Antibody-dependent cell-mediated cytotoxicity (ADCC) evolution under treatment by cetuximab and links with treatment outcome in colorectal cancer (CRC) patients.

2012 ◽  
Vol 30 (15_suppl) ◽  
pp. 2600-2600
Author(s):  
Marco Carlo Merlano ◽  
Martino Monteverde ◽  
Giuliana Strola ◽  
Jerome Barriere ◽  
Marie-Christine Etienne-Grimaldi ◽  
...  
Keyword(s):  
Treatment Outcome ◽  
Gene Polymorphisms ◽  
Immune Cell ◽  
Ex Vivo ◽  
Cancer Cell Line ◽  
Target Cells ◽  
Allelic Discrimination Assay ◽  
Allelic Discrimination ◽  
Significant Drop ◽  
Patient Gender

2600 Background: ADCC plays a role in antitumor activity of IgG1 mAb by inducing immune cell-mediated lysis of tumor cells. We evaluated ADCC ability before and under cetuximab-based treatment and examined its impact on treatment outcome. Methods: 29 patients (17 men, 12 women, median age 72, range 51-84) with metastatic wild-type KRAS CRC treated with chemotherapy (irinotecan or Folfiri) plus cetuximab were prospectively enrolled. ADCC ex-vivo was measured before starting treatment and every 2 months during treatment (1 to 7 measurements/patient, 12 patients with >2 measurements). 400 000 purified Natural Killer cells (CD3- CD56+) from patients were incubated with 10 000 target cells (CAL166 cancer cell line expressing EGFR) and 10 µg/ml cetuximab (triplicates). Cytotoxicity was measured by the LDH-release assay. ADCC was expressed as the % of lyzed target cells. Gene polymorphisms of Fcγ receptors FCGR2a (131Arg>His) and FCGR3a (158Phe>Val) were analyzed (Allelic Discrimination assay). Results: The feasibility rate of ADCC measurement was 88%. ADCC basal values ranged between 30% and 100% (mean 62%, median 66%). Basal ADCC was not influenced by patient gender. A tendency for an increased ADCC basal value was observed in younger patients: median was 76% in the 6 patients ≤ 60 vs 56% in the 23 patients over 60 years-old (p = 0.031). FCGR2A and FCGR3A gene polymorphisms were not linked to basal ADCC. The evolution of individual ADCC ability before treatment and 2 months later revealed a significant drop in ADCC following treatment initiation (intra-patient comparison, n=18, p=0.006), with an absolute median drop of 19%. This decrease was not sustained over time and intra-patient comparison between basal value and 4-month measurement was not significant. 25 patients were assessable for survival (11 deaths). Basal ADCC values were not related to survival. Conclusions: A new generation of mAb is currently being developed with the aim to amplify ADCC. Present data illustrate the feasibility of ADCC measurement in mAb-treated patients and reveal an initial drop in ADCC under treatment that may reflect the variable chemotherapy-induced impact on host immunity.

C-Reactive Protein Gene Polymorphisms in Biopsy-proven Giant Cell Arteritis from Northwestern Spain

2009 ◽  
Vol 36 (2) ◽  
pp. 341-346 ◽  
Author(s):  
ROGELIO PALOMINO-MORALES ◽  
TOMAS R. VAZQUEZ-RODRIGUEZ ◽  
JOSE A. MIRANDA-FILLOY ◽  
JAVIER MARTIN ◽  
MIGUEL A. GONZALEZ-GAY
Keyword(s):  
Giant Cell Arteritis ◽  
Giant Cell ◽  
Gene Polymorphisms ◽  
Reaction System ◽  
C Reactive Protein ◽  
Allelic Discrimination Assay ◽  
Allelic Discrimination ◽  
Potential Implication ◽  
Reactive Protein ◽  
Northwestern Spain

