Shedded neuronal ICAM-5 suppresses T-cell activation

Li Tian, Jani Lappalainen, Matti Autero, Satu Hänninen, Heikki Rauvala, Carl G Gahmberg

    Forskningsoutput: TidskriftsbidragArtikelVetenskapligPeer review

    Sammanfattning

    Intercellular adhesion molecules (ICAMs) bind to leukocyte beta 2 integrins, which, among other functions, provide costimulatory signals for T-cell activation. ICAM-5 (telencephalin) is expressed in the soma-dendritic region of neurons of the mammalian brain. The receptor for ICAM-5 is the integrin LFA-1, a major leukocyte integrin expressed in lymphocytes and microglia. In conditions of brain ischemia, epilepsy, and encephalitis, the soluble form of ICAM-5 (siCAM-5) has been detected in physiologic fluids. Here, we report that sICAM-5 attenuates the T-cell receptor-mediated activation of T cells as demonstrated by the decreased expression of the activation markers CD69, CD40L, and CD25 (IL-2R). This effect is most clearly seen in CD45RO(LOW) (naive), and not in CD45RO(High) (memory) T cells, and is most effective early in priming, but not in the presence of strong costimula- tory signals. Furthermore, sICAM-5 promotes the mRNA expression of the cytokines TGF-beta 1 and IFN-gamma, but not TNF. The formation of sICAM-5 is promoted by activated T cells through the cleavage of ICAM-5 from neurons. This suggests that ICAM-5 is involved in immune privilege of the brain and acts as an anti-inflammatory agent.
    Originalspråkengelska
    TidskriftBlood
    Volym111
    Utgåva7
    Sidor (från-till)3615-3625
    Antal sidor11
    ISSN0006-4971
    DOI
    StatusPublicerad - 2008
    MoE-publikationstypA1 Tidskriftsartikel-refererad

    Vetenskapsgrenar

    • 311 Basmedicin
    • 118 Biovetenskaper
    • 515 Psykologi

    Citera det här

    Tian, L., Lappalainen, J., Autero, M., Hänninen, S., Rauvala, H., & Gahmberg, C. G. (2008). Shedded neuronal ICAM-5 suppresses T-cell activation. Blood, 111(7), 3615-3625. https://doi.org/10.1182/blood-2007-09-111179
    Tian, Li ; Lappalainen, Jani ; Autero, Matti ; Hänninen, Satu ; Rauvala, Heikki ; Gahmberg, Carl G. / Shedded neuronal ICAM-5 suppresses T-cell activation. I: Blood. 2008 ; Vol. 111, Nr. 7. s. 3615-3625.
    @article{943f8f2392404761811e3bbd55dcc35f,
    title = "Shedded neuronal ICAM-5 suppresses T-cell activation",
    abstract = "Intercellular adhesion molecules (ICAMs) bind to leukocyte beta 2 integrins, which, among other functions, provide costimulatory signals for T-cell activation. ICAM-5 (telencephalin) is expressed in the soma-dendritic region of neurons of the mammalian brain. The receptor for ICAM-5 is the integrin LFA-1, a major leukocyte integrin expressed in lymphocytes and microglia. In conditions of brain ischemia, epilepsy, and encephalitis, the soluble form of ICAM-5 (siCAM-5) has been detected in physiologic fluids. Here, we report that sICAM-5 attenuates the T-cell receptor-mediated activation of T cells as demonstrated by the decreased expression of the activation markers CD69, CD40L, and CD25 (IL-2R). This effect is most clearly seen in CD45RO(LOW) (naive), and not in CD45RO(High) (memory) T cells, and is most effective early in priming, but not in the presence of strong costimula- tory signals. Furthermore, sICAM-5 promotes the mRNA expression of the cytokines TGF-beta 1 and IFN-gamma, but not TNF. The formation of sICAM-5 is promoted by activated T cells through the cleavage of ICAM-5 from neurons. This suggests that ICAM-5 is involved in immune privilege of the brain and acts as an anti-inflammatory agent.",
    keywords = "311 Basic medicine, 118 Biological sciences, 515 Psychology",
    author = "Li Tian and Jani Lappalainen and Matti Autero and Satu H{\"a}nninen and Heikki Rauvala and Gahmberg, {Carl G}",
    year = "2008",
    doi = "10.1182/blood-2007-09-111179",
    language = "English",
    volume = "111",
    pages = "3615--3625",
    journal = "Blood",
    issn = "0006-4971",
    publisher = "American Society of Hematology",
    number = "7",

