Human papilloma virus and lupus: the virus, the vaccine and the disease

Segal‬‏, Yahel; Calabrò, Michele; Kanduc, Darja; Shoenfeld, Yehuda

doi:10.1097/bor.0000000000000398

Cited by 37 publications

(19 citation statements)

References 112 publications

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“…Molecular mimicry is one mechanism implicated in the break of tolerance. A recent study identified a penta-peptide (SKVVS) in the human papillomavirus (HPV) protein L1 that is shared with KIR2DL1, 2DL2, 3DL1, 3DL2, and 2DL4 and suggested that HPV infection in genetically predisposed individuals may contribute to lupus via molecular mimicry (38, 39). In this light, it would be interesting to study whether the presence of anti-KIR autoantibodies correlates with HPV infection, but the lack of these data in our cohort preclude such analyses.…”

Section: Discussionmentioning

confidence: 99%

“…However, the fact that the effect of anti-KIR-containing IgG was observed on isolated NK cells, that IgG had opposite effects in educated and tolerized subsets of NK cells and that NK cells retuned following wash-out of IgG strongly suggest that the effect on NK cells were at least in part the result of antibody-mediated blockade of KIR/KIR-ligand interactions. This speculation is not unlikely given the clear data on the effect on NK cells that are triggered upon exposure to the anti-KIR2D antibody lirilumab (39).…”

Section: Discussionmentioning

confidence: 99%

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Autoantibodies to Killer Cell Immunoglobulin-Like Receptors in Patients With Systemic Lupus Erythematosus Induce Natural Killer Cell Hyporesponsiveness

et al. 2019

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Natural killer (NK) cell cytotoxicity toward self-cells is restrained by the inhibitory HLA class I-binding receptors CD94/NKG2A and the killer cell immunoglobulin-like receptors (KIRs). CD94/NKG2A and KIRs are also essential for NK cell education, which is a dynamic functional maturation process where a constitutive binding of inhibitory receptors to cognate HLA class I molecules is required for NK cells to maintain their full cytotoxic capacity. Previously, we described autoantibodies to CD94/NKG2A in patients with systemic lupus erythematosus (SLE). In this study we analyzed sera from 191 patients with SLE, 119 patients with primary Sjögren's syndrome (pSS), 48 patients with systemic sclerosis (SSc), and 100 healthy donors (HD) for autoantibodies to eight different KIRs. Anti-KIR autoantibodies were identified in sera from 23.0% of patients with SLE, 10.9% of patients with pSS, 12.5% of patients with SSc, and 3.0% of HD. IgG from anti-KIR-positive SLE patients reduced the degranulation and cytotoxicity of NK cells toward K562 tumor cells. The presence of anti-KIR-autoantibodies reacting with >3 KIRs was associated with an increased disease activity (p < 0.0001), elevated serum levels of IFN-α (p < 0.0001), nephritis (p = 0.001), and the presence of anti-Sm (p = 0.007), and anti-RNP (p = 0.003) autoantibodies in serum. Together these findings suggest that anti-KIR autoantibodies may contribute to the reduced function of NK cells in SLE patients, and that a defective NK cell function may be a risk factor for the development of lupus nephritis.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Autoantibodies to Killer Cell Immunoglobulin-Like Receptors in Patients With Systemic Lupus Erythematosus Induce Natural Killer Cell Hyporesponsiveness

et al. 2019

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“…TLR4 signaling was increased with transgenic mice for a TLR chaperone molecule (gp96), which resulted in a lupus-like autoimmune glomerulonephritis 26 . Flares of autoimmune diseases have been observed with infection 82 in humans and also is an inducer of autoimmunity in mice. Decreased anti-dsDNA antibodies were observed in TLR2 and TLR4 knockout C57BL/6 (lpr/lpr) mice; and autoantibodies were induced by LPS stimulation through the TLR4-dependent cell signaling pathway in lupus-prone mice 83 , 84 .…”

