Genetic polymorphism of immunogenic signaling system
https://doi.org/10.22625/2072-6732-2011-3-2-21-27
Abstract
The functional studies underline the importance of maintaining structural integrity of the innate immune components of intracellular signaling. The molecular structures for a number of proteins and protein domains in immune signaling have been determined. These structures have assisted us in understanding innate immunity at the molecular level. A polymorphisms modulating innate immunity signal transduction has recently been shown to influence human susceptibility to many different infections, providing one more indication of the potential of host genetics to reveal physiological pathways and mechanisms that influence resistance
to infectious diseases. This lection describes recently determined structures involved in TLR signaling.
About the Authors
V. N. Tzygan
Military Medical Academy by S.M. Kirov, S.Petersburg
Russian Federation
Russian Federation
A. M. Ivanov
Military Medical Academy by S.M. Kirov, S.Petersburg
Russian Federation
Russian Federation
T. A. Kamilova
Military Medical Academy by S.M. Kirov, S.Petersburg
Russian Federation
Russian Federation
E. A. Коjuhova
Military Medical Academy by S.M. Kirov, S.Petersburg
Russian Federation
Russian Federation
N. N. Мurashkin
Military Medical Academy by S.M. Kirov, S.Petersburg
Russian Federation
Russian Federation
N. V. Tsygan
Military Medical Academy by S.M. Kirov, S.Petersburg
Russian Federation
Russian Federation
References
1. Akira, S. Pathogen recognition and innate immunity / S. Akira, S. Uematsu, O. Takeuchi // Cell. – 2006. – V. 124. –P. 783–801.
2. Artis, D. The intestinal epithelium: sensors to effectors in nematode infection / D. Artis, R.K. Grencis // Mucos. Immunol. – 2008. – V. 1, №4. – P. 252–262.
3. Baima, E.T. Novel insights into the cellular mechanismsof the anti-inflammatory effects of NF-[kappa]B essential modulator (NEMO) binding domain peptides / E.T. Baima [et al.] // J. Biol. Chem. – 2010. – V. 285. – P. 13498–13506.
4. Brandl, K. MyD88-mediated signals induce the bactericidal lectin RegIII gamma and protect mice against intestinal Listeria monocytogenes infection / K. Brandl [et al.] // J. Exp. Med. – 2007. – V. 204. – P. 1891–1900.
5. Burns, K. Inhibition of interleukin 1 receptor/Toll-like receptor signaling through the alternatively spliced, short form of MyD88 is due to its failure to recruit IRAK-4 / K. Burns [et al.] // J. Exp. Med. – 2003. – V. 197. – P. 263–268.
6. Burns, K. Tollip, a new component of the IL-1RI pathway, links IRAK to the IL-1 receptor / K. Burns [et al.] // Nat. Cell Biol. – 2000. – V. 2, № 6. – P. 346–351.
7. Casanova, J.L. Genetic dissection of immunity to mycobacteria: the human model / J.L. Casanova, L. Abel // Annu. Rev. Immunol. – 2002. – V. 20. – P. 581–620.
8. Caws, M. The influence of host and bacterial genotype on the development of disseminated disease with Mycobacterium tuberculosis / M. Caws [et al.] // PLoS Pathog. – 2008. – V. 4, № 3. – P. e1000034.
9. Coban, C. Toll-like receptor 9 mediates innate immune activation by the ma-laria pigment hemozoin / C. Coban [et al.] // J. Exp. Med. – 2005. – V. 201, №1. – P. 19–25.
10. Dean, M. Balanced polymorphism selected by genetic versus infectious human disease / M. Dean, M. Carrington, S.J. O’Brien // Annu. Rev. Genom Hum. Ge-net. – 2002. – V. 3. – P. 263–292.
11. Dhiman, N. Associations between SNPs in toll-like receptors and related intracel-lular signaling molecules and immune responses to measles vaccine: preliminary results / N. Dhiman [et al.] // Vaccine. – 2008. – V. 26, № 14. –P. 1731–1736.
12. Didierlaurent, A. Tollip regulates proinflammatory responses to interleukin-1 and lipopolysaccharide /A. Didierlaurent [et al.] // Mol. Cell Biol. – 2006. – V. 26. – P. 735–742.
13. Dunne, A. Structural complementarity of Toll /interleukin-1 receptor domains in Toll-like receptors and the adaptors Mal and MyD88 / A. Dunne [et al.] // J. Bi-ol. Chem. – 2003. – V. 278. – P. 41443–41451.
14. Fellay, J. Host genetics: fine-tuning innate signaling /J. Fellay, D.B. Goldstein // Curr. Biol. – 2007. – V. 17, № 13. –P. R516–R518.
15. Guay, H.M. MyD88 is required for the formation of longterm humoral immu-nity to virus infection H.M. Guay [et al.] //J. Immunol. – 2007. – V. 178, № 8. – P. 5124–5131.
16. Hamann, L. Low frequency of the TIRAP S180L polymorphism in Africa, and its potential role in malaria, sepsis, and leprosy / L. Hamann [et al.] // BMC Med. Genet. –2009. – V. 10. – P. 65.
17. Hawn, T.R. A polymorphism in Toll-interleukin 1 receptor domain containing adaptor protein is associated with susceptibility to meningeal tuberculosis / T.R. Hawn [et al.] // J. Infect. Dis. – 2006. – V. 194. – P. 1127–1134.
18. Higashimoto, T. Regulation of I(kappa)B kinase complex by phosphorylation of (gamma)-binding domain of I(kappa)B kinase (beta) by Polo-like kinase 1 / T. Higashimoto [et al.] // J. Biol. Chem. – 2008. – V. 283, № 51. – P. 35354– 35367.
