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390 results on '"Gariglio, M."'

4. 277 HPV8 E6 induced STAT3 activation leads to hair follicle junctional zone keratinocyte stem cell proliferation and expansion in actinic keratoses

Author

Olivero, C., primary, Morgan, H., additional, Martuscelli, L., additional, Gibbs, A., additional, Shorning, B., additional, Borgogna, C., additional, De Andrea, M., additional, Hufbauer, M., additional, Smola, S., additional, Pfister, H., additional, Akgul, B., additional, Gariglio, M., additional, and Patel, G., additional

Published
2023
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6. Effects of a Functional Protein on Gut Local Immune Response and Morphometrical Indices in Poultry

Author

Colombino, E., primary, Biasato, I., additional, Karimi, M., additional, Ton Nu, M.A., additional, Bellezza Oddon, S., additional, Gariglio, M., additional, Bergamino, C., additional, Battisti, E., additional, Zanet, S., additional, Fiorilla, E., additional, Gai, F., additional, Gasco, L., additional, Schiavone, A., additional, and Capucchio, M.T., additional

Published
2022
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19. Strategy of Human Cytomegalovirus To Escape Interferon Beta-Induced APOBEC3G Editing Activity

Author

Pautasso, S, Galitska, G, Dell'Oste, V, Biolatti, M, Cagliani, R, Forni, D, De Andrea, M, Gariglio, M, Sironi, M, Landolfo, S, Pautasso S, Galitska G, Dell'Oste V, Biolatti M, Cagliani R, Forni D, De Andrea M, Gariglio M, Sironi M, Landolfo S, Pautasso, S, Galitska, G, Dell'Oste, V, Biolatti, M, Cagliani, R, Forni, D, De Andrea, M, Gariglio, M, Sironi, M, Landolfo, S, Pautasso S, Galitska G, Dell'Oste V, Biolatti M, Cagliani R, Forni D, De Andrea M, Gariglio M, Sironi M, and Landolfo S

Abstract

The apolipoprotein B editing enzyme catalytic subunit 3 (APOBEC3) is a family of DNA cytosine deaminases that mutate and inactivate viral genomes by single-strand DNA editing, thus providing an innate immune response against a wide range of DNA and RNA viruses. In particular, APOBEC3A (A3A), a member of the APOBEC3 family, is induced by human cytomegalovirus (HCMV) in decidual tissues where it efficiently restricts HCMV replication, thereby acting as an intrinsic innate immune effector at the maternal-fetal interface. However, the widespread incidence of congenital HCMV infection implies that HCMV has evolved to counteract APOBEC3-induced mutagenesis through mechanisms that still remain to be fully established. Here, we have assessed gene expression and deaminase activity of various APOBEC3 gene family members in HCMV-infected primary human foreskin fibroblasts (HFFs). Specifically, we show that APOBEC3G (A3G) gene products and, to a lesser degree, those of A3F but not of A3A, are upregulated in HCMV-infected HFFs. We also show that HCMV-mediated induction of A3G expression is mediated by interferon beta (IFN-), which is produced early during HCMV infection. However, knockout or overexpression of A3G does not affect HCMV replication, indicating that A3G is not a restriction factor for HCMV. Finally, through a bioinformatics approach, we show that HCMV has evolved mutational robustness against IFN- by limiting the presence of A3G hot spots in essential open reading frames (ORFs) of its genome. Overall, our findings uncover a novel immune evasion strategy by HCMV with profound implications for HCMV infections. IMPORTANCE APOBEC3 family of proteins plays a pivotal role in intrinsic immunity defense mechanisms against multiple viral infections, including retroviruses, through the deamination activity. However, the currently available data on APOBEC3 editing mechanisms upon HCMV infection remain unclear. In the present study, we show that particularly the APOBEC3G (A3G)

Published
2018

28. Serum IFI16 and anti-IFI16 antibodies in psoriatic arthritis

Author

De Andrea, M, primary, De Santis, M, additional, Caneparo, V, additional, Generali, E, additional, Sirotti, S, additional, Isailovic, N, additional, Guidelli, G M, additional, Ceribelli, A, additional, Fabbroni, M, additional, Simpatico, A, additional, Cantarini, L, additional, Gisondi, P, additional, Idolazzi, L, additional, Gariglio, M, additional, and Selmi, C, additional

Published
2019
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29. PROTEIN LEVELS AND AUTOANTIBODIES AGAINST LL37 AND IFI16 NUCLEIC ACID SENSORS IN PSORIATIC ARTHRITIS

Author

Meroni, M., Isailovic, N., De Santis, M., Ceribelli, A., Generali, E., Altamore, L., Sabatino, G., Rovero, P., Papini, A. M., Caneparo, V., Landolfo, S., Gariglio, M., De Andrea, M., and Selmi, C.

