Involvement of Th1 cells and heat shock protein 60 in the pathogenesis of intestinal Behçet's disease

Imamura, Yoshiaki; Kurokawa, Manae S.; Yoshikawa, Hideshi; Nara, Kazuhiko; Takada, Erika; Masuda, Chieko; Tsukikawa, Satoshi; Ozaki, S.; Matsuda, Takahide; Suzuki, Noboru

doi:10.1111/j.1365-2249.2005.02695.x

Cited by 110 publications

(91 citation statements)

References 37 publications

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“…We have also observed heavy infiltration of CD4 + and CD8 + T cells into the intestinal lesions of BD patients, and have detected the expression of mRNAs for proinflammatory and Th1 cytokines/chemokines 12) . Kobayashi et al observed the accumulation of lymphocytes around the vasa vasorum in six patients with vascular BD, as well as expression of proinflammatory cytokines by these cells, including IL-1 alpha, TNF-alpha, and IFN-gamma 13) .…”

Section: Th1 Cell Dominance In Bdmentioning

confidence: 91%

Unbalanced helper T cell function in Behcet's disease

Shimizu

Yoshikawa

Takada

et al. 2011

Inflammation and Regeneration

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Behcet's disease (BD) is a multisystem inflammatory disease that is characterized by recurrent attacks of uveitis, oral apthous ulcers, genital ulcers, and erythema nodosum. The etiology and pathogenesis of BD are largely unknown. We have presented evidence that supports a role of excessive Th1 cell activity in BD. Recently, it has been suggested that Th17 cells are associated with several autoimmune diseases, such as multiple sclerosis, rheumatoid arthritis, and inflammatory bowel disease, all of which are considered to be Th1 diseases. Therefore, it is interesting to study the role of Th17-related cytokines and Th17-associated signaling molecules in BD. Major Th17-related cytokines were not detected in peripheral blood mononuclear cells (PBMCs) and in skin lesions of BD patients. Expression of TGF-beta receptor and Smad2 mRNA was significantly higher in BD patients compared with the levels in normal controls. Interleukin (IL)-23 receptor, ROR-C, and Foxp3 are key transcription factors expressed by Th17 cells and regulatory T cells, respectively, and their expression was decreased in BD. These findings suggest that T cell function may be unbalanced in BD.Rec.1/15

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Section: Th1 Cell Dominance In Bdmentioning

confidence: 91%

Unbalanced helper T cell function in Behcet's disease

Shimizu

Yoshikawa

Takada

et al. 2011

Inflammation and Regeneration

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“…Histopathological studies also point to a Th1 type tissue infiltration in ABD, possibly driven by the highly expressed IL-12 and IL-23 in intestinal and cutaneous lesions. Interestingly, both streptococcal antigens and auto-antigens, such as aB-crystallin also drive an IL-12 mediated response in ABD (Imamura et al, 2005;Kulaber et al, 2007;Lew et al, 2008;Yanagihori et al, 2006). Concerning Th2 type of immune response, both, cells and signature cytokines, such as IL-4, IL-10 and IL-13 are reported to be unaffected or decreased in ABD by most researchers in the serum or in the aqueous humor.…”

Section: T Cell Abnormalitiesmentioning

confidence: 99%

Immunopathogenesis Based Adamantiades- Behcet Disease Vasculitis Treatment

Boura¹,

Tselios²,

Gkougkourelas³

et al. 2011

Advances in the Diagnosis and Treatment of Vasculitis

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“…Functional abnormalities of these receptors or different activation cascades by different microorganisms are associated with disease pathogenesis in BD [73]. Human HSP60 induces a potent inflammatory response in the innate immune system via its ligands, TLRs, and operates in a similar manner to that of classical pathogen-derived ligands and can thus activate nonspecifically the innate immune system and stimulates the maturation of dendritic cells [6]. In some studies, the expression of TLR1, TLR2, TLR4, and TLR6 on monocytes and granulocytes in patients with BD was investigated, which showed increased expression of TLR4, but not TLR2 and others, by peripheral blood mononuclear cells [73,74].…”

Section: Heat Shock Proteinsmentioning

confidence: 99%

“…Today, BD is considered a more complicated entity [2] and is defined as a chronic, relapsing, multisystemic idiopathic inflammatory problem with mucocutaneous (erythema nodosum, pustular vasculitis), ocular (anterior and posterior uveitis), arthritic, vascular (both arterial and venous vasculitis), and central nervous system (meningoencephalitis) involvements [3][4][5]. The etiology and pathogenesis of this disease have been explored extensively [6]; genetic susceptibility, environmental factors (viral and/or bacterial infections), inflammatory response abnormalities (heat shock proteins (HSPs), dysregulated nitric oxide production) and abnormal immune responses play a major role in BD pathogeny [7]. Current evidence lends increasing support to immunoinflammatory mechanisms as one of the prime pathogenic processes involved in the development and progression of BD [8].…”

mentioning

confidence: 99%

Behcet’s disease: from heat shock proteins to infections

2014

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Background: Behcet's disease (BD) is a chronic, inflammatory multisystemic condition of unknown etiology. Although the cause of BD is not clear, it is believed to be the result of an autoimmune process triggered by an infectious or environmental agent (possibly local to a geographic region) in a genetically predisposed individual. Objective: To detail current knowledge of the role of microorganisms in the pathogenesis of BD and review the infectious etiology of this disease. Methods: The review based on publication in SCOPUS, Science direct, and PubMed. Results: A microbial infection has been implicated in the development of the disease to explain the strong inflammatory reactions observed, the activation of monocytes and macrophages, and the induction of proinflammatory cytokines and chemokines detected. Common factors linking some of the possible pathogenetic agents are extrinsically induced tissue stress or heat shock proteins, which react with host tissues and elicit significant T-helper type 1 cell responses. Conclusion: Based on collected data, we conclude that the microorganisms discussed seem to participate and, at least in part, act as triggers during the course of BD. By clarifying the microbial associations of BD and finding its etiology, particularly the causative antigens leading to BD, it would be easier to suggest more effective treatment and preventive strategies for this disease.

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Involvement of Th1 cells and heat shock protein 60 in the pathogenesis of intestinal Behçet's disease

Abstract: Summary Involvement of excessive

Cited by 110 publications

References 37 publications

Unbalanced helper T cell function in Behcet's disease

Unbalanced helper T cell function in Behcet's disease

Immunopathogenesis Based Adamantiades- Behcet Disease Vasculitis Treatment

Behcet’s disease: from heat shock proteins to infections

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