Section: Discussionmentioning

confidence: 99%

Distinct systemic microbiome and microbial translocation are associated with plasma level of anti-CD4 autoantibody in HIV infection

Luo

Alekseyenko

et al. 2018

Sci Rep

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Microbial signals have been linked to autoantibody induction. Recently, we found that purified anti-CD4 autoantibodies from the plasma of chronic HIV-1-infected patients under viral-suppressed antiretroviral therapy (ART) play a pathologic role in poor CD4+ T cell recovery. The purpose of the study was to investigate the association of systemic microbiome and anti-CD4 autoantibody production in HIV. Plasma microbiome from 12 healthy controls and 22 HIV-infected subjects under viral-suppressed ART were analyzed by MiSeq sequencing. Plasma level of autoantibodies and microbial translocation (LPS, total bacterial 16S rDNA, soluble CD14, and LPS binding protein) were analyzed by ELISA, limulus amebocyte assay, and qPCR. We found that plasma level of anti-CD4 IgGs but not anti-CD8 IgGs was increased in HIV+ subjects compared to healthy controls. HIV+ subjects with plasma anti-CD4 IgG > 50 ng/mL (high) had reduced microbial diversity compared to HIV+ subjects with anti-CD4 IgG ≤ 50 ng/mL (low). Moreover, plasma anti-CD4 IgG level was associated with elevated microbial translocation and reduced microbial diversity in HIV+ subjects. The Alphaproteobacteria class was significantly enriched in HIV+ subjects with low anti-CD4 IgG compared to patients with high anti-CD4 IgG even after controlling for false discovery rate (FDR). The microbial components were different from the phylum to genus level in HIV+ subjects with high anti-CD4 IgGs compared to the other two groups, but these differences were not significant after controlling for FDR. These results suggest that systemic microbial translocation and microbiome may associate with anti-CD4 autoantibody production in ART-treated HIV disease.

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“…This has included high-profile coverage of individuals who died after HPV vaccination. 88,89 The main concerns raised about the safety of HPV vaccination have focused on death following vaccination, 88,89 autoimmune and neurological conditions, [90][91][92][93][94][95][96][97][98] and premature ovarian insufficiency (POI) or ovarian failure. [99][100][101][102][103][104][105] Addressing myth 3…”

Section: Mythmentioning

confidence: 99%

Addressing HPV vaccine myths: practical information for healthcare providers

Bednarczyk

2019

Human Vaccines & Immunotherapeutics

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Human papillomavirus (HPV) vaccine uptake consistently lags behind that of other adolescent vaccines. In 2017, uptake of a single HPV vaccine dose and HPV vaccine series completion was 66% and 49%, respectively, compared to uptake of tetanus, diphtheria, and acellular pertussis vaccine (89%) and quadrivalent meningococcal conjugate vaccine (85%). Reasons for not vaccinating adolescents again HPV are varied, and in many cases, are rooted in commonly spread myths and misperceptions about the vaccine. In this review, we address five key myths-HPV vaccination is not effective at preventing cancer; Pap smears are sufficient to prevent cervical cancer; HPV vaccination is not safe; HPV vaccination is not needed since most infections are naturally cleared by the immune system; 11-12 years of age is too young to vaccinate. For each myth, we summarize the scientific evidence refuting the myth and provide speaking prompts for healthcare professionals to communicate about HPV vaccination.

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Human papilloma virus and lupus: the virus, the vaccine and the disease

Cited by 37 publications

References 112 publications

Autoantibodies to Killer Cell Immunoglobulin-Like Receptors in Patients With Systemic Lupus Erythematosus Induce Natural Killer Cell Hyporesponsiveness

Autoantibodies to Killer Cell Immunoglobulin-Like Receptors in Patients With Systemic Lupus Erythematosus Induce Natural Killer Cell Hyporesponsiveness

Distinct systemic microbiome and microbial translocation are associated with plasma level of anti-CD4 autoantibody in HIV infection

Addressing HPV vaccine myths: practical information for healthcare providers

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