Objective.To investigate the potential implication of several polymorphisms of the C-reactive protein (CRP) gene in the predisposition to or clinical expression of giant cell arteritis (GCA).Methods.A total of 125 patients diagnosed with biopsy-proven GCA and 234 ethnically matched controls from the Lugo region of Northwestern Spain were included in our study. Four functional gene polymorphisms for CRP rs1417938, rs1800947, rs1205, and rs3093059 variants were assessed using a polymerase chain reaction system with predeveloped TaqMan allelic discrimination assay.Results.Although we observed a significant increase in the frequency of heterozygotes for rs1417938 A/T [odds ratio (OR) = 1.70; 95% confidence interval (CI) 1.04–2.80; p = 0.03] and rs1205 C/T (OR 1.73; 95% CI 1.07–2.78; p = 0.02) in patients with GCA, no statistically significant differences in the allelic frequencies of these 2 polymorphisms were found between patients with GCA and controls. A marginal significant increase in the frequency of rs3093059 allele T in patients with GCA compared to controls was observed (OR 1.81; 95% CI 0.97–3.39; p = 0.04). However, the increased frequency of patients with GCA homozygous for rs3093059 T/T in patients with GCA compared to controls was out of the range of significance (OR 1.77; 95% CI 0.92–3.40; p = 0.07). No significant differences were found when we stratified patients with GCA according to the presence of polymyalgia rheumatica or severe ischemic complications of the disease.Conclusion.The functional CRP gene polymorphisms assessed in our study do not seem to play a major role in the pathogenesis of GCA in individuals from Northwestern Spain.

HLA-DQ gene polymorphisms are associated with hepatitis B virus in patients with hepatocellular carcinoma progression

2020 ◽  
Vol 16 ◽  
Author(s):  
Amal A. Mohamed ◽  
Adel Abdel Hady ◽  
Somia Saad ◽  
Shrouk Mausa ◽  
Omnia Tantawi ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Hepatitis B Virus ◽  
Hepatitis B ◽  
Gene Polymorphisms ◽  
Strong Association ◽  
Control Group ◽  
Allelic Discrimination Assay ◽  
Allelic Discrimination ◽  
Hla Dq ◽  
B Virus

Background & Aims: The main cause of chronic hepatitis is Hepatitis B virus (HBV). The progression and development of hepatitis B related diseases are included liver cirrhosis (LC) and hepatocellular carcinoma (HCC). Human leukocyte antigen-(HLA) DQ polymorphism has been observed in other recent studies dealing with the association between HBV and liver disease. Our study of Egyptian population was introduced to assess the strong association between HLA-DQ polymorphism and HBV infection in addition to the progression of HCC. The aim of this work was to estimate HLA-DQ gene polymorphisms in HBV and HCC. Methods: HLA-DQ genotype polymorphism assayed by using the ABI Taq Man allelic discrimination assay in different groups under this study. According to the relevant HLA Class II SNP literature, one single nucleotide polymorphism (SNPs) was selected as candidate sites; it is an HLA-DQ, which showed minor allele frequency AA, GA, and GG. Results: We performed haplotype analysis to all subjects, the most frequent AA haplotype in HCC cases (18%) in comparison with HBV and healthy individuals (3%). The haplotype GA was more frequent in HCC group and slightly frequency in LC related to HBV only cases in comparison with the control group. In contrast, the GG haplotype recorded less frequently in HCC individuals, but the HBV and LC groups showed more frequency in comparison with HCC group. There is a correlation between AFP serum elevated levels of most frequency in GA and AA polymorphism for HCC cases. Conclusion: We found AA and GA haplotype were significantly most frequent in HCC. Our findings HLA-DQ AA and GG polymorphism might serve as a novel potential predictive marker for HCC and may function in tumorigenesis of HBV.

scholarly journals Polygenic Study of Endurance‐Associated Genetic Markers NOS3 (Glu298Asp), BDKRB2 (‐9/+9), UCP2 (Ala55Val), AMPD1 (Gln45Ter) and ACE (I/D) in Polish Male Half Marathoners

2018 ◽  
Vol 64 (1) ◽  
pp. 87-98 ◽  
Author(s):  
Piotr Gronek ◽  
Joanna Gronek ◽  
Ewelina Lulińska-Kuklik ◽  
Michał Spieszny ◽  
Marta Niewczas ◽  
...  
Keyword(s):  
Genetic Markers ◽  
Gene Polymorphisms ◽  
Endurance Performance ◽  
Study Group ◽  
Buccal Cells ◽  
Allelic Discrimination Assay ◽  
Allelic Discrimination ◽  
Running Performance ◽  
Thermal Cycler ◽  
Combined Impact