Subjects
biomarkers, antibodies, innate immunity
Abstract

The etiopathogenesis of psoriatic disease, including psoriasis and psoriatic arthritis (PsA), is still unclear, but recently it has been clarified why self-DNA become immunogenic in psoriatic disease, suggesting an important role of nucleic acid sensors such as LL37 and IFI16, in psoriatic disease. We aimed at investigating humoral and cellular response to LL37 and IFI16 in PsA.

Published
2018

33. HPV8 field cancerization in a transgenic mouse model is due to Lrig1+Keratinocyte stem cell expansion

Author

Lanfredini, S, Olivero, C, Borgogna, C, Calati, F, Powell, K, Davies, K, De Andrea, M, Harries, S, Tang, H, Pfister, H, Gariglio, M, and Patel, G

Subjects
WT, wild type, Keratinocytes, Actinic, Skin Neoplasms, Mice, Transgenic, HPV, human papillomavirus, Nerve Tissue Proteins, KSC, keratinocyte stem cell, Biochemistry, Transgenic, EV, epidermodysplasia verruciformis, Mice, Experimental, Neoplasms, SCC, cutaneous squamous cell carcinoma, Animals, TA, transcriptional activation, Papillomaviridae, Molecular Biology, Cell Proliferation, Membrane Glycoproteins, integumentary system, HF, hair follicle, IFE, interfollicular epidermis, Neoplasms, Experimental, Keratosis, Cell Biology, Keratosis, Actinic, AK, actinic keratosis, Neoplastic Stem Cells, 2708, Tumor Biology, Original Article
Abstract

β-Human papillomaviruses (HPVs) cause near ubiquitous latent skin infection within long-lived hair follicle (HF) keratinocyte stem cells. In patients with epidermodysplasia verruciformis, β-HPV viral replication is associated with skin keratosis and cutaneous squamous cell carcinoma. To determine the role of HF keratinocyte stem cells in β-HPV-induced skin carcinogenesis, we utilized a transgenic mouse model in which the keratin 14 promoter drives expression of the entire HPV8 early region (HPV8tg). HPV8tg mice developed thicker skin in comparison with wild-type littermates consistent with a hyperproliferative epidermis. HF keratinocyte proliferation was evident within the Lrig1+ keratinocyte stem cell population (69 vs. 55%, P < 0.01, n = 7), and not in the CD34+, LGR5+, and LGR6+ keratinocyte stem cell populations. This was associated with a 2.8-fold expansion in Lrig1+ keratinocytes and 3.8-fold increased colony-forming efficiency. Consistent with this, we observed nuclear p63 expression throughout this population and the HF infundibulum and adjoining interfollicular epidermis, associated with a switch from p63 transcriptional activation isoforms to ΔNp63 isoforms in HPV8tg skin. Epidermodysplasia verruciformis keratosis and in some cases actinic keratoses demonstrated similar histology associated with β-HPV reactivation and nuclear p63 expression within the HF infundibulum and perifollicular epidermis. These findings would suggest that β-HPV field cancerization arises from the HF junctional zone and predispose to squamous cell carcinoma.

Published
2017

37. Serum IFI16 and anti‐IFI16 antibodies in psoriatic arthritis.

Author

De Andrea, M., De Santis, M., Caneparo, V., Generali, E., Sirotti, S., Isailovic, N., Guidelli, G. M., Ceribelli, A., Fabbroni, M., Simpatico, A., Cantarini, L., Gisondi, P., Idolazzi, L., Gariglio, M., and Selmi, C.

