摘要:

Anterior uveitis describes inflammation that involves the iris or ciliary body. Anterior uveitis may be part of a systemic illness such as a spondyloarthropathy. It may also arise from an infection such as herpes simplex; be part of an ocular syndrome, such as Fuchs' heterochromic iridocyclitis; be part of trauma, as in cataract surgery; or result from an idiopathic eye disease with a presumed immune pathogenesis. During 2001, progress has been made understanding uveitis in general, as well as specifically, in association with spondyloarthropathy. Here, we review recent insights into anterior uveitis with regard to clinical presentation, immune mechanisms, genetics, and anti-tumor necrosis factor therapy.

ISSN:1040-8711    

出版商:OVID    

年代:2002

数据来源: OVID

摘要:

Gut involvement is a prominent feature of spondyloarthropathy (SpA). Analysis of immune alterations of the gut in SpA have shown two distinct aspects. On the one hand, gut inflammation in SpA seems closely related with gut inflammation seen in Crohn disease. On the other hand, gut inflammation in SpA is associated with peripheral joint inflammation. Recent studies have provided new insights into this gut–synovium axis. First, there is little new evidence to support the concept of viable microbial pathogens recirculating to the joint. In contrast, it seems likely that both bacterial antigens and reactive T cell clones home to the joint, and that adhesion molecules such as the &bgr;7 integrins and VAP1 play an important role in this process. Second, there is increasing evidence that the different disease localizations in SpA are characterized by alterations of the innate immune system, which contribute to a breakdown of the immune tolerance and the creation of an inflammation-prone environment. Mediators of the innate immune system, such as scavenger receptors, interleukin-10 (IL-10), and tumor necrosis factor &agr; (TNF-&agr;), may therefore be interesting targets for therapeutic intervention, as illustrated by the effect of TNF-&agr; blockade in SpA.

ISSN:1040-8711    

出版商:OVID    

年代:2002

数据来源: OVID

摘要:

Synovitis of recent onset is a challenging problem, both from a diagnostic and a mechanistic point of view. The role of the immune system in mediating the systemic and synovial inflammatory response remains an area of active investigation. Studies in early synovitis cohorts have confirmed the relatively specific association of rheumatoid factor positive polyarthritis with a number of autoantibodies, particularly anticyclical citrullinated peptide (CCP) antibodies, antifilaggarin antibodies (AFA), and anti-Sa antibodies. Immunopathologic studies of synovial tissue samples from patients with early synovitis have generally suggested quantitative rather than qualitative differences between various forms of synovitis. In particular, Th1 cytokines appear to predominate in rheumatoid arthritis and psoriatic synovitis, while Th2 cytokines are more often detectable in the synovium of reactive arthritis patients. This latter observation is consistent with an immune response profile that favors persistence of intracellular organisms.

ISSN:1040-8711    

出版商:OVID    

年代:2002

数据来源: OVID

摘要:

While twin studies have previously demonstrated high heritability of susceptibility to ankylosing spondylitis (AS), it is only recently that the involvement of genetic factors in determining the severity of the disease has been demonstrated. The genes involved in determining the rate of ankylosis in AS are likely to be different from those involved in the underlying immunologic events, and represent important potential targets for treatment of AS. This article will describe the progress that has been made in the genetic epidemiology of AS, and in identifying the genes involved.

ISSN:1040-8711    

出版商:OVID    

年代:2002

数据来源: OVID

摘要:

This review summarizes articles written about psoriatic arthritis in the past year. It concentrates on clinical and epidemiologic issues, pathogenesis and treatment, and updates the reader regarding new concepts in psoriatic arthritis.

ISSN:1040-8711    

出版商:OVID    

年代:2002

数据来源: OVID

摘要:

Although the influence of HLA-B27 on the development of spondyloarthropathies is undisputed, its role in pathogenesis remains unclear. New ideas have focused on abnormal characteristics of HLA-B27 resulting from aberrant folding, disulfide bond formation, or both, rather than a predilection for selecting arthritogenic peptides. This reflects, in part, unanswered questions about whether immunologic recognition of HLA-B27 is required for disease. Recent studies suggest that CD4+ T cells, immunomodulatory killer cell Ig receptors, and Ig-like transcript receptors may recognize aberrant forms of HLA-B27. Other reports suggest that HLA-B27 expression can alter cytokine production from monocytes and T cells—effects that appear unrelated to antigen presentation. Novel bioinformatics approaches have led to the identification of HLA-B27-restricted pathogen-derived peptides and may prove useful in determining whether HLA-B27 presents arthritogenic peptides. Elucidating the role of HLA-B27 in the pathogenesis of these conditions will require an integration of information from animal models, genome-wide screens for susceptibility alleles, and translational studies using human samples.

