cases of NSCLE with similar outcomes and minimal adverse effects. Immunologic profiling pointed to an increase in intermediate and non-classical and decreased PD-1 expression in monocytes and NK cells after 12 weeks of treatment. Conclusions: Anifrolumab appears effective and relatively safe in refractory NSCLE. Preliminary immunologic data suggest changes in peripheral blood monocyte subsets and NK cells. However, these findings must be confirmed in prospective, controlled clinical trials. Full article

Background: Chronic cytomegalovirus (CMV) infection may favor the development of immunosenescence and inflammation that impair vaccine responses, including COVID-19. In addition, the polymorphism of the interferon-lambda gene (IFNλ) affects COVID-19 immune responses in older adults. Objective: We aimed to investigate the impact of IFNλ polymorphism (IL28B gene-rs12979860) on the immune/inflammatory response to vaccination with CoronaVac for COVID-19 in older adults who were CMV-seropositive. Methods: Blood samples from 42 CMV-seropositive older adults (73.7 ± 4.5 years) were collected before and 30 days after immunization with a second dose of the CoronaVac vaccine to evaluate the immune/inflammatory response. Results: At genotyping, 20 subjects were homozygous for the C/C alleles (Allele-1 group), 5 were homozygous for the T/T Alleles (Allele-2 group), and 17 were heterozygous (C/T, Alleles-1/2 group). The Allele-1 group showed higher IgG levels for COVID-19 (p = 0.0269) and intermediate monocyte percentage (p = 0.017), in contrast to a lower non-classical monocyte percentage (p = 0.0141) post-vaccination than pre-vaccination. Also, this group showed that IgG levels for CMV were positively associated with a systemic pro-inflammatory state and senescent T cells (CD4+ and CD8+). The Allele-2 group presented higher IFN-β levels at pre- (p = 0.0248) and post-vaccination (p = 0.0206) than the values in the Allele-1 and Alleles-1/2 groups, respectively. In addition, the Allele-2 and Alleles-1/2 groups showed that IgG levels for COVID-19 were positively associated with a balanced systemic inflammatory state. Conclusion: CMV-seropositivity in older adults who had Allele-1 could lead to an unbalanced systemic inflammatory state, which may impair their antibody response to COVID-19 vaccination compared to other volunteer groups. Full article

Innate immune cells appear to have an important implication in the resolution and/or the aggravation of the COVID-19 pathogenesis after infection with SARS-CoV-2. To better appreciate the role of these cells during COVID-19, changes in blood eosinophil, the neutrophil and monocyte count, and levels of surface protein markers have been reported. However, analyses at several timepoints of multiple surface markers on granulocytes and monocytes over a period of one month after a SARS-CoV-2 infection are missing. Therefore, in this study, we performed blood eosinophil, neutrophil, and monocyte phenotyping using a list of surface proteins and flow cytometry during a period of 30 days after the hospitalization of patients with severe SARS-CoV-2 infections. Blood cell counts were reported at seven different timepoints over the 30-day period as well as measures of multiple mediators in serum using a targeted multiplex assay approach. Our results indicate a 95% drop in the blood eosinophil count by D1, with eosinophils displaying a phenotype defined as CD69/CD63/CD125^high and CCR3/CD44^low during the early phases of hospitalization. Conversely, by D7 the neutrophil count increased significantly and displayed an immature, activated, and immunosuppressive phenotype (i.e., 3% of CD10/CD16^low and CD10^lowCD177^high, 6.7% of CD11b^highCD62L^low, and 1.6% of CD16^highCD62L^low), corroborated by enhanced serum proteins that are markers of neutrophil activation. Finally, our results suggest a rapid recruitment of non-classical monocytes leaving CD163/CD64^high and CD32^low monocytes in circulation during the very early phase. In conclusion, our study reveals potential very early roles for eosinophils and monocytes in the pathogenesis of COVID-19 with a likely reprogramming of eosinophils in the bone marrow. The exact roles of the pro-inflammatory neutrophils and the functions of the eosinophils and the monocytes, as well as these innate immune cell types, interplays need to be further investigated. Full article

