Pathogenesis of spondylarthropathies

Sieper, Joachim; Braun, Jürgen

doi:10.1002/art.1780381105

Cited by 152 publications

(19 citation statements)

References 72 publications

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“…The termini of the peptide are bound in the characteristic binding modes that have been observed previously (14,15,37). Most notably, the side chain of pArg 1 is sandwiched between the HC residues Arg 62 and Trp 167 , resulting in an energetically favorable stabilization (38), whereas the side chain of pLeu 9 does not contact the floor of the F pocket (Figs. 2A, 3A, and 3B) but is firmly anchored by numerous hydrophobic interactions.…”

Section: Nh2mentioning

confidence: 68%

“…In case of the human MHC class I allele HLA-B27, which is very strongly associated with ankylosing spondylitis (AS) (5,6), autoimmunity and in particular molecular mimicry between foreign and self-proteins or their fragments have long been suspected to play a role in pathogenetic processes (7)(8)(9)(10)(11). Cytotoxic T lymphocytes (CTLs) directed against the self-antigen pVIPR (RRKWRRWHL, derived from vasoactive intestinal peptide type 1 receptor (residues 400 -408)) have been found in healthy individuals with the AS-associated HLA-B27 subtype B*2705, and their number is increased in AS patients (12).…”

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confidence: 99%

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Conformational Dimorphism of Self-peptides and Molecular Mimicry in a Disease-associated HLA-B27 Subtype

Rückert

Fiorillo

Loll

et al. 2006

Journal of Biological Chemistry

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Section: Nh2mentioning

confidence: 68%

mentioning

confidence: 99%

Conformational Dimorphism of Self-peptides and Molecular Mimicry in a Disease-associated HLA-B27 Subtype

Rückert

Fiorillo

Loll

et al. 2006

Journal of Biological Chemistry

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“…The complexes are then expressed on the cell surface and presented to cytotoxic T cells. It has been suggested that the immune system of people with this tissue type responds abnormally to an antigenic stimulus in that autoreactive T cells are activated by an external microbial antigen and then recognise crossreactive endogenous peptides presented by HLA-B27 [14]. This somehow triggers the processes which result in the pathological changes seen in the condition.…”

Section: Pathophysiologymentioning

confidence: 99%

Inflammatory Mediators as Potential Therapeutic Targets in the Spine

Roberts

Butler²

2005

CDTIA

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Inflammation plays a variable part in the pathogenesis of several spinal disorders. Ankylosing spondylitis is a chronic inflammatory arthropathy of the spine and rheumatoid arthritis, whilst affecting predominantly limb joints, also affects the cervical spine in a significant proportion of people. Inflammation is also involved in disorders such as disc herniation and sciatica, which have previously been thought of as being primarily mechanical or degenerative. Anti-inflammatory agents which have been shown to be effective elsewhere in the body are discussed in this review as possible therapeutic agents in the spine. As the inflammatory cascade and immunopathology of these conditions continue to be elucidated, it has become apparent that individual molecules may be potential targets for inactivation or down-regulation. Candidates include pro-inflammatory cytokines, such as TNF-alpha, cytokines, e.g. IL-1 and IL-15, or enzymes enhancing the inflammation pathway such as the cyclooxygenases. Hence treatments based on inactivation of these molecules by various mechanisms, including antibodies, receptor antagonists, enzyme inhibitors or gene therapy, are being introduced. However, the mode of action of a particular molecule can be complex and sometimes apparently contradictory. For example, TNF-alpha is known to play an important role in promoting inflammation by upregulating expression of cell adhesion molecules on endothelial cells and stimulating the production of reactive oxygen intermediates, nitric oxide and prostaglandins. However, it can also have an immunosuppressive and anti-inflammatory role after prolonged release. Therefore, although inhibitors of many of these molecules are now in clinical application and trials (many with promising results in rheumatoid arthritis), it is important to remain vigilant and monitor long-term outcomes particularly when these treatments are used in clinical syndromes with relatively poorly defined immunopathology such as spinal disorders.

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“…A wide range of infections especially with intracellular bacteria have been shown to be involved in the pathogenesis of spondylarthropathies and reactive arthritis. 16 One of our cases suffered from an infection with Yersinia enterocolitica, which is known to favor the outbreak of rheumatic symptoms in HLA-B27-positive individuals. In the other patients no infections known to trigger the development of spondylarthropathies could be demonstrated.…”

Section: Discussionmentioning

confidence: 92%

First manifestations of seronegative spondylarthropathy following autologous stem cell transplantation in HLA-B27-positive patients

Koch

Kranzhöfer

Pfreundschu

et al. 2000

Bone Marrow Transplant

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Summary:Two male patients with non-Hodgkin's lymphoma (NHL, follicular NHL, diffuse large B cell NHL, both in 2nd complete remission) and one female patient with acute myeloid leukemia in 1st complete remission developed arthralgias and enthesopathy following autologous stem cell transplantation. In 2/3 patients, sacroiliitis could be demonstrated on X-ray. In both patients, the rheumatic symptoms were classified as manifestations of a spondylarthropathy. All three patients were subsequently shown to be HLA-B27-positive. The patients were successfully treated with non-steroidal anti-inflammatory drugs. The differential diagnosis of joint pain following autologous stem cell transplantation should include HLA-B27-associated spondylarthropathies in addition to the more commonly seen bone and joint pain due to immobilization and medication. Bone Marrow Transplantation (2000) 26, 673-675.

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Pathogenesis of spondylarthropathies

Cited by 152 publications

References 72 publications

Conformational Dimorphism of Self-peptides and Molecular Mimicry in a Disease-associated HLA-B27 Subtype

Conformational Dimorphism of Self-peptides and Molecular Mimicry in a Disease-associated HLA-B27 Subtype

Inflammatory Mediators as Potential Therapeutic Targets in the Spine

First manifestations of seronegative spondylarthropathy following autologous stem cell transplantation in HLA-B27-positive patients

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