Abstract The purpose of this study was to investigate individually and in combination the association between the ACE (I/D), NOS3 (Glu298Asp), BDKRB2 (-9/+9), UCP2 (Ala55Val) and AMPD1 (Gln45Ter) variants with endurance performance in a large, performance-homogenous cohort of elite Polish half marathoners. The study group consisted of 180 elite half marathoners: 76 with time < 100 minutes and 104 with time > 100 minutes. DNA of the subjects was extracted from buccal cells donated by the runners and genotyping was carried out using an allelic discrimination assay with a C1000 Touch Thermal Cycler (Bio-Rad, Germany) instrument with TaqMan® probes (NOS3, UCP2, and AMPD1) and a T100™ Thermal Cycler (Bio-Rad, Germany) instrument (ACE and BDKRB2). We found that the UCP2 Ala55Val polymorphism was associated with running performance, with the subjects carrying the Val allele being overrepresented in the group of most successful runners (<100 min) compared to the >100 min group (84.2 vs. 55.8%; OR = 4.23, p < 0.0001). Next, to assess the combined impact of 4 gene polymorphisms, all athletes were classified according to the number of 'endurance' alleles (ACE I, NOS3 Glu, BDKRB2 -9, UCP2 Val) they possessed. The proportion of subjects with a high (4-7) number of 'endurance' alleles was greater in the better half marathoners group compared with the >100 min group (73.7 vs. 51.9%; OR = 2.6, p = 0.0034). These data suggest that the likelihood of becoming an elite half marathoner partly depends on the carriage of a high number of endurance-related alleles.

scholarly journals The Clinical Value of Ficolin-3 Gene Polymorphism in Rheumatic Heart Disease. An Egyptian Adolescents Study

2020 ◽  
Author(s):  
Maher H. Gomaa ◽  
Emad Gamil Khidr ◽  
Ahmed Elshafei ◽  
Hala S. Hamza ◽  
Aya M. Fattouh ◽  
...  
Keyword(s):  
Heart Disease ◽  
Rheumatic Heart Disease ◽  
Gene Polymorphisms ◽  
Early Recognition ◽  
Elevated Serum ◽  
High Serum ◽  
Clinical Value ◽  
Allelic Discrimination Assay ◽  
Allelic Discrimination ◽  
Rheumatic Heart

Abstract Background: The innate immunity molecules against Streptococcus pyogenes infections include ficolin-3 that was thought to have a role in autoimmune diseases resulting from this infection such as rheumatic fever (RF) which goes on and leads to its most serious sequel, rheumatic heart disease (RHD). We aimed in this study to disclose if there is an association between ficolin-3 gene polymorphisms (rs4494157 and rs10794501) and RF with or without RHD for the first time in Egyptian adolescents. Methods: This study was carried out on 160 RF patients; eighty patients had RHD and eighty didn't have RHD. Besides, eighty ethnically and age-matched healthy subjects were selected as control. Ficolin-3 gene polymorphisms (rs4494157 and rs10794501) were genotyped by TaqMan® allelic discrimination assay. Serum ficolin-3 was quantitatively determined by ELISA. Results: Regarding ficolin-3 gene polymorphisms; no differences in the frequency of rs10794501 were found between the investigated groups, while polymorphism of rs4494157 showed a significant correlation between AA homozygous genotype, high serum ficolin-3, and RHD risk. Conclusion: Elevated serum ficolin-3 and carriage of AA genotype of rs4494157 appeared to be involved in RF and RHD pathogenesis and may be predictive tools for early recognition of RHD prone RF patients, and subsequent early prophylactic interventions.

scholarly journals Inflamm-Aging Is Associated with Lower Plasma PTX3 Concentrations and an Impaired Capacity of PBMCs to Express hTERT following LPS Stimulation

2019 ◽  
Vol 2019 ◽  
pp. 1-13 ◽  
Author(s):  
Aaron L. Slusher ◽  
Tiffany M. Zúñiga ◽  
Edmund O. Acevedo
Keyword(s):  
Gene Expression ◽  
Young Adults ◽  
Telomere Length ◽  
Immune Cell ◽  
Ex Vivo ◽  
Middle Aged ◽  
Human Telomerase Reverse Transcriptase ◽  
Negatively Associated ◽  
Htert Gene ◽  
Age Related