Muscle dystrophies are a group of genetic disorders characterized by progressive muscle degeneration. Prednisone is a glucocorticoid drug widely used to prevent muscle weakness in these diseases. Despite its known beneficial role, the effect of intermittent delivery on monocytes’ polarization and on dystrophic muscle microenvironment has not yet been thoroughly investigated. In this study, our aim was to identify the phenotype of monocyte subsets in blood and the expression of fibrosis-related genes in dystrophic muscle biopsies in patients receiving intermittent prednisone therapy. We found an increased rate of classical monocytes and a decreased rate of non-classical monocytes that expressed anti-inflammatory marker CD206 in treated patients. In dystrophic muscles, 21 fibrosis-related genes were altered, among which we identified CCAAT/enhancer-binding protein beta CEBPB. Both classical monocytes and CEBPB are known for their roles in stimulating collagen 1 production, a probable marker hampering monocyte/macrophage function. Hence, in some patients with muscular dystrophy, intermittent prednisone treatment could shift the monocytes’ phenotype toward an M2, senescent-like profile. This seems to decrease the inflammatory infiltrate in muscle tissue, an observation that needs to be further confirmed. Full article

Elite controllers (ECs) represent a unique subset of people living with HIV (PLWHs), who can suppress viral replication without requiring antiretroviral therapy (ART). However, despite this viral control, ECs exhibit increased incidences of various comorbid conditions and heightened systemic inflammation, which has been linked to monocyte activation. In this study, we performed an in-depth phenotypic analysis of monocytes in a cohort of long-term ECs (LTECs) and compared them to non-controller patients with ART-mediated control of HIV replication and to non-controller patients with uncontrolled viral replication. A total of 67 participants were included: 22 LTECs, 15 non-controllers on ART (onART), 10 non-controllers without ART (offART), and 20 uninfected controls (UCs) as a reference group. Monocyte phenotypes were analyzed using spectral flow cytometry with a 13-marker panel. The data were analyzed using two approaches: (a) FCS Express software v.7 to define different subsets of monocytes and assess the levels of expression of eight different monocyte functional markers and (b) R software v.4.1.1 for unsupervised multidimensional analysis, including batch correction, dimensionality reduction, and clustering analysis. Monocyte phenotypic profiling was conducted using three different approaches: (1) assessment of monocyte subsets (classical, intermediate, and non-classical monocytes); (2) evaluation of the levels of expression of eight monocyte functional markers, and (3) characterization of monocyte clusters defined through the dimensionality reduction of flow cytometry data (56 different clusters). The monocyte phenotype of the onART group closely resembled that of the UC group. In contrast, LTECs exhibited important alterations in the monocyte phenotype compared to that of the UCs, including (a) an increased proportion of intermediate monocytes and a decreased proportion of classical monocytes (p < 0.01), (b) altered expressions of functional markers across monocyte subsets (p < 0.05), and (c) alterations in sixteen different monocyte clusters (twelve decreased and four increased, p < 0.05). Many of these alterations were also observed when comparing the LTEC and onART groups. Our findings suggest that monocyte-driven mechanisms may contribute to HIV control in LTECs; however, some of these alterations could also promote systemic inflammation and immune activation. These observations provide a compelling rationale for considering therapeutic interventions in this unique population of PLWHs. Full article

