Toll-like receptors

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Toll-like receptors:

Toll-like receptors Eman abd El- raouf ahmed

The content::

The content: 1-introduction 2-

Introduction October 3, 2011 — The Nobel prize for medicine was awarded today to 3 scientists whose discoveries about the immune system are expanding how clinicians prevent and treat infection, inflammatory diseases, and cancer,:

Introduction October 3, 2011 — The Nobel prize for medicine was awarded today to 3 scientists whose discoveries about the immune system are expanding how clinicians prevent and treat infection, inflammatory diseases, and cancer , The work of Dr. Beutler and Dr. Hoffmann has "triggered an explosion of research in innate immunity" and the identification of dozen or so different receptor proteins called Toll-like receptors in humans and mice, according to the Nobel Foundation. Each Toll-like receptor recognizes certain types of molecules found in trespassing microorganisms. Genetic variations in these Toll-like receptors come with an increased risk for infection or chronic inflammatory disease .

introduction:

introduction

introduction:

introduction

http://www.proteinlounge.com/PBTool/ListPathwayThumb.aspx Pathway Builder Online:

http:// www.proteinlounge.com/PBTool/ListPathwayThumb.aspx Pathway Builder Online

PowerPoint Presentation:

http:// www.youtube.com/watch?v=iVMIZy-Y3f8

introduction:

introduction

introduction:

introduction

*definition:

*definition

Types of toll-like receptor:

Types of toll-like receptor

Types of TLR continue..:

Types of TLR continue..

TLR-3 (types continue…):

TLR-3 (types continue…)

TLR-2 AND 4(types continue…):

TLR-2 AND 4(types continue…)

Type 4 TLR:

Type 4 TLR

Dendritic cell and toll-like receptor:

Dendritic cell and toll-like receptor

TLR-domain:

TLR-domain

Structure of toll-like receptor:

Structure of toll-like receptor

3D -structure:

3D -structure

function:

function

Figure 3. Potential mechanism for the role of Toll-like receptors (TLRs) in intestinal defence and tolerance. Interleukin 1 receptor (IL-1R)-associated kinase (IRAK) appears to be an important negative regulator of TLR signalling. Thus, following short-term TLR stimulation (a), expression of IRAK and NF-kB might be appropriately upregulated, thereby rapidly and efficiently defending the host against an acute threat; this acute defence mechanism might be dysregulated in disease, leading to exaggerated immune responses. Following long-term TLR stimulation (b), expression of IRAK and NF-kB might be appropriately downregulated, maintaining hyporesponsiveness in health; again, this might be dysregulated in disease:

Figure 3. Potential mechanism for the role of Toll-like receptors (TLRs) in intestinal defence and tolerance. Interleukin 1 receptor (IL-1R)-associated kinase (IRAK) appears to be an important negative regulator of TLR signalling . Thus, following short-term TLR stimulation (a), expression of IRAK and NF- kB might be appropriately upregulated , thereby rapidly and efficiently defending the host against an acute threat; this acute defence mechanism might be dysregulated in disease, leading to exaggerated immune responses. Following long-term TLR stimulation (b), expression of IRAK and NF- kB might be appropriately downregulated , maintaining hyporesponsiveness in health; again, this might be dysregulated in disease

TLR AND signals:

TLR AND signals

Signals of TLR:

Signals of TLR

Fig. 4. TLR signaling pathway. TLR signaling pathways originate from the cytoplasmic TIR domain. A TIR domain-containing adaptor, MyD88, associates with the cytoplasmic TIR domain of TLRs, and recruits IRAK to the receptor upon ligand binding. IRAK then activates TRAF6, leading to the activation of the IκB kinase (IKK) complex consisting of IKKα, IKKβ and NEMO/IKKγ. The IKK complex phosphorylates IκB, resulting in nuclear translocation of NF-κB which induces expression of inflammatory cytokines. TIRAP, a second TIR domain-containing adaptor, is involved in the MyD88-dependent signaling pathway via TLR2 and TLR4. In TLR3- and TLR4-mediated signaling pathways, activation of IRF-3 and induction of IFN-β are observed in a MyD88-independent manner. A third TIR domain-containing adaptor, TRIF, is essential for the MyD88-independent pathway. Non-typical IKKs, IKKi/IKKε and TBK1, mediate activation of IRF-3 downstream of TRIF. A fourth TIR domain-containing adaptor, TRAM, is specific to the TLR4-mediated MyD88-independent/TRIF-dependent pathway.:

Fig. 4. TLR signaling pathway. TLR signaling pathways originate from the cytoplasmic TIR domain. A TIR domain-containing adaptor, MyD88, associates with the cytoplasmic TIR domain of TLRs, and recruits IRAK to the receptor upon ligand binding. IRAK then activates TRAF6, leading to the activation of the I κ B kinase (IKK) complex consisting of IKK α, IKK β and NEMO/IKK γ. The IKK complex phosphorylates I κ B, resulting in nuclear translocation of NF- κ B which induces expression of inflammatory cytokines. TIRAP, a second TIR domain-containing adaptor, is involved in the MyD88-dependent signaling pathway via TLR2 and TLR4. In TLR3- and TLR4-mediated signaling pathways, activation of IRF-3 and induction of IFN- β are observed in a MyD88-independent manner. A third TIR domain-containing adaptor, TRIF, is essential for the MyD88-independent pathway. Non-typical IKKs, IKKi/IKK ε and TBK1, mediate activation of IRF-3 downstream of TRIF. A fourth TIR domain-containing adaptor, TRAM, is specific to the TLR4-mediated MyD88-independent/TRIF-dependent pathway .

mechanism of TLR4:

mechanism of TLR4

mechanism-TLR continue:

mechanism-TLR continue

TLR4- mechanism continue:

TLR4- mechanism continue

TLR -antibody:

TLR -antibody

Research Summary It is well known that macrophages and dendritic cells play important roles in host defense. Some reports indicate that some proteins can modify the activation status of these cells. We are analyzing physiological functions of molecules which expressed on these innate immune cells. To clarify their function, we are utilizing in vitro techniques and also the gene knocked out mice. Also, osteoclasts are thought to belong to similar cell lineage to macrophages and dendritic cells. We are also analyzing on the function of a new immunoglobulin superfamily molecule in osteolastogenesis and bone metabolisms. :

Research Summary It is well known that macrophages and dendritic cells play important roles in host defense. Some reports indicate that some proteins can modify the activation status of these cells. We are analyzing physiological functions of molecules which expressed on these innate immune cells. To clarify their function, we are utilizing in vitro techniques and also the gene knocked out mice. Also, osteoclasts are thought to belong to similar cell lineage to macrophages and dendritic cells. We are also analyzing on the function of a new immunoglobulin superfamily molecule in osteolastogenesis and bone metabolisms.

Toll-like receptors (TLRs) are a family of ten evolutionarily conserved receptors expressed either on the cell surface or in intracellular endocytic vesicles or organelles, and which collectively recognize a diverse range of microbial ligands. Recognition by TLRs triggers the rapid, orchestrated production of chemokines, cytokines, and other inflammatory mediators that leads to the generation of cellular immune responses.:

Toll-like receptors (TLRs) are a family of ten evolutionarily conserved receptors expressed either on the cell surface or in intracellular endocytic vesicles or organelles, and which collectively recognize a diverse range of microbial ligands. Recognition by TLRs triggers the rapid, orchestrated production of chemokines , cytokines, and other inflammatory mediators that leads to the generation of cellular immune responses .

TLR AND cancer:

TLR AND cancer

references:

references http:// www.ventirx.com/product/toll-receptors.htm http://my.ilstu.edu/~ ddwilso2/nur475/Skin_Cancers.htm http:// intimm.oxfordjournals.org/content/17/1/1.full http:// www.proteinlounge.com/Animation/Animation.aspx http://www.uthsc.edu/molecular_sciences/directories/faculty/f_re.php

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