Age-related elevations in proinflammatory cytokines, known as inflamm-aging, are associated with shorter immune cell telomere lengths. Purpose. This study examined the relationship of plasma PTX3 concentrations, a biomarker of appropriate immune function, with telomere length in 15 middle-aged (40-64 years) and 15 young adults (20-31 years). In addition, PBMCs were isolated from middle-aged and young adults to examine their capacity to express a key mechanistic component of telomere length maintenance, human telomerase reverse transcriptase (hTERT), following ex vivo cellular stimulation. Methods. Plasma PTX3 and inflammatory cytokines (i.e., IL-6, IL-10, TGF-β, and TNF-α), PBMC telomere lengths, and PBMC hTERT gene expression and inflammatory protein secretion following exposure to LPS, PTX3, and PTX3+LPS were measured. Results. Aging was accompanied by the accumulation of centrally located visceral adipose tissue, without changes in body weight and BMI, and alterations in the systemic inflammatory milieu (decreased plasma PTX3 and TGF-β; increased TNF-α (p≤0.050)). In addition, shorter telomere lengths in middle-aged compared to young adults (p=0.011) were negatively associated with age, body fat percentages, and plasma TNF-α (r=−0.404, p=0.027; r=−0.427, p=0.019; and r=−0.323, p=0.041, respectively). Finally, the capacity of PBMCs to increase hTERT gene expression following ex vivo stimulation was impaired in middle-aged compared to young adults (p=0.033) and negatively associated with telomere lengths (r=0.353, p=0.028). Conclusions. Proinflammation and the impaired hTERT gene expression capacity of PBMCs may contribute to age-related telomere attrition and disease.

scholarly journals 602 STING agonist-based treatment promotes vascular normalization and tertiary lymphoid structure formation in the therapeutic melanoma microenvironment

2020 ◽  
Vol 8 (Suppl 3) ◽  
pp. A637-A637
Author(s):  
Manoj Chelvanambi ◽  
Ronald Fecek ◽  
Jennifer Taylor ◽  
Walter Storkus
Keyword(s):  
T Cells ◽  
T Cell ◽  
Cd8 T Cells ◽  
Immune Cell ◽  
Ex Vivo ◽  
In Vitro Assays ◽  
Type I ◽  
Vascular Normalization ◽  
S 100 ◽  
Transcriptional Changes

BackgroundThe degree of immune infiltration in tumors, especially CD8+ T cells, greatly impacts patient disease course and response to interventional immunotherapy. Hence, enhancement of TIL prevalence is a preferred clinical endpoint, one that may be achieved via administration of agents that normalize the tumor vasculature (VN) leading to improved immune cell recruitment and/or that induce the development of local tertiary lymphoid structures (TLS) within the tumor microenvironment (TME).MethodsLow-dose STING agonist ADU S-100 (5 μg/mouse) was delivered intratumorally to established s.c. B16.F10 melanomas on days 10, 14 and 17 post-tumor inoculation under an IACUC-approved protocol. Treated and control, untreated tumors were isolated at various time points to assess transcriptional changes associated with VN and TLS formation via qPCR, with corollary immune cell composition changes determined using flow cytometry and immunofluorescence microscopy. In vitro assays were performed on CD11c+ BMDCs treated with 2.5 μg/mL ADU S-100 (vs PBS control) and associated transcriptional changes analyzed via qPCR or profiled using DNA microarrays. For TCRβ-CDR3 analyses, CDR3 was sequenced from gDNA isolated from enzymatically digested tumors and splenocytes.ResultsWe report that activation of STING within the TME leads to slowed melanoma growth in association with increased production of angiostatic factors including Tnfsf15 (Vegi), Cxcl10 and Angpt1, and TLS inducing factors including Ccl19, Ccl21, Lta, Ltb and Tnfsf14 (Light). Therapeutic responses from intratumoral STING activation were characterized by increased vascular normalization (VN), enhanced tumor infiltration by CD8+ T cells and CD11c+ DCs and local TLS neo-genesis, all of which were dependent on host expression of STING. Consistent with a central role for DC in TLS formation, ex vivo ADU S-100-activated mCD11c+ DCs also exhibited upregulated expression of TLS promoting factors including lymphotoxin-α (LTA), IL-36, inflammatory chemokines and type I interferons. TLS formation was associated with the development of a therapeutic TIL TCR repertoire enriched in T cell clonotypes uniquely detected within the tumor but not the peripheral circulation in support or local T cell cross-priming within the TME.ConclusionsOur data support the premise that i.t. delivery of STING agonist promotes a pro-inflammatory TME in support of VN and TLS formation, leading to the local expansion of unique TIL repertoire in association with superior anti-melanoma efficacy.

