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  1. Article: The Contribution of Bullying Involvement and Alexithymia to Somatic Complaints in Preadolescents.

    Levantini, Valentina / Camodeca, Marina / Iannello, Nicolò Maria

    Children (Basel, Switzerland)

    2023  Volume 10, Issue 5

    Abstract: ... extant research highlights the relevance of alexithymia and bullying involvement ... outsiders-and alexithymia on somatic complaints in a sample of 179 Italian middle-school students (aged 11 ... complaints through alexithymia. We also found a significant direct association between victimization and ...

    Abstract Somatic complaints during preadolescence are connected to individual and contextual factors, and extant research highlights the relevance of alexithymia and bullying involvement. In this cross-sectional study, we explored the joint and unique influence of bullying involvement-as perpetrators, victims, or outsiders-and alexithymia on somatic complaints in a sample of 179 Italian middle-school students (aged 11-15). Findings revealed an indirect association between bullying perpetration and victimization complaints through alexithymia. We also found a significant direct association between victimization and somatic complaints. No significant association between outsider behavior and somatization was found. Our results revealed that bullying perpetration and victimization could increase youths' risk for somatic complaints and clarify one of the processes underlying this association. The current findings further emphasize the relevance of emotional awareness for youths' well-being and propose that implementing social-emotional skills might prevent some of the adverse consequences of being involved in bullying episodes.
    Language English
    Publishing date 2023-05-21
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2732685-8
    ISSN 2227-9067
    ISSN 2227-9067
    DOI 10.3390/children10050905
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article: Immunosurveillance of senescent cancer cells by natural killer cells.

    Iannello, Alexandre / Raulet, David H

    Oncoimmunology

    2014  Volume 3, Issue 1, Page(s) e27616

    Abstract: We recently dissected how senescent tumors can trigger complementing signaling pathways that mobilize natural killer (NK) cells to eliminate malignant cells. In addition to cell-intrinsic effects on proliferation, senescence induces the production of ... ...

    Abstract We recently dissected how senescent tumors can trigger complementing signaling pathways that mobilize natural killer (NK) cells to eliminate malignant cells. In addition to cell-intrinsic effects on proliferation, senescence induces the production of chemokine (C-C motif) ligand 2 (CCL2), which recruits NK cells to mediate direct tumoricidal effects. Hence, senescence activates a cancer cell-extrinsic oncosuppression program.
    Language English
    Publishing date 2014-01-06
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
    ZDB-ID 2645309-5
    ISSN 2162-402X ; 2162-4011
    ISSN (online) 2162-402X
    ISSN 2162-4011
    DOI 10.4161/onci.27616
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Immune surveillance of unhealthy cells by natural killer cells.

    Iannello, Alexandre / Raulet, David H

    Cold Spring Harbor symposia on quantitative biology

    2013  Volume 78, Page(s) 249–257

    Abstract: Pathogenic and oncogenic insults result in the induction of intrinsic defense mechanisms such as cell-death pathways and senescence, and extrinsic pathways that mobilize immune responses to destroy unhealthy cells. Both protective mechanisms presumably ... ...

    Abstract Pathogenic and oncogenic insults result in the induction of intrinsic defense mechanisms such as cell-death pathways and senescence, and extrinsic pathways that mobilize immune responses to destroy unhealthy cells. Both protective mechanisms presumably evolved to limit the damage these insults could inflict on the host. After viral infection or malignant transformation, unhealthy cells can be directly sensed by natural killer (NK) and some T cells via the activating receptor NKG2D. All NK cells and subsets of T cells express NKG2D. The NKG2D/ligand system represents a major recognition mechanism for detection and elimination of unhealthy cells. Here we discuss different pathways, including stress pathways, that are responsible for cell-surface display of ligands for NKG2D, which are self-proteins that are minimally expressed by normal cells. We also discuss new results indicating that efficient elimination of tumor cells that display NKG2D ligands depends on the recruitment of NK cells and other immune cells to the tumor, which can be regulated by distinct mechanisms, including the p53-dependent production of chemokines by senescent tumors. The cooperative effect of pathways that induce the display of NKG2D ligands and distinct pathways that mobilize immune cells provides a higher degree of specificity to the NK cell response.
    MeSH term(s) Animals ; Cellular Senescence ; Humans ; Immunologic Surveillance ; Killer Cells, Natural/cytology ; Ligands ; Lymphocytes/immunology ; Mice ; NK Cell Lectin-Like Receptor Subfamily K/metabolism ; Neoplasms/immunology ; Neoplasms/metabolism ; RNA, Messenger/metabolism ; Signal Transduction ; T-Lymphocytes/cytology ; Tumor Suppressor Protein p53/metabolism
    Chemical Substances KLRK1 protein, human ; Ligands ; NK Cell Lectin-Like Receptor Subfamily K ; RNA, Messenger ; TP53 protein, human ; Tumor Suppressor Protein p53
    Language English
    Publishing date 2013-10-17
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Review
    ISSN 1943-4456 ; 0091-7451
    ISSN (online) 1943-4456
    ISSN 0091-7451
    DOI 10.1101/sqb.2013.78.020255
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article: L'interleukine-21, un nouvel adjuvant contre le cancer ?

