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  1. Article ; Online: 1,25(OH)

    Sanseverino, Isabella / Rinaldi, Arturo Ottavio / Purificato, Cristina / Cortese, Antonio / Millefiorini, Enrico / Gauzzi, Maria Cristina

    International journal of molecular sciences

    2023  Volume 24, Issue 7

    Abstract: Immune mechanisms play an essential role in driving multiple sclerosis (MS) and altered trafficking and/or activation of dendritic cells (DC) were observed in the central nervous system and cerebrospinal fluid of MS patients. Interferon β (IFNβ) has been ...

    Abstract Immune mechanisms play an essential role in driving multiple sclerosis (MS) and altered trafficking and/or activation of dendritic cells (DC) were observed in the central nervous system and cerebrospinal fluid of MS patients. Interferon β (IFNβ) has been used as a first-line therapy in MS for almost three decades and vitamin D deficiency is a recognized environmental risk factor for MS. Both IFNβ and vitamin D modulate DC functions. Here, we studied the response to 1,25-dihydoxyvitamin D3 (1,25(OH)
    MeSH term(s) Humans ; Vitamin D/pharmacology ; Vitamins/pharmacology ; Multiple Sclerosis ; Cytokines ; Chemokines
    Chemical Substances Vitamin D (1406-16-2) ; Vitamins ; Cytokines ; Chemokines
    Language English
    Publishing date 2023-04-04
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms24076717
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Erratum to: Endogenous CCL2 neutralization restricts HIV-1 replication in primary human macrophages by inhibiting viral DNA accumulation.

    Sabbatucci, Michela / Covino, Daniela Angela / Purificato, Cristina / Mallano, Alessandra / Federico, Maurizio / Lu, Jing / Rinaldi, Arturo Ottavio / Pellegrini, Matteo / Bona, Roberta / Michelini, Zuleika / Cara, Andrea / Vella, Stefano / Gessani, Sandra / Andreotti, Mauro / Fantuzzi, Laura

    Retrovirology

    2015  Volume 12, Page(s) 47

    Language English
    Publishing date 2015-06-09
    Publishing country England
    Document type Published Erratum
    ISSN 1742-4690
    ISSN (online) 1742-4690
    DOI 10.1186/s12977-015-0166-4
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Endogenous CCL2 neutralization restricts HIV-1 replication in primary human macrophages by inhibiting viral DNA accumulation.

    Sabbatucci, Michela / Covino, Daniela Angela / Purificato, Cristina / Mallano, Alessandra / Federico, Maurizio / Lu, Jing / Rinaldi, Arturo Ottavio / Pellegrini, Matteo / Bona, Roberta / Michelini, Zuleika / Cara, Andrea / Vella, Stefano / Gessani, Sandra / Andreotti, Mauro / Fantuzzi, Laura

    Retrovirology

    2015  Volume 12, Page(s) 4

    Abstract: Background: Macrophages are key targets of HIV-1 infection. We have previously described that the expression of CC chemokine ligand 2 (CCL2) increases during monocyte differentiation to macrophages and it is further up-modulated by HIV-1 exposure. ... ...