Background: Based on CD14/CD16 expression, monocytes can be divided into the following three functionally distinct subsets: classical (MO1, CD14++/CD16-), intermediate (MO2, CD14+/CD16+) and non-classical (MO3, CD14^dim/CD16-). An expanded MO1 subset (cutoff, ≥94%) was found to be predictive of CMML. However, the utility of this test in routine practice has important limitations, with some reporting low sensitivity or a lack of correlation. Here, we sought to evaluate the practical usefulness of this test by using our routine antibody panel and a new gating strategy. Methods: Our study included 56 peripheral blood (PB) and 69 bone marrow (BM) samples. The PB cohort included 20 patients with CMML, 21 with no myeloid neoplasms (non-MN) and 15 with other myeloid neoplasms (non-CMML-MN). The BM cohort included 25 CMML, 16 non-MN and 28 non-CMML-MN cases. Taking advantage of an existing 8-color myelomonocytic tube routinely used in our lab, we conducted a retrospective monocyte subset analysis using a new sequential gating strategy. Results: The assay was able to distinguish CMML from non-CMML cases with high sensitivity (90.0%) and specificity (88.9%) in blood samples using a cutoff value of MO1 > 94%. For BM samples, a reduced MO3 < 1.24% was more closely associated with CMML with a sensitivity of 96.0% and a specificity of 79.5%. A side-by-side comparison of our assay with the original “monocyte assay” showed strong agreement. Conclusions: Our study demonstrates the utility of a practical and robust approach for monocyte subset analysis in the diagnosis of CMML. Full article

Background: Patients with chronic kidney disease (CKD) exhibit changes in leukocyte dynamics, leading to altered hematological and biochemical parameters and deteriorating kidney function. In this study, we aim to investigate the correlation between leukocyte subpopulations and hematological and biochemical parameters in patients with end-stage CKD undergoing hemodialysis. Methods: This descriptive, analytical, cross-sectional study included 20 end-stage CKD patients on hemodialysis. Leukocyte subpopulations, including classical monocytes (CD14⁺⁺/CD16⁻), intermediate monocytes (CD14⁺⁺/CD16⁺), non-classical monocytes (CD14⁺/CD16⁺⁺), CD4 T lymphocytes (CD3⁺/CD4⁺), CD8 T lymphocytes (CD3⁺/CD8⁺), B lymphocytes (CD3⁻/CD19⁺), NK cells (CD56⁺/CD16⁺), and iNKT cells (CD3⁺/CD56⁺), were analyzed using flow cytometry. Results: Patients with end-stage CKD on hemodialysis have decreased classical monocytes and increased non-classical monocytes frequency. A positive correlation was observed between non-classical monocytes and total lymphocytes (Rho-Spearman: R = 0.495, p = 0.027) as well as B lymphocytes (R = 0.567, p < 0.05). We discerned the immunological characteristics of diabetic kidney disease (DKD) and CKD due to other causes in this balanced cohort: B lymphocytes negatively correlate with alkaline phosphatase (R = −0.764, p < 0.05), parathyroid hormone (R = −0.929, p < 0.05), and ferritin (R = −0.893, p < 0.05). Additionally, in DKD, non-classical monocytes positively correlate with eosinophils (R = +0.691; p = 0.019) and classic monocytes with neutrophils (R = +0.627, p = 0.039). Meanwhile, a correlation between either total T lymphocytes or helper T lymphocytes and serum albumin was detected on patients with nephropathy due to other causes. Conclusions: CKD alters classical and non-classical monocyte frequency, whilst T and B lymphocyte frequency positively correlates to the proinflammatory non-classical monocytes. In DKD patients, the uremic environment increases classic monocytes, CD16+ inflammatory monocytes, neutrophils, eosinophils, and B lymphocytes. The described leukocyte dynamic correlates with alkaline phosphatase, parathyroid hormone, iron, and serum albumin serological concentration. Full article

Classic congenital adrenal hyperplasia due to 21-hydroxylase deficiency (CAH) requires lifelong glucocorticoid replacement to manage cortisol deficiency and excessive androgen production. Conventional circadian treatment (CT) tries to mimic natural cortisol rhythms, whereas reverse-circadian treatment (RC) prioritizes the suppression of adrenal androgen excess overnight through evening dosing. Limited data exist on the immunological impact of these regimens. A bi-centric study was conducted, including 41 pediatric and adolescent CAH patients. Peripheral blood samples were collected from patients on conventional treatment (n = 38) or RC (n = 16), with 11 RC patients switching to conventional treatment. Immune cell phenotypes, cytokine profiles, and natural killer (NK) cell cytotoxicity were assessed. Patients receiving RC showed lower percentages of CD4+CD25+ T cells (p = 0.0139). After the switch, patients with RC presented with a higher percentage of non-classical monocytes (p = 0.0255) and a lower percentage of Th17 cells (p = 0.0195). A lower expression of CD107 was observed with RC (p < 0.0001), as well as a higher percentage of NKp30 (p = 0.0189). Comparing patients after the switch from RC to HC, patients with RC presented with a lower NKG2D expression (p = 0.0420). Both conventional treatment and RC exhibited distinct immunological impacts, with CT showing modest advantages in normalizing immune phenotypes. These findings suggest that CT may offer immunological benefits for managing young patients with congenital adrenal hyperplasia. Full article