    Iannello, Alexandre / Ahmad, Ali

    Medecine sciences : M/S

    2009  Volume 25, Issue 4, Page(s) 341–343

    Title translation Interleukin-21, new adjuvant for cancer therapy?.
    MeSH term(s) Animals ; Antibodies, Monoclonal/administration & dosage ; Antineoplastic Agents/therapeutic use ; Antineoplastic Combined Chemotherapy Protocols/therapeutic use ; Carcinoma/drug therapy ; Clinical Trials as Topic ; Drug Screening Assays, Antitumor ; Female ; Humans ; Immunity, Cellular/drug effects ; Immunity, Cellular/physiology ; Interleukins/administration & dosage ; Interleukins/physiology ; Interleukins/therapeutic use ; Lymphoma, B-Cell/drug therapy ; Mammary Neoplasms, Experimental/drug therapy ; Melanoma/drug therapy ; Mice ; Neoplasms/drug therapy
    Chemical Substances Antibodies, Monoclonal ; Antineoplastic Agents ; Interleukins ; interleukin-21
    Language French
    Publishing date 2009-04
    Publishing country France
    Document type News
    ZDB-ID 632733-3
    ISSN 1958-5381 ; 0767-0974
    ISSN (online) 1958-5381
    ISSN 0767-0974
    DOI 10.1051/medsci/2009254341
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article: Rova-T enhances the anti-tumor activity of anti-PD1 in a murine model of small cell lung cancer with endogenous Dll3 expression.

    Vitorino, Philip / Chuang, Chen-Hua / Iannello, Alexandre / Zhao, Xi / Anderson, Wade / Ferrando, Ronald / Zhang, Zhaomei / Madhavan, Shravanthi / Karsunky, Holger / Saunders, Laura R

    Translational oncology

    2020  Volume 14, Issue 1, Page(s) 100883

    Abstract: Rovalpituzumab tesirine (Rova-T) offers a targeted therapy for ~85% of SCLC patients whose tumors express DLL3, but clinical dosing is limited due to off-target toxicities. We hypothesized that a sub-efficacious dose of Rova-T combined with anti-PD1, ... ...

    Abstract Rovalpituzumab tesirine (Rova-T) offers a targeted therapy for ~85% of SCLC patients whose tumors express DLL3, but clinical dosing is limited due to off-target toxicities. We hypothesized that a sub-efficacious dose of Rova-T combined with anti-PD1, which alone shows a clinical benefit to ~15% of SCLC patients, might elicit a novel mechanism of action and extend clinical utility. Using a pre-clinical murine SCLC tumor model that expresses Dll3 and has an intact murine immune system, we found that sub-efficacious doses of Rova-T with anti-PD1 resulted in enhanced anti-tumor activity, compared to either monotherapy. Multiplex immunohistochemistry (IHC) showed CD4 and CD8 T-cells primarily in normal tissue immediately adjacent to the tumor. Combination treatment, but not anti-PD1 alone, increased Ki67+/CD8 T-cells and Granzyme B+/CD8 in tumors by flow cytometry and IHC. Antibody depletion of T-cell populations showed CD8+ T-cells are required for in vivo anti-tumor efficacy. Whole transcriptome analysis as well as flow cytometry and IHC showed that Rova-T activates dendritic cells and increases Ccl5, Il-12, and Icam more than anti-PD1 alone. Increased tumor expression of PDL1 and MHC1 following Rova-T treatment also supports combination with anti-PD1. Mice previously treated with Rova-T + anti-PD1 withstood tumor re-challenge, demonstrating sustained anti-tumor immunity. Collectively our pre-clinical data support clinical combination of sub-efficacious Rova-T with anti-PD1 to extend the benefit of immune checkpoint inhibitors to more SCLC patients.
    Language English
    Publishing date 2020-10-15
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2443840-6
    ISSN 1936-5233
    ISSN 1936-5233
    DOI 10.1016/j.tranon.2020.100883
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Immunosurveillance and immunotherapy of tumors by innate immune cells.