ISSN:1040-8711    

出版商:OVID    

年代:2002

数据来源: OVID

摘要:

The spondyloarthropathies are diseases influenced by genetic predisposition and, to a varying extent, infectious triggers. A causal role for bacterial infections is most clear for reactive arthritis. Recent insights into arthritogenic components of bacteria may set the stage for a better understanding of disease pathogenesis, the role of heat shock proteins in antigen processing and immune activation, and the adjuvant effect of CpG-DNA. Recent developments in the area of innate immunity broaden current concepts of genetically defined factors in host-pathogen interactions. In particular, the biology of toll-like receptors as important elements in the innate immune response to pathogens is being defined. These factors in innate immunity may have important implications for sequelae of infections, such as reactive arthritis.

ISSN:1040-8711    

出版商:OVID    

年代:2002

数据来源: OVID

摘要:

In the United States, intermittent or chronic mono- or oligoarthritis, particularly affecting the knee, is the most common manifestation of late Lyme disease (LD). Lyme arthritis (LA) can usually be prevented by early treatment of acute LD. However, the erythema migrans rash may go undetected in children and in the dark skin of African Americans, leading to delayed treatment and a relatively increased incidence in LA. Virtually all untreated patients with LA have high levels of serum immunoglobulin G antibodies, and sometimes low levels of immunoglobulin M antibodies, toBorrelia burgdorferi(Bb) by ELISA and Western blot. These responses may persist for many years after antibiotic treatment, and therefore, serologic results do not accurately distinguish between active or past infection. Most patients with LA respond well to standard courses of antibiotic treatment, but a small percentage have persistent knee synovitis, in some cases possibly related to the triggering of intrasynovial autoimmunity. Other patients develop a syndrome of diffuse arthralgia, myalgia, fatigue, and subjective cognitive difficulty during or soon after LD, which persists despite antibiotic treatment. Patients with this post-treatment, post-LD syndrome were recently studied in a placebo-controlled double-blind antibiotic trial. There was no evidence of Borrelial infection in these patients by culture or detection of Bb DNA in blood or spinal fluid. Furthermore, there was no difference in responsiveness of these patients to a 3-month course of antibiotic compared with placebo treatment. Thus, LA caused by active Bb infection, post-treatment LA with persistent knee synovitis and post-LD syndrome are distinct and distinguishable clinical entities.

ISSN:1040-8711    

出版商:OVID    

年代:2002

数据来源: OVID

摘要:

Treatment-resistant Lyme arthritis (TRLA) develops in 10% of Lyme arthritis patients and is characterized by continuous joint inflammation that does not resolve with antibiotic therapy. TRLA is associated with HLA-DRB1*0401 and related alleles, as well as with an immune response to theBorrelia burgdorferi (Bb)outer surface protein A (OspA). The immunodominant epitope of OspA in the context of HLA-DRB1*0401 corresponds to amino acids 165–173 (OspA165–173). The human Lymphocyte Function Antigen-1 (hLFA1&agr;) contains a peptide with homology to OspA165–173. Treatment-resistant Lyme arthritis patients' T cells, cloned based on their ability to bind OspA165–173-loaded HLA-DRB1*0401 tetramers, respond to OspA and hLFA1&agr; with a different cytokine profile, suggesting that hLFA1&agr; acts as a partial agonist with a potential role in the perpetuation of joint inflammation.

ISSN:1040-8711    

出版商:OVID    

年代:2002

数据来源: OVID

摘要:

Borrelia burgdorferi,the spirochete that causes Lyme disease, has evolved elegant strategies for interacting with its mammalian hosts. Among them are several distinct mechanisms of adhesion to cells and extracellular matrix components. The mammalian receptors forB. burgdorferithat have been most thoroughly studied, and for which candidate bacterial ligands have been identified, are decorin, fibronectin, glycosaminoglycans, and &bgr;3-chain integrins. This diversity of adhesion mechanisms allowsB. burgdorferito infect multiple tissues, including the synovial tissues of the joints.

ISSN:1040-8711    

出版商:OVID    

年代:2002

数据来源: OVID