The immune system plays a crucial role in the pathogenesis of neurodegenerative diseases. Here, we explored whether blood immune cell profiles are already altered in healthy individuals with a genetic predisposition to amyotrophic lateral sclerosis (ALS) or Alzheimer’s disease (AD). Using multicolor flow cytometry, we analyzed 92 immune cell phenotypes in the blood of 448 healthy participants from the Berlin Aging Study II. We calculated polygenic risk scores (PGSs) using genome-wide significant SNPs from recent large genome-wide association studies on ALS and AD. Linear regression analyses were then performed of the immune cell types on the PGSs in both the overall sample and a subgroup of older participants (>60 years). While we did not find any significant associations between immune cell subtypes and ALS and AD PGSs when controlling for the false discovery rate (FDR = 0.05), we observed several nominally significant results (p < 0.05) with consistent effect directions across strata. The strongest association was observed with CD57+ CD8+ early-memory T cells and ALS risk (p = 0.006). Other immune cell subtypes associated with ALS risk included PD-1+ CD8+ and CD57+ CD4+ early-memory T cells, non-classical monocytes, and myeloid dendritic cells. For AD, naïve CD57+ CD8+ T cells and mature NKG2A+ natural killer cells showed nominally significant associations. We did not observe major immune cell changes in individuals at high genetic risk of ALS or AD, suggesting they may arise later in disease progression. Additional studies are required to validate our nominally significant findings. Full article

Autism spectrum disorder (ASD) is an early-onset neurodevelopmental condition that now impacts 1 in 36 children in the United States and is characterized by deficits in social communication, repetitive behaviors, and restricted interests. Children with ASD also frequently experience co-morbidities including anxiety and ADHD, and up to 80% experience gastrointestinal (GI) symptoms such as constipation, diarrhea, and/or abdominal pain. Systemic immune activation and dysregulation, including increased pro-inflammatory cytokines, are frequently observed in ASD. Evidence has shown that the innate immune system may be impacted in ASD, as altered monocyte gene expression profiles and cytokine responses to pattern recognition ligands have been observed compared to typically developing (TD) children. In humans, circulating monocytes are often categorized into three subpopulations—classical, transitional (or “intermediate”), and nonclassical monocytes, which can vary in functions, including archetypal inflammatory and/or reparative functions, as well as their effector locations. The potential for monocytes to contribute to immune dysregulation in ASD and its comorbidities has so far not been extensively studied. This study aims to determine whether these monocyte subsets differ in frequency in children with ASD and if the presence of GI symptoms alters subset distribution, as has been seen for T cell subsets. Whole blood from ASD children with (ASD⁺GI⁺) and without gastrointestinal symptoms (ASD⁺GI⁻) and their TD counterparts was collected from children enrolled in the Childhood Autism Risk from Genetics and Environment (CHARGE) study. Peripheral blood mononuclear cells were isolated and stained for commonly used subset identifiers CD14 and CD16 as well as activation state markers CCR2, HLA-DR, PD-1, and PD-L1 for flow cytometry analysis. We identified changes in monocyte subpopulations and their expression of surface markers in children with ASD compared to TD children. These differences in ASD appear to be dependent on the presence or absence of GI symptoms. We found that the ASD⁺GI⁺ group have a different monocyte composition, evident in their classical, transitional, and nonclassical populations, compared to the ASD⁺GI⁻ and TD groups. Both the ASD⁺GI⁺ and ASD⁺GI⁻ groups exhibited greater frequencies of classical monocytes compared to the TD group. However, the ASD⁺GI⁺ group demonstrated lower frequencies of transitional and nonclassical monocytes than their ASD⁺GI⁻ and TD counterparts. CCR2⁺ classical monocyte frequencies were highest in the ASD⁺GI⁻ group. HLA-DR⁺ classical, transitional, and nonclassical monocytes were statistically comparable between groups, however, HLA-DR⁻ nonclassical monocyte frequencies were lower in both ASD groups compared to TD. The frequency of classical monocytes displaying exhaustion markers PD-1 and PD-L1 were increased in the ASD⁺GI⁺ group compared to ASD⁺GI⁻ and TD, suggesting potentially impaired ability for clearance of foreign pathogens or debris, typically associated with worsened inflammation. Taken together, the findings of differential proportions of the monocyte subpopulations and altered surface markers may explain some of the characteristics of immune dysregulation, such as in the gastrointestinal tract, observed in ASD. Full article