scholarly journals TAMI-28. DIFFERENTIAL MIGRATION MECHANICS AND IMMUNE RESPONSES OF GLIOMA SUBTYPES

2020 ◽  
Vol 22 (Supplement_2) ◽  
pp. ii219-ii219
Author(s):  
Ghaidan Shamsan ◽  
Chao Liu ◽  
Brooke Braman ◽  
Susan Rathe ◽  
Aaron Sarver ◽  
...  
Keyword(s):  
Tumor Cells ◽  
Immune Cell ◽  
Molecular Subtypes ◽  
Ex Vivo ◽  
Brain Slices ◽  
Traction Force ◽  
Genetic Alterations ◽  
Sleeping Beauty ◽  
Brain Parenchyma ◽  
Biophysical Modeling

Abstract In Glioblastoma (GBM), tumor spreading is driven by tumor cells’ ability to infiltrate healthy brain parenchyma, which prevents complete surgical resection and contributes to tumor recurrence. GBM molecular subtypes, classical, proneural and mesenchymal, were shown to strongly correlate with specific genetic alterations (Mesenchymal: NF1; Classical: EGFRVIII; Proneural: PDGFRA). Here we tested the hypothesis that a key mechanistic difference between GBM molecular subtypes is that proneural cells are slow migrating and mesenchymal cells are fast migrating. Using Sleeping Beauty transposon system, immune-competent murine brain tumors were induced by SV40-LgT antigen in combination with either NRASG12V (NRAS) or PDGFB (PDGF) overexpression. Cross-species transcriptomic analysis revealed NRAS and PDGF-driven tumors correlate with human mesenchymal and proneural GBM, respectively. Similar to human GBM, CD44 expression was higher in NRAS tumors and, consistent with migration simulations of varying CD44 levels, ex vivo brain slice live imaging showed NRAS tumors cells migrate faster than PDGF tumors cells (random motility coefficient = 30µm2/hr vs. 2.5µm2/hr, p &lt; 0.001). Consistent with CD44 function as an adhesion molecule, migration phenotype was independent of the tumor microenvironment. NRAS and human PDX/MES tumor cells were found to migrate faster and have larger cell spread area than PDGF and human PDX/PN tumors cells, respectively, in healthy mouse brain slices. Furthermore, traction force microscopy revealed NRAS tumor cells generate larger traction forces than PDGF tumors cells which further supports our theoretical mechanism driving glioma migration. Despite increased migration, NRAS cohort had better survival than PDGF which was attributed to enhanced antitumoral immune response in NRAS tumors, consistent with increased immune cell infiltration found in human mesenchymal GBM. Overall our work identified a potentially actionable difference in migration mechanics between GBM subtypes and establishes an integrated biophysical modeling and experimental approach to mechanically parameterize and simulate distinct molecular subtypes in preclinical models of cancer.

scholarly journals Targeting Haemagglutinin Antigen of Avian Influenza Virus to Chicken Immune Cell Receptors Dec205 and CD11c Induces Differential Immune-Potentiating Responses

Vaccines ◽  
2021 ◽  
Vol 9 (7) ◽  
pp. 784
Author(s):  
Angita Shrestha ◽  
Jean-Remy Sadeyen ◽  
Deimante Lukosaityte ◽  
Pengxiang Chang ◽  
Marielle Van Hulten ◽  
...  
Keyword(s):  
Influenza A ◽  
Immune Cell ◽  
Ex Vivo ◽  
Protective Efficacy ◽  
Haemagglutination Inhibition ◽  
Primary Vaccination ◽  
Antigen Delivery ◽  
Single Chain ◽  
Protective Antigens ◽  
Single Chain Fragment Variable

