Tumor necrosis factor‐<i>α</i> increases chemokine gene expression and production in synovial fibroblasts from human temporomandibular joint

Ogura, Naomi; Tobe, Makiko; Sakamaki, Hiroyuki; Nagura, Hideaki; Abiko, Yoshimitsu; Kondoh, Toshirou

doi:10.1111/j.1600-0714.2005.00302.x

Cited by 42 publications

(40 citation statements)

References 34 publications

(58 reference statements)

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“…Although the expression of RANTES was first thought to be limited to active T cells, recent data have shown that it is produced by a variety of tissue types in response to specific stimuli. RANTES mRNA is expressed late (3-5 d) after activation of resting T cells, whereas in fibroblasts, renal epithelial, and mesangial cells, RANTES mRNA is quickly up-regulated by TNF-␣ stimulation (Hirano et al 2003;Ogura et al 2005).…”

Section: Discussionmentioning

confidence: 99%

Unphosphorylated STAT3 accumulates in response to IL-6 and activates transcription by binding to NFκB

Yang¹,

Liao²,

Agarwal³

et al. 2007

Genes Dev.

546

496

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Section: Discussionmentioning

confidence: 99%

Unphosphorylated STAT3 accumulates in response to IL-6 and activates transcription by binding to NFκB

Yang¹,

Liao²,

Agarwal³

et al. 2007

Genes Dev.

546

496

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“…Strong evidence shows that these epidermis-derived cytokines are essential for the migration of LC out of the epidermis [41][42][43]. Furthermore, these cytokines have been reported to increase secretion of many chemokines by fibroblasts [44,45] and this would explain the increased LC migration towards fibroblasts after allergen exposure. Indeed, here we show that one of these chemokines is CXCL12, which is induced by TNF-a.…”

Section: Discussionmentioning

confidence: 99%

CXCL12 is essential for migration of activated Langerhans cells from epidermis to dermis

et al. 2008

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The initial step in Langerhans cell (LC) migration from the epidermis to the lymph node involves migration of maturing LC into the dermis. Here, we investigated the migration of LC out of the epidermis after exposure of the skin to contact allergens. Ex vivo intact human skin, epidermal sheets, and LC derived from the MUTZ-3 cell line (MUTZ-LC) were used to determine whether dermal fibroblasts play a role in mediating LC migration towards the dermis. Exposure of epidermal sheets or MUTZ-LC to allergens (nickel sulphate, 2,4-dinitrochlorobenzene, and cinnamaldehyde) or a cytokine maturation cocktail resulted in LC migration towards dermal fibroblasts. This was due to upregulation of CXCR4 on maturing LC and secretion of CXCL12/stromal derived factor-1 chemokine by fibroblasts. Neutralizing antibodies to either CXCL12 or CXCR4 completely blocked migration. Injection of CXCL12 neutralizing antibodies into intact human skin totally inhibited LC migration into the dermis. In contrast, neutralizing antibodies to CCL19/ CCL21 did not inhibit migration into the dermis. We describe a novel and essential role of dermis-derived CXCL12 in initiating migration of maturing human LC to the dermis thus permitting their further journey to the draining lymph nodes.Key words: Allergy . Chemotaxis . Cytokines . DC . Skin See accompanying commentary by Villablanca and Rodrigo IntroductionHuman skin is the external barrier to harmful environmental factors. Upon environmental assault (e.g. exposure to pathogens or allergens), Langerhans cells (LC) residing in the epidermis start to mature and migrate through the dermis [1,2]. Pathogenor allergen-exposed LC then migrate further into the afferent lymphatics towards the local lymph node where they are able to initiate a T-cell-mediated response [3]. LC migration is regulated by the sequential and differential expression of chemokines and their receptors [4,5]. Although migration to the lymph node is well documented, the chemokine ligands/receptors involved in the initial step of human LC migration out of the epidermis and into the dermis are as yet unknown.Several studies describe an essential role of CCR7 in mediating migration of mature LC towards the lymphatics [6][7][8][9][10]. CCR7 is highly expressed on fully mature, but not on immature LC, and is the chemokine receptor for the ligands CCL19 (MIP-3b) and CCL21 (6Ckine) [11][12][13]. Both of these chemokines are upregulated by lymphatic endothelial cells in response to allergen exposure [14]. Simultaneously, the chemokine receptor CCR6 on LC is downregulated upon maturation [15]. CCR6 is the receptor for CCL20 , which is mainly produced by keratinocytes (KC) in clinically normal human skin. CCR6/CCL20 is thought to 3050be of importance for epidermal homeostasis and homing of immature LC [16][17][18][19]. Taken together these reports show that loss of CCR6 and gain of CCR7 play important roles in the migration of mature LC out of the epidermis and into the lymphatic vessels. However, it is probable that other as yet unidentified sig...

