Skip to main content

Mechanisms Regulating TNF-Driven Gut and Joint Inflammation

  • Conference paper
  • First Online:
Advances in TNF Family Research

Part of the book series: Advances in Experimental Medicine and Biology ((AEMB,volume 691))

Abstract

Chronic inflammatory arthritis, a hallmark of a variety of inflammatory rheumatic diseases and inflammatory bowel disease, is a lifelong condition, often with onset in early adulthood, with an important morbidity and even mortality in our society. It is estimated that approximately 2–3% suffers from chronic arthritis in our society. The coexistence of gut and joint inflammation is well established in spondyloarthritis (SpA), a cluster of interrelated rheumatologic diseases, characterized by a number of clinical and genetic features including peripheral arthritis (typical of lower limb joints) as well as inflammation of the axial skeleton (e.g., spine). Remarkably, other organs including skin (psoriasis) or the eye (anterior uveitis) may also be affected, indicating the systemic nature of these diseases. Various subtypes of SpA can be distinguished based upon clinical features, but an important overlap between them exists. The clinical subtypes include an kylosing spondylitis (AS, characterized by prominent inflammation of the axial skeleton – spine, sacroiliac joints, although other joints may also be affected), infection triggered reactive arthritis, some forms of juvenile chronic arthritis, arthritis in association with inflammatory bowel diseases (IBD), and some types of psoriatic arthritis.

This is a preview of subscription content, log in via an institution to check access.

Access this chapter

Chapter
USD 29.95
Price excludes VAT (USA)
  • Available as PDF
  • Read on any device
  • Instant download
  • Own it forever
eBook
USD 259.00
Price excludes VAT (USA)
  • Available as EPUB and PDF
  • Read on any device
  • Instant download
  • Own it forever
Softcover Book
USD 329.99
Price excludes VAT (USA)
  • Compact, lightweight edition
  • Dispatched in 3 to 5 business days
  • Free shipping worldwide - see info
Hardcover Book
USD 329.99
Price excludes VAT (USA)
  • Durable hardcover edition
  • Dispatched in 3 to 5 business days
  • Free shipping worldwide - see info

Tax calculation will be finalised at checkout

Purchases are for personal use only

Institutional subscriptions

References

  1. Cuvelier C et al (1987) Histopathology of intestinal inflammation related to reactive arthritis. Gut 28:394–401

    Article  CAS  PubMed  Google Scholar 

  2. De Vos M et al (1989) Ileocolonoscopy in seronegative spondylarthropathy. Gastroenterology 96:339–344

    PubMed  Google Scholar 

  3. Mielants H, Veys EM, Cuvelier C, De Vos M,, Botelberghe L (1985) HLA-B27 related arthritis and bowel inflammation. Part 2. Ileocolonoscopy and bowel histology in patients with HLA-B27 related arthritis. J Rheumatol 12:294–298

    CAS  PubMed  Google Scholar 

  4. Mielants H, Veys EM, Joos R, Cuvelier C, De Vos M (1987) Repeat ileocolonoscopy in reactive arthritis. J Rheumatol 14:456–458

    CAS  PubMed  Google Scholar 

  5. Mielants H, Veys EM, Cuvelier C, De Vos M (1989) Subclinical involvement of the gut in undifferentiated spondylarthropathies. Clin Exp Rheumatol 7:499–504

    CAS  PubMed  Google Scholar 

  6. Mielants H, Veys EM, Cuvelier C, de Vos M (1988) Ileocolonoscopic findings in seronegative spondylarthropathies. Br J Rheumatol 27 Suppl 2:95–105

    Google Scholar 

  7. Mielants H et al (1995) The evolution of spondyloarthropathies in relation to gut histology. II. Histological aspects. J Rheumatol 22:2273–2278

    CAS  PubMed  Google Scholar 

  8. Mielants H et al (1995) The evolution of spondyloarthropathies in relation to gut histology. III. Relation between gut and joint. J Rheumatol 22:2279–2284

    CAS  PubMed  Google Scholar 

  9. Mielants H et al (1995).The evolution of spondyloarthropathies in relation to gut histology. I. Clinical aspects. J Rheumatol 22:2266–2272

    CAS  PubMed  Google Scholar 

  10. De Vos M, Mielants H, Cuvelier C, Elewaut A, Veys E (1996) Long-term evolution of gut inflammation in patients with spondyloarthropathy. Gastroenterology 110:1696–1703

