Role of Toll-Like Receptors in Innate Immunity Essay

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Before discussing the role of toll like receptors in innate immunity it might be prudent to know a little about the toll like receptors themselves. Toll like receptors are a class of receptors which recognize molecules derived from microbes when they have breached the normal defense mechanisms of the body (Lewinson, 2004, pp.50-75). Toll like receptors are pattern recognition receptors which function along with the HLA typing system to identify host tissue from that of the foreign inciting agent. There are certain subtypes of TLR which act in conjunction with the organism they are supposed to identify (Davidson, 2006, pp.140-160).

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Basically three subgroups of the TLR exist; Protein with subgroup 1 TLR are receptors for interleukins produced by macrophages, monocytes, dendrite cells and have an extra cellular Immunoglobulin domain. Type 2 protein domains bind to molecules of microbial origin and the 3rd subgroup consists of adaptor proteins concerned with signaling from proteins 1 and 2. These are the types and some properties of the TLR. They have an integral role when it comes to innate immunity (Cotran, 2006, pp. 260-350).

Now the question as to what is innate immunity and how TLR serve to enhance immunity? Innate immunity is one of the natural host immune systems developed by nature for the protection of the different species. It is present in both vertebrates and invertebrates. Innate immunity basically consists of natural host defenses which protect the body from foreign invasion. The other type of immunity is classified as the acquired immunity. This type of immunity stems from the factors acquired through the lifetime of the individual and forms only after exposure to a certain micro organism, whereas innate immunity is inbuilt and does not require repeated stimulus to come into play (Lewinson, 2004, pp. 200).

Both of the mechanisms act independently of each other. The concept of innate immunity has been well understood and researched in the invertebrates. The concept first emerged through studies undertaken on Drosophila. This was done at the end of the 20th century and the research centered on the antifungal action of Drosophila (Lemaitre, et.al, 1996, n.p.) After that the mammalian homolog of the Toll receptor was discovered and showed to induce expression of genes involved in inflammatory responses.

Further more researches on the subject proved it beyond doubt that innate immunity is indeed closely related to the TLR system and the system works in conjunction with the TLR. Of all the TLRs a total of 11 have been identified with the humans containing 10 and certain lower specie having the total of 11 tolls like receptors (Poltorak, 1998). The intracellular portion of the TLR is termed as TLR IL-1 receptor in accordance with it’s similarity to the interleukin agents.

The extra cellular domain mainly consists of Leucine rich repeats while the intracellular ones consist of an immunoglobulin like domain. Thus individual TLR play a definitive role in thru recognition of foreign microbial agents and in the subsequent activation of the immunity cascade (Smith, et.al, 2003, pp. 50-56). TLR 2 is concerned with the recognition of the lipoproteins from the various microorganisms. TLR 3 is concerned with the identification of the RNA which is used by various viruses for their replication.

This property of the TLR 3 helps the host to identify viruses ion different phases of their replication and results in the activation of the host T-cell immunity cascade. TLR 4 is involved in the recognition of the lipopolysacharides (Netea, et.al, 2002, pp.135). It recognizes taxi, which is an important constituent of the microorganisms. However a high concentration of the above mentioned substances are required to bring about an effect by TLR 4.

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Bacterial flagella are composed of a protein called Flagellin and it is this Flagellin which is recognized by TLR 5. The TLR 5 thus activates the natural host immune system on contact with a bacterial flagellum (Kiyoshi, 2004, pp. 50-75). TLR 6 works along with TLR 2 and the two tolls like receptors work to identify lipids on the cellular walls of the bacteria or the inciting organisms and work accordingly to activate the host T-cell. TLR 7 and TLR 8 are concerned with the identification of materials contained in viral inclusion cell bodies like imidazoquinolones which are important constituents of the nucleic acids in viruses (Hashimoto, et.al, 2004, n.p.).

TLR 9 is associated with recognition of CpG DNA which is an integral constituent of the bacterial DNA. TLR 11 has not been as yet associated with recognition systems in humans but is found to act in a cohesive manner to identify pathogens associated with bladder infection in mice (Lutz, 2004, n.p.). The different receptors are placed at different strategic location throughout the host cell so much so that the part involved in the recognition system may easily come into contact with the specific subtype of the molecule it is intended to identify.

The TLR 1, 2 and 4 are present on the cell surface while 3, 7, 8 and 9 are located morewhatsover intracellularly. The recognition of the foreign inciting agent by the TLR and its subsequent destruction involves several steps (Ahmad, et.al, 2002, n.p.). TLR recognition of the pathogen leads to the expression of genes which are inflammatory mediators. These mediators along with the HLA recognition system presents the inciting agents to the binding domain and activates the antigen specific acquired immunity through Tcell activation and B cell activation.