Subjects
PSORIATIC arthritis, SYNOVIAL fluid, NUCLEAR proteins, ENZYME-linked immunosorbent assay, IMMUNOGLOBULINS, RHEUMATISM
Abstract

Summary: Nuclear interferon‐inducible protein 16 (IFI16) and anti‐IFI16 antibodies have been detected in subjects with several rheumatic diseases, often correlating with disease severity, and in this study we investigated their prevalence and clinical associations in psoriatic arthritis (PsA) compared to psoriasis (Pso). We tested sera and synovial fluids of patients with PsA for IFI16 protein levels by capture enzyme‐linked immunosorbent assay (ELISA) and for anti‐IFI16 immunoglobulin (Ig)G and IgA by ELISA, protein radio‐immunoprecipitation and immunoprecipitation‐Western blot of IgG. Sera from patients with Pso and healthy subjects were used as controls, and in a subgroup of patients with PsA we also studied sera after treatment with etanercept. IFI16 was detectable in the sera of 66% of patients with Pso, 46% with PsA and 19% of controls. Among PsA cases, 51% of IFI16‐positive cases had elevated levels of C‐reactive protein (CRP) compared to 31% of patients with undetectable IFI16. Anti‐IFI16 of both IgG and IgA isoforms were detected with significantly higher frequency in PsA and Pso compared to healthy controls, with higher IgG titres in patients with elevated C‐reactive protein (CRP) (P = 0·015). Immunoprecipitation confirmed the presence of anti‐IFI16 IgG antibodies and these preferentially recognized epitopes outside the N‐terminus of the protein. Lastly, IFI16 was detected in one of seven and anti‐IFI16 in three of seven synovial fluids from patients with PsA. Therefore, IFI16 and anti‐IFI16 are detectable in serum and synovial fluid of PsA patients, especially in cases of elevated CRP. [ABSTRACT FROM AUTHOR]

Published
2020
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38. The transgenic HPV8 mouse skin is associated with LRIG1 keratinocyte stem cell expansion

Author

Patel, G., Lanfredini, S., Olivera, C., Borgogna, C., Calati, F., Powell, K., Davies, K-J., De Andrea, M., Harries, S., Tang, H. K. C., Pfister, H., Gariglio, M., Patel, G., Lanfredini, S., Olivera, C., Borgogna, C., Calati, F., Powell, K., Davies, K-J., De Andrea, M., Harries, S., Tang, H. K. C., Pfister, H., and Gariglio, M.

Published
2017

39. Human Beta-papillomavirus infection and keratinocyte carcinomas

Author

Quint, K.D., Genders, R.E., Koning, M.N.C. de, Borgogna, C., Gariglio, M., Bavinck, J.N.B., Doorbar, J., and Feltkamp, M.C.

Subjects
Beta-papillomavirus, squamous cell carcinoma, skin cancer, basal cell carcinoma, human papillomavirus, keratinocyte carcinoma
Published
2015

46. The interferon-inducible DNa-sensor protein IFI16: a key player in the antiviral response

Author

Oste, V., Gatti, D., Giorgio, A. G., Gariglio, M., Landolfo, S., and Marco De Andrea

Subjects
DNA, Viral, Animals, Humans, Nuclear Proteins, Herpesviridae Infections, Phosphoproteins, Herpesviridae, Immunity, Innate
Abstract

IFI16, a member of the IFN-inducible PYHIN-200 gene family, displays multifaceted activity due to its ability to bind to various target proteins and, in turn, modulate a variety cell functions including proliferation, differentiation, apoptosis/pyroptosis, senescence, and in? ammation. The last few year have seen major advances in our knowledge of IFI16 antiviral activity and its role in the immune response. Indeed, a wealth of evidence now supports a key role of IFI16 in the activation of innate immunity and viral restriction against Herpesviruses and Lentiviruses, such that the definition of IFI16 as a "restriction factor" is now widely accepted. However, most viruses have developed their own unique strategy to antagonize IFI16, leading to a modification or disruption of its function. This review summarizes our current understanding of how viral replication is sensed and then inhibited by IFI16 protein and the viral strategies employed to defeat this host defense mechanism. We will focus mainly on Herpesviruses, although recent discoveries on the role of IFI16 in lentiviral infection will also be considered.

Published
2015

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