    }

    Tian, L, Lappalainen, J, Autero, M, Hänninen, S, Rauvala, H & Gahmberg, CG 2008, 'Shedded neuronal ICAM-5 suppresses T-cell activation', Blood, vol. 111, nr. 7, s. 3615-3625. https://doi.org/10.1182/blood-2007-09-111179

    Shedded neuronal ICAM-5 suppresses T-cell activation. / Tian, Li; Lappalainen, Jani; Autero, Matti; Hänninen, Satu; Rauvala, Heikki; Gahmberg, Carl G.

    I: Blood, Vol. 111, Nr. 7, 2008, s. 3615-3625.

    Forskningsoutput: TidskriftsbidragArtikelVetenskapligPeer review

    TY - JOUR

    T1 - Shedded neuronal ICAM-5 suppresses T-cell activation

    AU - Tian, Li

    AU - Lappalainen, Jani

    AU - Autero, Matti

    AU - Hänninen, Satu

    AU - Rauvala, Heikki

    AU - Gahmberg, Carl G

    PY - 2008

    Y1 - 2008

    N2 - Intercellular adhesion molecules (ICAMs) bind to leukocyte beta 2 integrins, which, among other functions, provide costimulatory signals for T-cell activation. ICAM-5 (telencephalin) is expressed in the soma-dendritic region of neurons of the mammalian brain. The receptor for ICAM-5 is the integrin LFA-1, a major leukocyte integrin expressed in lymphocytes and microglia. In conditions of brain ischemia, epilepsy, and encephalitis, the soluble form of ICAM-5 (siCAM-5) has been detected in physiologic fluids. Here, we report that sICAM-5 attenuates the T-cell receptor-mediated activation of T cells as demonstrated by the decreased expression of the activation markers CD69, CD40L, and CD25 (IL-2R). This effect is most clearly seen in CD45RO(LOW) (naive), and not in CD45RO(High) (memory) T cells, and is most effective early in priming, but not in the presence of strong costimula- tory signals. Furthermore, sICAM-5 promotes the mRNA expression of the cytokines TGF-beta 1 and IFN-gamma, but not TNF. The formation of sICAM-5 is promoted by activated T cells through the cleavage of ICAM-5 from neurons. This suggests that ICAM-5 is involved in immune privilege of the brain and acts as an anti-inflammatory agent.

    AB - Intercellular adhesion molecules (ICAMs) bind to leukocyte beta 2 integrins, which, among other functions, provide costimulatory signals for T-cell activation. ICAM-5 (telencephalin) is expressed in the soma-dendritic region of neurons of the mammalian brain. The receptor for ICAM-5 is the integrin LFA-1, a major leukocyte integrin expressed in lymphocytes and microglia. In conditions of brain ischemia, epilepsy, and encephalitis, the soluble form of ICAM-5 (siCAM-5) has been detected in physiologic fluids. Here, we report that sICAM-5 attenuates the T-cell receptor-mediated activation of T cells as demonstrated by the decreased expression of the activation markers CD69, CD40L, and CD25 (IL-2R). This effect is most clearly seen in CD45RO(LOW) (naive), and not in CD45RO(High) (memory) T cells, and is most effective early in priming, but not in the presence of strong costimula- tory signals. Furthermore, sICAM-5 promotes the mRNA expression of the cytokines TGF-beta 1 and IFN-gamma, but not TNF. The formation of sICAM-5 is promoted by activated T cells through the cleavage of ICAM-5 from neurons. This suggests that ICAM-5 is involved in immune privilege of the brain and acts as an anti-inflammatory agent.

    KW - 311 Basic medicine

    KW - 118 Biological sciences

    KW - 515 Psychology

    U2 - 10.1182/blood-2007-09-111179

    DO - 10.1182/blood-2007-09-111179

    M3 - Article

    VL - 111

    SP - 3615

    EP - 3625

    JO - Blood

    JF - Blood

    SN - 0006-4971

    IS - 7

    ER -