    Iannello, Alexandre / Thompson, Thornton W / Ardolino, Michele / Marcus, Assaf / Raulet, David H

    Current opinion in immunology

    2016  Volume 38, Page(s) 52–58

    Abstract: Increasing evidence supports a role for innate immune effector cells in tumor surveillance. Natural killer (NK) cells and myeloid cells represent the two main subsets of innate immune cells possessing efficient but quite different tumor suppressive ... ...

    Abstract Increasing evidence supports a role for innate immune effector cells in tumor surveillance. Natural killer (NK) cells and myeloid cells represent the two main subsets of innate immune cells possessing efficient but quite different tumor suppressive abilities. Here, we describe the germline-encoded NK cell receptors that play a role in suppressing tumor development and describe briefly the cellular pathways leading to the upregulation of their ligands in tumor cells. We also describe mechanisms underlying the elimination of tumor cells by macrophages and a recently characterized mechanism dedicated to sensing cytosolic DNA that is implicated in antitumor immune responses.
    MeSH term(s) Animals ; Antigens, Differentiation, T-Lymphocyte/genetics ; Antigens, Differentiation, T-Lymphocyte/immunology ; DNA, Neoplasm/genetics ; DNA, Neoplasm/immunology ; Gene Expression Regulation, Neoplastic ; Humans ; Immunity, Innate ; Immunologic Surveillance ; Immunotherapy/methods ; Killer Cells, Natural/immunology ; Killer Cells, Natural/pathology ; Macrophages/immunology ; Macrophages/pathology ; Neoplasm Proteins/genetics ; Neoplasm Proteins/immunology ; Neoplasms/genetics ; Neoplasms/immunology ; Neoplasms/pathology ; Neoplasms/therapy ; Receptors, Natural Killer Cell/genetics ; Receptors, Natural Killer Cell/immunology ; Signal Transduction
    Chemical Substances Antigens, Differentiation, T-Lymphocyte ; CD226 antigen ; DNA, Neoplasm ; Neoplasm Proteins ; Receptors, Natural Killer Cell
    Language English
    Publishing date 2016-02
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Review
    ZDB-ID 1035767-1
    ISSN 1879-0372 ; 0952-7915
    ISSN (online) 1879-0372
    ISSN 0952-7915
    DOI 10.1016/j.coi.2015.11.001
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article: L'interleukine-21, une cytokine clé dans le contrôle du VIH et d'autres infections virales chroniques.

    Iannello, Alexandre / Allam, Ossama / Samarani, Suzanne / Ahmad, Ali

    Medecine sciences : M/S

    2012  Volume 28, Issue 6-7, Page(s) 605–611

    Abstract: The differentiation, homeostatic proliferation and effector functions of different immune cells are controlled, to a large extent, by cytokines. Viruses often cause immune response dysfunctions by causing defects in the cytokine networks. The defects are ...

    Title translation Interleukin-21: a key cytokine for controlling HIV and other chronic viral infections.
    Abstract The differentiation, homeostatic proliferation and effector functions of different immune cells are controlled, to a large extent, by cytokines. Viruses often cause immune response dysfunctions by causing defects in the cytokine networks. The defects are often manifested by altered cytokine secretion and/or responsiveness to the cytokine. Among these cytokines, Interleukin-21 (IL-21) is a relatively recently discovered cytokine, which is mainly produced by CD4(+) T cells in the body, and exerts multiple and pleiotropic effects on various immune cells. Recent studies have shown that the cytokine is indispensable for controlling chronic viral infections. This review summarizes current knowledges concerning the biological effects of this cytokine on different components of the immune system. We also discuss how it contributes toward mounting efficient antiviral immunity and controlling chronic viral infections, especially HIV-1. The IL-1 cytokine represents a novel therapeutic agent for virus-infected patients as well as an adjuvant in antiviral vaccination strategies.
    MeSH term(s) Adaptive Immunity/genetics ; Chronic Disease ; HIV Infections/immunology ; HIV Infections/prevention & control ; HIV-1/drug effects ; HIV-1/immunology ; Humans ; Interleukins/genetics ; Interleukins/physiology ; Interleukins/therapeutic use ; Models, Biological ; Vaccination/methods ; Virus Diseases/immunology ; Virus Diseases/prevention & control
    Chemical Substances Interleukins ; interleukin-21
    Language French
    Publishing date 2012-06
    Publishing country France
    Document type English Abstract ; Journal Article ; Review
    ZDB-ID 632733-3
    ISSN 1958-5381 ; 0767-0974
    ISSN (online) 1958-5381
    ISSN 0767-0974
    DOI 10.1051/medsci/2012286013
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Online: A potentially protective role of IL-18 Binding Protein in HIV-infected Long-Term Non-Progressors.