19. Hoarau, C. TLR9 activation induces normal neutrophil responses in a child with IRAK-4 deficiency: involvement of the direct PI3K pathway / C. Hoarau [et al.] // J. Immunol. – 2007. – V. 179, № 7. – P. 4754–4765.
20. Janssen, R. Genetic susceptibility to respiratory syncytial virus bronchiolitis is predominantly associated with innate immune genes / R. Janssen [et al.] // J. In-fect. Dis. – 2007. –V. 196. – P. 826–834.
21. Khor, C.C. A Mal functional variant is associated with protection against inva-sive pneumococcal disease, bacteremia, malaria and tuberculosis / C.C. Khor [et al.] // Nat. Genet. –2007. – V. 39. – P. 523–528.
22. Kimman, T.G. Association of interacting genes in the Toll-like receptor signal-ing pathway and the antibody response to pertussis vaccination / T.G. Kimman [et al.] // PLoS ONE. – 2008. – V. 3, № 11. – P. e3665.
23. Lammers, K.M. Combined carriership of TLR9 -1237C and CD14 -260T alleles enhances the risk of developing chronic relapsing pouchitis / K.M. Lammers [et al.] // World J. Gastroenterol. – 2005. – V. 11, № 46. – P. 7323–7329.
24. Lasker, M.V. Intracellular TLR signaling: a structural perspective on human disease / M.V. Lasker [et al.] //J. Immunol. – 2006. – V. 177, № 1. – P. 11–16.
25. Lebeis, S.L. TLR signaling mediated by MyD88 is required for a protective in-nate immune response by neutrophils to Citrobacter rodentium / S.L. Lebeis [et al.] // J. Immunol. – 2007. – V. 179. – P. 566–577.
26. Loiarro, M. Peptide-mediated interference of TIR domain dimerization in MyD88 inhibits interleukin-1-dependent activation of NF-κB / M. Loiarro [et al.] // J. Biol. Chem. – 2005. – V. 280. – P. 15809–15814.
27. Madge, L.A. Inhibiting proinflammatory NF-kappaB signaling using cell-penetrating NEMO binding domain peptides / L.A. Madge [et al.] // Methods Mol. Biol. – 2009. – V. 512. – P. 209–232.
28. Magnusson, M. Cutting edge: natural DNA repetitive extragenic sequences from Gram-negative pathogens strongly stimulate TLR91 / M. Magnusson [et al.] // J. Immunol. – 2007. – V. 179. – P. 31–35.
29. Medvedev, A.E. Cutting edge: expression of IL-1 receptor-associated kinase-4 (IRAK-4) proteins with mutations identified in a patient with recurrent bacterial infections alters normal IRAK-4 interaction with components of the IL-1 receptor complex / A.E. Medvedev [et al.] // J. Immunol. – 2005. – V. 174. – P. 6587–6591.
30. Nagpal, K. A TIR domain variant of MyD88 adapter-like (Mal)/TIRAP results in loss of MyD88 binding and reduced TLR2/TLR4 signaling / K. Nagpal [et al.] // J. Biol. Chem. – 2009. – V. 284, № 38. – P. 25742–25748.
31. Núñez, M.R. A dimer of the Toll-like receptor 4 cytoplasmic domain provides a specific scaffold for the recruitment of signalling adaptor proteins / M.R. Núñez [et al.] // PLoS One. – 2007. – V. 2, № 8. – P. e788.
32. Picard, C. Pyogenic bacterial infections in humans with IRAK-4 deficiency / C. Picard [et al.] // Science. – 2003. – V. 299. – P. 2076–2079.
33. Ronni, T.V. Common interaction surfaces of the Tolllike receptor 4 cytoplas-mic domain stimulate multiple nucleartargets / T.V. Ronni [et al.] // Mol. Cell. Biol. – 2003. –V. 23. – P. 2543–2555.
34. Spolarics, Z. The X-files of inflammation: cellular mosaicism of X-linked po-lymorphic genes and the female advantage in the host response to injury and in-fection /Z. Spolarics // Shock. – 2007. – V. 27, № 6. – P. 597–604.
35. Stack, J. Vaccinia virus protein A46R targets multiple Toll-like-interleukin-1 receptor adaptors and contributes to virulence / J. Stack [et al.] // J. Exp. Med. – 2005. – V. 201. – P. 1007–1018.
36. Takeda, K. Toll-like receptors in innate immunity /K. Takeda, S. Akira // Int. Immunol. – 2005. – V. 17. – P. 1–14.
37. Tosh, K. Variants in the SP110 gene are associated with genetic susceptibility to tuberculosis in West Africa / K. Tosh [et al.] // Proc. Natl. Acad. Sci. USA. – 2006. – V. 103. – P. 10364–10368.
38. Weighardt, H. Type I IFN modulates host defense and late hyperinflammation in septic peritonitis / H. Weighardt [et al.] // J. Immunol. – 2006. – V. 177. – P. 5623–5630.
39. Weighardt, H. Role of Toll-like receptor responses for sepsis pathogenesis / H. Weighardt, B. Holzmann //Immunobiology. – 2007. – V 212, № 9–10. – P. 715– 722.
40. West, A.P. Recognition and signaling by toll-like receptors / A.P. West [et al.] // Annu. Rev. Cell Dev. Biol. –2006. – V. 22. – P. 409–437.
Review
For citations:
Tzygan V.N., Ivanov A.M., Kamilova T.A., Коjuhova E.A., Мurashkin N.N., Tsygan N.V. Genetic polymorphism of immunogenic signaling system. Journal Infectology. 2011;3(2):21-27. (In Russ.) https://doi.org/10.22625/2072-6732-2011-3-2-21-27
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