    Article  PubMed  Google Scholar 

  11. Brewerton DA et al (1973) Ankylosing spondylitis and HL-A 27. Lancet 1:904–907

    Article  CAS  PubMed  Google Scholar 

  12. Palm O, Moum B, Ongre A, Gran JT (2002) Prevalence of ankylosing spondylitis and other spondyloarthropathies among patients with inflammatory bowel disease: a population study (the IBSEN study). J Rheumatol 29:511–515

    PubMed  Google Scholar 

  13. Purrmann J et al (1988) HLA antigens in ankylosing spondylitis associated with Crohn’s disease. Increased frequency of the HLA phenotype B27,B44. J Rheumatol 15:1658–1661

    CAS  PubMed  Google Scholar 

  14. Steer S et al (2003) Low back pain, sacroiliitis, and the relationship with HLA-B27 in Crohn’s disease. J Rheumatol 30:518–522

    PubMed  Google Scholar 

  15. Burton PR et al (2007) Association scan of 14,500 nonsynonymous SNPs in four diseases identifies autoimmunity variants. Nat Genet 39:1329–1337

    Article  CAS  PubMed  Google Scholar 

  16. Duerr RH et al (2006) A genome-wide association study identifies IL23R as an inflammatory bowel disease gene. Science 314:1461–1463

    Article  CAS  PubMed  Google Scholar 

  17. Rahman P et al (2008) Association of interleukin-23 receptor variants with ankylosing spondylitis. Arthritis Rheum 58:1020–1025

    Article  CAS  PubMed  Google Scholar 

  18. Jacques P, Elewaut D (2008) Joint expedition: linking gut inflammation to arthritis. Mucosal Immunol 1:364–371

    Article  CAS  PubMed  Google Scholar 

  19. Jacques P, Mielants H, Coppieters K, De Vos M, Elewaut D (2007) The intimate relationship between gut and joint in spondyloarthropathies. Curr Opin Rheumatol 19:353–357

    Article  PubMed  Google Scholar 

  20. Kontoyiannis D, Pasparakis M, Pizarro TT, Cominelli F, Kollias G (1999) Impaired on/off regulation of TNF biosynthesis in mice lacking TNF AU-rich elements: implications for joint and gut-associated immunopathologies. Immunity 10:387–398

    Article  CAS  PubMed  Google Scholar 

  21. Armaka M et al (2008) Mesenchymal cell targeting by TNF as a common pathogenic principle in chronic inflammatory joint and intestinal diseases. J Exp Med 205:331–337

    Article  CAS  PubMed  Google Scholar 

  22. Melis L, Elewaut D (2009) Progress in spondylarthritis. Immunopathogenesis of spondyloarthritis: which cells drive disease? Arthritis Res Ther 11:233

    Google Scholar 

  23. Brown MA (2009) Progress in spondylarthritis. Progress in studies of the genetics of ankylosing spondylitis. Arthritis Res Ther 11:254

    Article  PubMed  Google Scholar 

  24. Kawano T et al (1997) CD1d-restricted and TCR-mediated activation of valpha14 NKT cells by glycosylceramides. Science 278:1626–1629

    Article  CAS  PubMed  Google Scholar 

  25. Godfrey DI, Hammond KJ, Poulton LD, Smyth MJ, Baxter AG (2000) NKT cells: facts, functions and fallacies. Immunol Today 21:573–583

    Article  CAS  PubMed  Google Scholar 

  26. Bendelac A, Rivera MN, Park SH, Roark JH (1997) Mouse CD1-specific NK1 T cells: development, specificity, and function. Annu Rev Immunol 15:535–562

    Article  CAS  PubMed  Google Scholar 

  27. Rachitskaya AV et al (2008) Cutting edge: NKT cells constitutively express IL-23 receptor and RORgammat and rapidly produce IL-17 upon receptor ligation in an IL-6-independent fashion. J Immunol 180:5167–5171

    CAS  PubMed  Google Scholar 

  28. Akbari O et al (2003) Essential role of NKT cells producing IL-4 and IL-13 in the development of allergen-induced airway hyperreactivity. Nat Med 9:582–588