    Iannello, Alexandre / Samarani, Suzanne / Allam, Ossama / Jenabian, Mohammad-Ali / Mehraj, Vikram / Amre, Devendra / Routy, Jean-Pierre / Tremblay, Cécile / Ahmad, Ali

    Cytokine

    2017  Volume 90, Page(s) 96–99

    Abstract: An imbalance between IL-18 and its antagonist, IL-18 Binding Protein, occurs in the circulation of HIV-infected individuals. We show here for the first time that HIV-infected Long Term Non-Progressors (LTNPs) do not develop this imbalance, and maintain ... ...

    Abstract An imbalance between IL-18 and its antagonist, IL-18 Binding Protein, occurs in the circulation of HIV-infected individuals. We show here for the first time that HIV-infected Long Term Non-Progressors (LTNPs) do not develop this imbalance, and maintain normal levels of IL-18BP in the circulation. Their circulating levels of the antagonist correlate negatively with viral loads and show a positive trend with CD4+ T cells counts. The maintenance of normal production of IL-18BP may contribute, at least in part, to the ability of LTNPs to delay AIDS progression.
    Language English
    Publishing date 2017-02
    Publishing country England
    Document type Journal Article
    ZDB-ID 1018055-2
    ISSN 1096-0023 ; 1043-4666
    ISSN (online) 1096-0023
    ISSN 1043-4666
    DOI 10.1016/j.cyto.2016.10.018
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article ; Online: New molecular semi-quantification tool provides reliable microbiological evidence for pulmonary infection.

    Yugueros-Marcos, Javier / Barraud, Olivier / Iannello, Alexandra / Ploy, Marie Cécile / Ginocchio, Christine / Rogatcheva, Margarita / Alberti-Segui, Cristina / Pachot, Alexandre / Moucadel, Virginie / François, Bruno

    Intensive care medicine

    2018  Volume 44, Issue 12, Page(s) 2302–2304

    MeSH term(s) Bacteria/isolation & purification ; Cell Culture Techniques/standards ; Diagnostic Techniques and Procedures/standards ; Healthcare-Associated Pneumonia/diagnosis ; Humans ; Pneumonia, Ventilator-Associated/diagnosis ; Practice Guidelines as Topic
    Language English
    Publishing date 2018-10-22
    Publishing country United States
    Document type Letter
    ZDB-ID 80387-x
    ISSN 1432-1238 ; 0340-0964 ; 0342-4642 ; 0935-1701
    ISSN (online) 1432-1238
    ISSN 0340-0964 ; 0342-4642 ; 0935-1701
    DOI 10.1007/s00134-018-5417-0
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: Comment on "HIV-specific IL-21 producing CD4+ T cells are induced in acute and chronic progressive HIV infection and are associated with relative viral control".

    Iannello, Alexandre / Samarani, Suzanne / Ahmad, Ali

    Journal of immunology (Baltimore, Md. : 1950)

    2010  Volume 185, Issue 10, Page(s) 5675; author reply 5675

    MeSH term(s) CD4-Positive T-Lymphocytes/drug effects ; CD4-Positive T-Lymphocytes/immunology ; Cell Separation/methods ; Chronic Disease ; Disease Progression ; Enterotoxins/pharmacology ; Flow Cytometry/methods ; HIV Infections/blood ; HIV Infections/immunology ; Humans ; Interleukins/biosynthesis ; Interleukins/immunology ; Ionomycin/pharmacology ; Ionophores
    Chemical Substances Enterotoxins ; Interleukins ; Ionophores ; interleukin-21 ; enterotoxin B, staphylococcal (39424-53-8) ; Ionomycin (56092-81-0)
    Language English
    Publishing date 2010-11-15
    Publishing country United States
    Document type Comment ; Letter
    ZDB-ID 3056-9
    ISSN 1550-6606 ; 0022-1767 ; 1048-3233 ; 1047-7381
    ISSN (online) 1550-6606
    ISSN 0022-1767 ; 1048-3233 ; 1047-7381
    DOI 10.4049/jimmunol.1090103
    Database MEDical Literature Analysis and Retrieval System OnLINE

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