This ensues a phagocytic response and the subsequent engulfment of the pathogen by the macrophages and it’s destruction from the host cell. In the absence of TLR, the recognition and phagocytosis of the pathogen cannot take place (Underhil, et.al, 1999, n.p.). Thus TLR are involved at the highest level at the destruction of the inciting foreign agent. Innate immune cells such as dendrite cells and macrophages engulf pathogens by phagocytes and present pathogen derived peptide antigens to T- cells, for their ultimate disposal.

If the inflammatory cytokines are produced in excess then they might lead to the destruction of the cell itself. Thus TLR is a necessary evil with mandatory checks and balances to be imposed on the system for appropriate functioning of the defense mechanism (Doyle, et.al, 2002, n.p.). This is achieved through a negative regulation of the TLR system. The precise mechanism whereby this is achieved has not been understood properly as yet and is called as endotoxin tolerance. The molecules involved in the signaling mechanism of this feedback system have been identified and are found to consist of Seriene subtypes (Horng, et.al, 2001, n.p.).

Research however is underway to properly comprehend the total philosophy behind such a mechanism. Uphill now what is known about the TLR has shown that it is indeed an integral part of the host defense system and without appropriate recognition there is no way that the host cell can tell a friend from a foe (Anderson, 2000, n.p.). The presence of an independent identification system has enabled us to combat bacterial and viral infections at a new front. Fortunately, everyday new advancements are taking place in modern technology which is quite good for human. Day by day emerging technologies allow people from all over the globe to study and research new discoveries of infections and their cures.

In the future it is proposed that medicines at genetic level may function on similar grounds as that of the TLR system devised by nature (Goldstein, et.al, 2003, n.p.). The medicine of future is based on genetic level of treatment and this is what may totally revamp the concept of TLR. (Howland, 2005, pp. 341-350)

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References

  1. Ahmad-Nejad, P., Hacker, H., Rutz, M., Bauer, S., Vabulas, R. M. and Wagner, H. (2002), Bacterial CpG-DNA and lipopolysaccharides activate Toll-like receptors at distinct cellular compartments. Issue 32: Vol 1958
  2. Anderson, Kevin (2000) Is bacterial resistance an example of evolutionary.
  3. Doyle, S. E,. et.al (2002) IRF3 mediates a TLR3/TLR4-specific antiviral gene program. Issue 17: Vol 251
  4. Davidson’s Principles and practice of medicine, Churchill Livingstone, 19th edition, pg 147-164, 2006
  5. Goldstein, D. R., Tesar, B. M., Akira, S. and Lakkis, F. G. (2003), Critical role of the Toll-like receptor signal adaptor protein My D88 in acute allograft rejection. Issue 111:Vol. 1571
  6. Howland, Richard (2005), Lippincot Illustrated reviews, 3rd edition Aplleton and Lange, pg 341
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  11. Lemaitre, B., Nicolas, E., Michaut, L., Reichhart, J.-M. And Hoffmann, J. A. (1996), The dorsoventral regulatory gene cassette cactus controls the potent antifungal response in Drosophila adults published in Cell. Issue 86 Volume 973 Lemaitre.
  12. Latz, E. et al. (2004). TLR9 signals after translocating from the ER to CpG DNA in the lysosome. Issue 5: Vol 190
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  14. Poltorak, A. et al. (1998), Defective LPS signaling in C3H/HeJ and C57BL/10ScCr mice: mutation in Tlr4 gene. Issue 282 Vol. 2085
  15. Ramzi Kotran , Vinay Kumar , Stanley L Robbins (2006) Tucker Collins Robins Pathological Basis Of Disease, 7th Edition W.B.Saunders Company, pg 260-450
  16. Smith, M. F. Jr., Mitchell, A., Li, G., Ding, S., Fitzmaurice, A. M., Ryan, K., Crowe, S. and Goldberg, J. B. (2003). Toll-like receptor (TLR) 2 and TLR5, but TL4 are required for Helicobacter pylori-induced NF-B activation and chemokine expression by epithelial cells. Issue 278: Vol 32552, pg 50-56
  17. Underhill, D. M., Ozinsky, A., Hajjar, A. M., Stevens, A., Wilson, C. B., Bassetti, M. and Aderem, A. (1999), The Toll-like receptor 2 is recruited to macrophage phagosomes and discriminates between pathogens. 401:811
  18. Warren Lewiston, (2004) Microbiology and Immunology, Appleton and Lange, Sixth Edition, (pg 54-75)
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