    Abstract Background: Macrophages are key targets of HIV-1 infection. We have previously described that the expression of CC chemokine ligand 2 (CCL2) increases during monocyte differentiation to macrophages and it is further up-modulated by HIV-1 exposure. Moreover, CCL2 acts as an autocrine factor that promotes viral replication in infected macrophages. In this study, we dissected the molecular mechanisms by which CCL2 neutralization inhibits HIV-1 replication in monocyte-derived macrophages (MDM), and the potential involvement of the innate restriction factors protein sterile alpha motif (SAM) histidine/aspartic acid (HD) domain containing 1 (SAMHD1) and apolipoprotein B mRNA-editing, enzyme-catalytic, polypeptide-like 3 (APOBEC3) family members.
    Results: CCL2 neutralization potently reduced the number of p24 Gag+ cells during the course of either productive or single cycle infection with HIV-1. In contrast, CCL2 blocking did not modify entry of HIV-1 based Virus Like Particles, thus demonstrating that the restriction involves post-entry steps of the viral life cycle. Notably, the accumulation of viral DNA, both total, integrated and 2-LTR circles, was strongly impaired by neutralization of CCL2. Looking for correlates of HIV-1 DNA accumulation inhibition, we found that the antiviral effect of CCL2 neutralization was independent of the modulation of SAMHD1 expression or function. Conversely, a strong and selective induction of APOBEC3A expression, to levels comparable to those of freshly isolated monocytes, was associated with the inhibition of HIV-1 replication mediated by CCL2 blocking. Interestingly, the CCL2 neutralization mediated increase of APOBEC3A expression was type I IFN independent. Moreover, the transcriptome analysis of the effect of CCL2 blocking on global gene expression revealed that the neutralization of this chemokine resulted in the upmodulation of additional genes involved in the defence response to viruses.
    Conclusions: Neutralization of endogenous CCL2 determines a profound restriction of HIV-1 replication in primary MDM affecting post-entry steps of the viral life cycle with a mechanism independent of SAMHD1. In addition, CCL2 blocking is associated with induction of APOBEC3A expression, thus unravelling a novel mechanism which might contribute to regulate the expression of innate intracellular viral antagonists in vivo. Thus, our study may potentially lead to the development of new therapeutic strategies for enhancing innate cellular defences against HIV-1 and protecting macrophages from infection.
    MeSH term(s) Cells, Cultured ; Chemokine CCL2/antagonists & inhibitors ; Chemokine CCL2/immunology ; Cytidine Deaminase/antagonists & inhibitors ; Cytidine Deaminase/genetics ; DNA, Viral/metabolism ; Gene Expression ; Gene Expression Profiling ; HIV-1/physiology ; Humans ; Macrophages/virology ; Monomeric GTP-Binding Proteins/genetics ; Proteins/antagonists & inhibitors ; Proteins/genetics ; SAM Domain and HD Domain-Containing Protein 1 ; Virus Internalization ; Virus Replication
    Chemical Substances CCL2 protein, human ; Chemokine CCL2 ; DNA, Viral ; Proteins ; SAM Domain and HD Domain-Containing Protein 1 (EC 3.1.5.-) ; SAMHD1 protein, human (EC 3.1.5.-) ; APOBEC3A protein, human (EC 3.5.4.5) ; Cytidine Deaminase (EC 3.5.4.5) ; Monomeric GTP-Binding Proteins (EC 3.6.5.2)
    Language English
    Publishing date 2015-01-22
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ISSN 1742-4690
    ISSN (online) 1742-4690
    DOI 10.1186/s12977-014-0132-6
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Increased circulating levels of vitamin D binding protein in MS patients.

    Rinaldi, Arturo Ottavio / Sanseverino, Isabella / Purificato, Cristina / Cortese, Antonio / Mechelli, Rosella / Francisci, Silvia / Salvetti, Marco / Millefiorini, Enrico / Gessani, Sandra / Gauzzi, Maria Cristina

    Toxins

    2015  Volume 7, Issue 1, Page(s) 129–137

    Abstract: Vitamin D (vitD) low status is currently considered a main environmental factor in multiple sclerosis (MS) etiology and pathogenesis. VitD and its metabolites are highly hydrophobic and circulate mostly bound to the vitamin D binding protein (DBP) and ... ...

