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Details for receptor: TLR2

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EndoNet ID: ENR00841

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Synonyms

  • toll-like receptor 2
  • TLR2
  • TIL4
  • toll/interleukin 1 receptor-like protein 4

General information

  • Peripheral blood mononuclear cell (PBMC) TLR-2 expression was significantly increased in patients with cirrhosis. [1]
  • TLRs 2, 6. 7, 8, 9 and 10 mRNA levels were upregulated in monocytes in HCV-infected patients compared to controls. [2]
  • The expression of TLR-2 correlated significantly with soluble TNF-alpha and soluble TNF-receptor levels. [1]
  • Cooperates with LY96 to mediate the innate immune response to bacterial lipoproteins and other microbial cell wall components. Acts via MyD88 and TRAF6, leading to NF-kappa-B activation, cytokine secretion and the inflammatory response. [3]
  • Recognizes mycoplasmal macrophage-activating lipopeptide-2kD (MALP-2), soluble tuberculosis factor (STF), phenol-soluble modulin (PSM) and B.burgdorferi outer surface protein A lipoprotein (OspA-L) cooperatively with TLR6. [3]
  • TLR2 can recognize certain viruses such as cytomegalovirus, measles virus and core and NS3 proteins of HCV. [2]
  • The TLR2 protein level was upregulated at 24 and 48 h after stimulation with TNFalpha or IL-1beta in HSCs. [4]

Links to other resources

UniProt O60603
Ensembl ENST00000260010

Subunit information

Sequence 
KEESSNQAS LSCDRNGIC KGSSGSLNS 
IPSGLTEAV KSLDLSNNR ITYISNSDL 
QRCVNLQAL VLTSNGINT IEEDSFSSL 
GSLEHLDLS YNYLSNLSS SWFKPLSSL 
TFLNLLGNP YKTLGETSL FSHLTKLQI 
LRVGNMDTF TKIQRKDFA GLTFLEELE 
IDASDLQSY EPKSLKSIQ NVSHLILHM 
KQHILLLEI FVDVTSSVE CLELRDTDL 
DTFHFSELS TGETNSLIK KFTFRNVKI 
TDESLFQVM KLLNQISGL LELEFDDCT 
LNGVGNFRA SDNDRVIDP GKVETLTIR 
RLHIPRFYL FYDLSTLYS LTERVKRIT 
VENSKVFLV PCLLSQHLK SLEYLDLSE 
NLMVEEYLK NSACEDAWP SLQTLILRQ 
NHLASLEKT GETLLTLKN LTNIDISKN 
SFHSMPETC QWPEKMKYL NLSSTRIHS 
VTGCIPKTL EILDVSNNN LNLFSLNLP 
QLKELYISR NKLMTLPDA SLLPMLLVL 
KISRNAITT FSKEQLDSF HTLKTLEAG 
GNNFICSCE FLSFTQEQQ ALAKVLIDW 
PANYLCDSP SHVRGQQVQ DVRLSVSEC 
HRTALVSGM CCALFLLIL LTGVLCHRF 
HGLWYMKMM WAWLQAKRK PRKAPSRNI 
CYDAFVSYS ERDAYWVEN LMVQELENF 
NPPFKLCLH KRDFIPGKW IIDNIIDSI 
EKSHKTVFV LSENFVKSE WCKYELDFS 
HFRLFDENN DAAILILLE PIEKKAIPQ 
RFCKLRKIM NTKTYLEWP MDEAQREGF 
WVNLRAAIK S

Binding hormones

  • BD-3
    • Human β-defensin 3 (hBD-3) activates antigen-presenting cells through Toll-like receptors (TLRs) 1/2. [5]

Anatomical structures with this receptor

  • leukocyte

  • monocyte

    Induced phenotypes

    • monocyte activation
      • We provide evidence that hBD-3 activates cells in a TLR1- and TLR2-dependent manner. [6]
      • hBD-3 induces activation of monocytes and mDCs, but not pDCs or B cells, is consistent with the expected pattern of TLR2 and TLR1 expression on these cells. [6]

  • bone_marrow

  • spleen

  • lymph_node

  • lipocyte_of_liver

    Induced phenotypes

    • regulation of innate immune response
      • Upregulated TLR2 expression primes HSCs to increase NF-kappa B activation and IL-8 production in response to TLR2 ligands. This is important for the induction of potent innate immune response. [4]
      • HSCs barely respond to TLR2 ligands. Initiation by inflammatory mediators such as TNF-α, IL-1β, and LPS might be required for fulfilling TLR2 signaling in HSCs. [7]
    • HSCs express TLR2, a receptor for Gram-positive bacterial cell wall components, such as peptidoglycan and lipoteichoic acid. [8]

  • peripheral blood mononuclear cell (PBMC)

    Influences

    • positive TNF-alpha
      • The products of gram-positive bacteria may be promoting increases in circulating TNF-alpha and soluble TNF-alpha receptor via stimulation of TLR-2. [1]

  • neutrophil_granulocyte

  • continuous_vascular_endothelial_cell_of_blood_vessels_and_lymphatics

  • epithelial_cell_with_microvilli

  • vaginal_mucosa

  • cervical_canal_of_uterus

  • cholangiocyte

  • bronchial_epithelial_cell

  • alveolar_macrophage

    Influences

    • TNF-alpha
      • SP-A significantly reduced PGN-elicited tumor necrosis factor alpha (TNF-alpha) secretion by rat alveolar macrophages. The inhibitory effect on TNF-alpha secretion was dependent upon SP-A concentrations in physiological range. [9]
      • Direct interaction of SP-A with TLR2 alters PGN-induced cell signaling. [9]

  • macrophage

    Influences

    • positive IL-1 beta
      • IL-1β is first synthesized as biologically-inactive precursor (pro-IL-1β) in response to Toll-like receptor (TLR) agonists in macrophages. [10]
Reference