    Article  CAS  PubMed  Google Scholar 

  29. Korsgren M et al (1999) Natural killer cells determine development of allergen-induced eosinophilic airway inflammation in mice. J Exp Med 189:553–562

    Article  CAS  PubMed  Google Scholar 

  30. Coppieters K et al (2007) A single early activation of invariant NK T cells confers long-term protection against collagen-induced arthritis in a ligand-specific manner. J Immunol 179:2300–2309

    CAS  PubMed  Google Scholar 

  31. Duarte N et al (2004) Prevention of diabetes in nonobese diabetic mice mediated by CD1d-restricted nonclassical NKT cells. J Immunol 173:3112–3118

    CAS  PubMed  Google Scholar 

  32. Kawano T et al (1998) Natural killer-like nonspecific tumor cell lysis mediated by specific ligand-activated Valpha14 NKT cells. Proc Natl Acad Sci U S A 95:5690–5693

    Article  CAS  PubMed  Google Scholar 

  33. Amprey JL et al (2004) A subset of liver NK T cells is activated during Leishmania donovani infection by CD1d-bound lipophosphoglycan. J Exp Med 200:895–904

    Article  CAS  PubMed  Google Scholar 

  34. Fischer K et al (2004) Mycobacterial phosphatidylinositol mannoside is a natural antigen for CD1d-restricted T cells. Proc Natl Acad Sci U S A 101:10685–10690

    Article  CAS  PubMed  Google Scholar 

  35. Kinjo Y et al (2005) Recognition of bacterial glycosphingolipids by natural killer T cells. Nature 434:520–525

    Article  CAS  PubMed  Google Scholar 

  36. Gumperz JE et al (2000) Murine CD1d-restricted T cell recognition of cellular lipids. Immunity 12:211–221

    Article  CAS  PubMed  Google Scholar 

  37. Zhou D et al (2004) Lysosomal glycosphingolipid recognition by NKT cells. Science 306:1786–1789

    Article  CAS  PubMed  Google Scholar 

  38. Godfrey DI, Kronenberg M (2004) Going both ways: immune regulation via CD1d-dependent NKT cells. J Clin Invest 114:1379–1388

    CAS  PubMed  Google Scholar 

  39. Miyamoto K, Miyake S, Yamamura T (2001) A synthetic glycolipid prevents autoimmune encephalomyelitis by inducing TH2 bias of natural killer T cells. Nature 413:531–534

    Article  CAS  PubMed  Google Scholar 

  40. Chiba A et al (2004) Suppression of collagen-induced arthritis by natural killer T cell activation with OCH, a sphingosine-truncated analog of alpha-galactosylceramide. Arthritis Rheum 50:305–313

    Article  CAS  PubMed  Google Scholar 

  41. Burdin N, Brossay L, Kronenberg M (1999) Immunization with alpha-galactosylceramide polarizes CD1-reactive NK T cells towards Th2 cytokine synthesis. Eur J Immunol 29:2014–2025

    Article  CAS  PubMed  Google Scholar 

  42. Kim HY et al (2005) NKT cells promote antibody-induced joint inflammation by suppressing transforming growth factor beta1 production. J Exp Med 201:41–47

    Article  CAS  PubMed  Google Scholar 

  43. Kim HY, Kim S, Chung DH (2006) FcgammaRIII engagement provides activating signals to NKT cells in antibody-induced joint inflammation. J Clin Invest 116:2484–2492

    Article  CAS  PubMed  Google Scholar 

  44. Jacques P et al (2010) Invariant natural killer T cells are natural regulators of murine spondylarthritis. Arthritis Rheum 62(4):988–999

    Article  CAS  PubMed  Google Scholar 

Download references

Author information

Authors and Affiliations

Authors

Corresponding author

Correspondence to Dirk Elewaut .

Editor information

Editors and Affiliations

Rights and permissions

Reprints and permissions

Copyright information

© 2011 Springer Science+Business Media, LLC

About this paper

Cite this paper

Elewaut, D., Jacques, P., Melis, L., Venken, K. (2011). Mechanisms Regulating TNF-Driven Gut and Joint Inflammation. In: Wallach, D., Kovalenko, A., Feldmann, M. (eds) Advances in TNF Family Research. Advances in Experimental Medicine and Biology, vol 691. Springer, New York, NY. https://doi.org/10.1007/978-1-4419-6612-4_42

Download citation

Publish with us

Policies and ethics