    Abstract Vitamin D (vitD) low status is currently considered a main environmental factor in multiple sclerosis (MS) etiology and pathogenesis. VitD and its metabolites are highly hydrophobic and circulate mostly bound to the vitamin D binding protein (DBP) and with lower affinity to albumin, while less than 1% are in a free form. The aim of this study was to investigate whether the circulating levels of either of the two vitD plasma carriers and/or their relationship are altered in MS. We measured DBP and albumin plasma levels in 28 MS patients and 24 healthy controls. MS patients were found to have higher DBP levels than healthy subjects. Concomitant interferon beta therapy did not influence DBP concentration, and the difference with the control group was significant in both females and males. No significant correlation between DBP and albumin levels was observed either in healthy controls or in patients. These observations suggest the involvement of DBP in the patho-physiology of MS.
    MeSH term(s) Adult ; Albumins/metabolism ; Female ; Humans ; Interferon-beta/therapeutic use ; Male ; Multiple Sclerosis, Relapsing-Remitting/blood ; Multiple Sclerosis, Relapsing-Remitting/drug therapy ; Vitamin D-Binding Protein/blood
    Chemical Substances Albumins ; Vitamin D-Binding Protein ; Interferon-beta (77238-31-4)
    Language English
    Publishing date 2015-01-13
    Publishing country Switzerland
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2518395-3
    ISSN 2072-6651 ; 2072-6651
    ISSN (online) 2072-6651
    ISSN 2072-6651
    DOI 10.3390/toxins7010129
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Induction of human regulatory innate lymphoid cells from group 2 innate lymphoid cells by retinoic acid.

    Morita, Hideaki / Kubo, Terufumi / Rückert, Beate / Ravindran, Avinash / Soyka, Michael B / Rinaldi, Arturo Ottavio / Sugita, Kazunari / Wawrzyniak, Marcin / Wawrzyniak, Paulina / Motomura, Kenichiro / Tamari, Masato / Orimo, Keisuke / Okada, Naoko / Arae, Ken / Saito, Kyoko / Altunbulakli, Can / Castro-Giner, Francesc / Tan, Ge / Neumann, Avidan /
    Sudo, Katsuko / O'Mahony, Liam / Honda, Kenya / Nakae, Susumu / Saito, Hirohisa / Mjösberg, Jenny / Nilsson, Gunnar / Matsumoto, Kenji / Akdis, Mübeccel / Akdis, Cezmi A

    The Journal of allergy and clinical immunology

    2019  Volume 143, Issue 6, Page(s) 2190–2201.e9

    Abstract: Background: Group 2 innate lymphoid cells (ILC2s) play critical roles in induction and exacerbation of allergic airway inflammation. Thus clarification of the mechanisms that underlie regulation of ILC2 activation has received significant attention. ... ...

    Abstract Background: Group 2 innate lymphoid cells (ILC2s) play critical roles in induction and exacerbation of allergic airway inflammation. Thus clarification of the mechanisms that underlie regulation of ILC2 activation has received significant attention. Although innate lymphoid cells are divided into 3 major subsets that mirror helper effector T-cell subsets, counterpart subsets of regulatory T cells have not been well characterized.
    Objective: We sought to determine the factors that induce regulatory innate lymphoid cells (ILCregs).
    Methods: IL-10
    Results: RA induced IL-10 secretion by human ILC2s but not type 2 cytokines. IL-10
    Conclusion: We have identified a unique immune regulatory and anti-inflammatory pathway by which RA converts ILC2s to ILCregs. Interactions between airway epithelial cells and ILC2s play an important roles in the generation of ILCregs.
    MeSH term(s) Animals ; Anti-Inflammatory Agents/pharmacology ; Cell Line ; Cytokines/immunology ; Epithelial Cells/immunology ; Humans ; Immunity, Innate ; Lung/immunology ; Lymphocytes/drug effects ; Lymphocytes/immunology ; Mice, Inbred C57BL ; Paranasal Sinuses/immunology ; Tretinoin/pharmacology
    Chemical Substances Anti-Inflammatory Agents ; Cytokines ; Tretinoin (5688UTC01R)
    Language English
    Publishing date 2019-01-22
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 121011-7
    ISSN 1097-6825 ; 1085-8725 ; 0091-6749
    ISSN (online) 1097-6825 ; 1085-8725
    ISSN 0091-6749
    DOI 10.1016/j.jaci.2018.12.1018
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