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  1. Article ; Online: Negatywna regulacja sygnalizacji receptorów Toll-podobnych.

    Antosz, Halina / Choroszyńska, Dorota

    Postepy higieny i medycyny doswiadczalnej (Online)

    2013  Volume 67, Page(s) 339–350

    Abstract: The mechanism of innate immunity is based on the pattern recognition receptors (PRR) that recognize molecular patterns associated with pathogens (PAMPs). Among PRR receptors Toll-like receptors (TLR) are distinguished. As a result of contact with ... ...

    Title translation Negative regulation of Toll-like receptor signalling.
    Abstract The mechanism of innate immunity is based on the pattern recognition receptors (PRR) that recognize molecular patterns associated with pathogens (PAMPs). Among PRR receptors Toll-like receptors (TLR) are distinguished. As a result of contact with pathogens, TLRs activate specific intracellular signaling pathways. It happens through proteins such as adaptor molecules, e.g. MyD88, TIRAP, TRIF, TRAM, and IPS-1, which participate in the cascade activation of kinases (IKK, MAP, RIP-1, TBK-1) as well as transcription factors (NF-κB, AP-1) and regulatory factor (IRF3). The result of this activation is the production of active proinflammatory cytokines, chemokines, interferons and enzymes. The PRR pathways are controlled by extra- and intracellular molecules to prevent overexpression of PRR. They include soluble receptors (sTLR), transmembrane proteins (ST2, SIGIRR, RP105, TRAIL-R) and intracellular inhibitors (SOCS-1, SOCS-3, sMyD88, TOLLIP, IRAK-M, SARM, A20, β-arrestin, CYLD, SHP). These molecules maintain the balance between activation and inhibition and ensure balancing of the beneficial and adverse effects of antigen recognition.
    MeSH term(s) Antigen Presentation/immunology ; Cytokines/immunology ; Humans ; Immunity, Innate/immunology ; Interferon Regulatory Factor-3/metabolism ; Intracellular Signaling Peptides and Proteins ; NF-kappa B/metabolism ; Receptors, Pattern Recognition/immunology ; Signal Transduction/immunology ; Suppressor of Cytokine Signaling Proteins/immunology ; Toll-Like Receptors/immunology ; Transcription Factor AP-1/metabolism ; Transcription Factors/immunology
    Chemical Substances Cytokines ; IRF3 protein, human ; Interferon Regulatory Factor-3 ; Intracellular Signaling Peptides and Proteins ; NF-kappa B ; Receptors, Pattern Recognition ; Suppressor of Cytokine Signaling Proteins ; TOLLIP protein, human ; Toll-Like Receptors ; Transcription Factor AP-1 ; Transcription Factors
    Language Polish
    Publishing date 2013-04-25
    Publishing country Poland
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 418865-2
    ISSN 1732-2693 ; 0032-5449
    ISSN (online) 1732-2693
    ISSN 0032-5449
    DOI 10.5604/17322693.1046538
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: IL-6, IL-10, c-Jun and STAT3 expression in B-CLL.

    Antosz, Halina / Wojciechowska, Katarzyna / Sajewicz, Joanna / Choroszyńska, Dorota / Marzec-Kotarska, Barbara / Osiak, Magdalena / Pająk, Natalia / Tomczak, Waldemar / Jargiełło-Baszak, Małgorzata / Baszak, Jacek

    Blood cells, molecules & diseases

    2015  Volume 54, Issue 3, Page(s) 258–265

    Abstract: Chronic lymphocytic leukemia is characterized by the accumulation of functionally abnormal, monoclonal B lymphocytes in the peripheral blood, bone marrow, lymph nodes and spleen, resulting in a reduction count of normal immunocompetent cells and their ... ...

    Abstract Chronic lymphocytic leukemia is characterized by the accumulation of functionally abnormal, monoclonal B lymphocytes in the peripheral blood, bone marrow, lymph nodes and spleen, resulting in a reduction count of normal immunocompetent cells and their impaired immune function. The defect in transmission of signals from various types of extracellular receptors, leading to aberrant cytokines and transcription factors gene expression, may underlie the basis of immune failure in B-CLL. The aim of the study was to assess of IL-6, IL-10, c-Jun, and STAT3 expression. In response to antigenic stimulation IL-6, IL-10, c-Jun, and STAT3 proteins induce mutual activity. The subject of the study was subpopulations of leukemic lymphocytes (CD5+ CD19+) and CD19+ B cells from healthy donors (control group). Our results provide evidence that the regulation of IL-6, IL-10, c-Jun, and STAT3 gene expression in CLL B cells is clearly different from normal B lymphocytes. In B-CLL STAT3 expression in unstimulated lymphocytes is significantly higher (p<0.0001) compared with normal subpopulation of B cell. In contrast, IL-6, IL-10, and c-Jun mRNA expressions are statistically lower in B-CLL in comparison with the control group, in all cases (p<0.0001). When analyzing the relationship between c-Jun expression and B-CLL stage according Rai we revealed decreasing c-Jun expression, both at the mRNA and protein levels, along with advancing stage of disease.
    MeSH term(s) Aged ; Aged, 80 and over ; B-Lymphocytes/metabolism ; B-Lymphocytes/pathology ; Female ; Gene Expression Regulation, Leukemic ; Humans ; Interleukin-10/analysis ; Interleukin-10/genetics ; Interleukin-6/analysis ; Interleukin-6/genetics ; Leukemia, Lymphocytic, Chronic, B-Cell/genetics ; Leukemia, Lymphocytic, Chronic, B-Cell/pathology ; Male ; Middle Aged ; Proto-Oncogene Proteins c-jun/analysis ; Proto-Oncogene Proteins c-jun/genetics ; RNA, Messenger/genetics ; STAT3 Transcription Factor/analysis ; STAT3 Transcription Factor/genetics
    Chemical Substances Interleukin-6 ; Proto-Oncogene Proteins c-jun ; RNA, Messenger ; STAT3 Transcription Factor ; Interleukin-10 (130068-27-8)
    Language English
    Publishing date 2015-03
    Publishing country United States
    Document type Journal Article
    ZDB-ID 1237083-6
    ISSN 1096-0961 ; 1079-9796
    ISSN (online) 1096-0961
    ISSN 1079-9796
    DOI 10.1016/j.bcmd.2014.11.006
    Database MEDical Literature Analysis and Retrieval System OnLINE

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