Background/Objectives: Obesity is closely linked to chronic low-grade inflammation and the development of cardio-metabolic comorbidities. Monocyte subsets, which are crucial in immune responses, have been reported to be altered in individuals with obesity, potentially exacerbating inflammation. Although very-low-calorie ketogenic diets (VLCKDs) are recognized for their efficacy in promoting weight loss and improving metabolic health, their impact on circulating monocyte subsets remains poorly understood. The objective of our study is to investigate the impact of VLCKDs on monocyte subset distribution in people with obesity. Methods: Thirty-six participants were divided into four groups—healthy controls, individuals with obesity and no dietary intervention, and individuals with obesity following either a low-calorie diet (LCD) or VLCKD for 28 days. Blood samples were analyzed to assess the distribution of classical monocytes (CMs), intermediate monocytes (IMs), and non-classical monocytes (NCMs) using flow cytometry. Results: Individuals with obesity exhibited significant increases in IMs and NCMs, alongside a decrease in CMs compared to healthy controls. The VLCKD led to a notable shift in monocyte distribution, with increased CMs and reduced IMs and NCMs, restoring levels closer to those observed in healthy individuals. In contrast, the LCD group showed no significant changes in monocyte subsets. Conclusions: VLCKDs may exert anti-inflammatory effects by modulating monocyte subset distribution, offering potential therapeutic benefits in mitigating obesity-related inflammation. These preliminary findings suggest that VLCKDs could be an effective strategy for improving immune function in individuals with obesity. Full article

Background: The Epstein–Barr virus (EBV) infects more than 90 percent of the human population. In pediatric patients, the innate immune response against EBV primary infection plays a key role. Monocytes and macrophages can have distinct functions depending on the microenvironment surrounding them. At least three monocyte subpopulations can be differentiated depending on membrane protein expression: classical (C, CD14++CD16−), intermediate (I, CD14++CD16+), and non-classical (NC, CD14+CD16++). They also modulate T and B lymphocyte activation/inhibition through the expression of costimulatory molecules such as CD80, CD86, and PD-L1. Yet, little is known about monocytes’ role in EBV infection. Methods: Peripheral blood and tonsil biopsies of EBV primary infected (PI) patients, healthy carriers (HCs), and patients undergoing reactivation (R) were studied. Results: Classical monocytes prevailed in all infectious statuses. Tonsillar CD163 positively correlated with CD163 expression in NC monocytes in HCs. PD-L1+ cells in the tonsil positively correlated with PD-L1 expression in NC monocytes. LMP-1 viral latent protein presented a positive correlation with PD-L1, CD163, and CD206 expression in the NC subpopulation. Conclusions: Our results evidence the predominant role of I and NC monocytes’ response against EBV infection. Furthermore, the viral oncoprotein LMP-1 could be involved in the expression of regulatory proteins in I and NC monocytes. Full article