Improving the immunogenicity and protective efficacy of vaccines is critical to reducing disease impacts. One strategy used to enhance the immunogenicity of vaccines is the selective delivery of protective antigens to the antigen presenting cells (APCs). In this study, we have developed a targeted antigen delivery vaccine (TADV) system by recombinantly fusing the ectodomain of hemagglutinin (HA) antigen of H9N2 influenza A virus to single chain fragment variable (scFv) antibodies specific for the receptors expressed on chicken APCs; Dec205 and CD11c. Vaccination of chickens with TADV containing recombinant H9HA Foldon-Dec205 scFv or H9HA Foldon-CD11c scFv proteins elicited faster (as early as day 6 post primary vaccination) and higher anti-H9HA IgM and IgY, haemagglutination inhibition, and virus neutralisation antibodies compared to the untargeted H9HA protein. Comparatively, CD11c scFv conjugated H9HA protein showed higher immunogenic potency compared to Dec205 scFv conjugated H9HA protein. The higher immune potentiating ability of CD11c scFv was also reflected in ex-vivo chicken splenocyte stimulation assay, whereby H9HA Foldon-CD11c scFv induced higher levels of cytokines (IFNγ, IL6, IL1β, and IL4) compared to H9HA Foldon-Dec205 scFv. Overall, the results conclude that TADV could be a better alternative to the currently available inactivated virus vaccines.

scholarly journals Implications of hematopoietic stem cells heterogeneity for gene therapies

Gene Therapy ◽  
2021 ◽  
Author(s):  
Jeremy Epah ◽  
Richard Schäfer
Keyword(s):  
Immune Cell ◽  
Ex Vivo ◽  
Bone Marrow Failure ◽  
Cell Types ◽  
Blood Disorders ◽  
Hematopoietic Stem ◽  
Therapeutic Concept ◽  
Gene Therapies ◽  
Bone Marrow Failure Syndromes ◽  
Immunodeficiency Syndrome

AbstractHematopoietic stem cell transplantation (HSCT) is the therapeutic concept to cure the blood/immune system of patients suffering from malignancies, immunodeficiencies, red blood cell disorders, and inherited bone marrow failure syndromes. Yet, allogeneic HSCT bear considerable risks for the patient such as non-engraftment, or graft-versus host disease. Transplanting gene modified autologous HSCs is a promising approach not only for inherited blood/immune cell diseases, but also for the acquired immunodeficiency syndrome. However, there is emerging evidence for substantial heterogeneity of HSCs in situ as well as ex vivo that is also observed after HSCT. Thus, HSC gene modification concepts are suggested to consider that different blood disorders affect specific hematopoietic cell types. We will discuss the relevance of HSC heterogeneity for the development and manufacture of gene therapies and in exemplary diseases with a specific emphasis on the key target HSC types myeloid-biased, lymphoid-biased, and balanced HSCs.

scholarly journals HIV-1 subverts the complement system in semen to enhance viral transmission

2021 ◽  
Author(s):  
Bernadien M. Nijmeijer ◽  
Marta Bermejo-Jambrina ◽  
Tanja M. Kaptein ◽  
Carla M. S. Ribeiro ◽  
Doris Wilflingseder ◽  
...  
Keyword(s):  
Ex Vivo ◽  
Virus Transmission ◽  
Sexual Contact ◽  
Target Cells ◽  
People Living With Hiv ◽  
Lectin Receptor ◽  
Pre Treatment ◽  
Living With Hiv ◽  
Hiv 1

AbstractSemen is important in determining HIV-1 susceptibility but it is unclear how it affects virus transmission during sexual contact. Mucosal Langerhans cells (LCs) are the first immune cells to encounter HIV-1 during sexual contact and have a barrier function as LCs are restrictive to HIV-1. As semen from people living with HIV-1 contains complement-opsonized HIV-1, we investigated the effect of complement on HIV-1 dissemination by human LCs in vitro and ex vivo. Notably, pre-treatment of HIV-1 with semen enhanced LC infection compared to untreated HIV-1 in the ex vivo explant model. Infection of LCs and transmission to target cells by opsonized HIV-1 was efficiently inhibited by blocking complement receptors CR3 and CR4. Complement opsonization of HIV-1 enhanced uptake, fusion, and integration by LCs leading to an increased transmission of HIV-1 to target cells. However, in the absence of both CR3 and CR4, C-type lectin receptor langerin was able to restrict infection of complement-opsonized HIV-1. These data suggest that complement enhances HIV-1 infection of LCs by binding CR3 and CR4, thereby bypassing langerin and changing the restrictive nature of LCs into virus-disseminating cells. Targeting complement factors might be effective in preventing HIV-1 transmission.

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