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“…IL-8 is one of the most potent chemo-attracting factors for neutrophils and T cells, both in vitro and in vivo (Endo et al, 1991;Larsen et al, 1989;Akahoshi et al, 1994). In the presence of IL-1, TNF-a and lipopolysaccharide, IL-8 is produced by a variety of cells, including leukocytes, fibroblasts, endothelial cells, chondrocytes, and synoviocytes (Sukedai et al, 2004;Furuzawa and Alocer, 1999;Hirota et al, 1992;Deleuran et al, 1994a;Van Damme, 1994;Ogura et al, 2005). Besides attracting polymorphonuclear cells, IL-8 also induces expression of adhesion molecules, neutrophil degranulation and production of oxygen metabolites (Baggiolini et al, 1994), thereby able to cause tissue damage.…”

Section: Pro-inflammatory Cytokinesmentioning

confidence: 99%

Immunopathological mechanisms in dogs with rupture of the cranial cruciate ligament

Doom

Bruin

Rooster

et al. 2008

Veterinary Immunology and Immunopathology

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The majority of studies on cranial cruciate ligament (CrCL) disease to date have been carried out on dogs that already sustained a CrCL rupture, which is the end-stage of the disease. Investigations have recently been carried out to study humoral and cellular immunopathological mechanisms in predisposed dogs before clinical rupture of the contralateral CrCL. The cruciate ligaments are mainly composed of collagen type I, and immune responses to collagen have been suggested as a cause of CrCL degradation in dogs. None of these investigations showed evidence that anticollagen type I antibodies alone initiate CrCL damage. However, in predisposed dogs a distinct anticollagen type I antibody gradient was found towards the contralateral stifle joint that eventually sustained a CrCL rupture, suggesting that there was an inflammatory process present in these joints before detectable joint instability occurred. The importance of cellular reactivity to collagen type I in cruciate disease also remains unclear. Peripheral blood mononuclear cell proliferation to collagen type I was very diverse in dogs with cruciate disease whereas some sham operated dogs and healthy dogs tested positive as well. It is not yet determined whether cellular reactivity to collagen type I exists locally in the stifle joints nor whether this could initiate CrCL degradation.Inflammatory processes within the stifle joint can alter the composition of the cruciate ligaments. In animal models of immunemediated synovitis, the mechanical strength of the CrCL is significantly reduced. Immunohistochemical studies on synovial tissues from dogs with rheumatoid arthritis and dogs with cruciate disease revealed that the pathologic features are similar in both joint pathologies and that the differences are mainly quantitative. Joint inflammation induced by biochemical factors such as cytokines has been implied in CrCL degeneration. In several studies, the levels of pro-inflammatory and T helper cytokines were measured in dogs that sustained a CrCL rupture, but the exact role of the various cytokines in the pathogenesis of CrCL disease remains inconclusive. More recently, the levels of the cytokines have been investigated over time in predisposed dogs before and after CrCL rupture. IL-8 expression tended to be higher in stifle joints that will rupture their CrCL during the next 6 months than in those that will not, indicating an inflammatory process in these joints before clinical rupture.

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Tumor necrosis factor‐α increases chemokine gene expression and production in synovial fibroblasts from human temporomandibular joint

Abstract: Increased protein production and gene expression of chemokines by synovial fibroblasts in response to TNF-alpha treatment appears to play an important role in recruitment of inflammatory cells into synovium and the progression of synovitis in the TMJ.

Cited by 42 publications

References 34 publications

Unphosphorylated STAT3 accumulates in response to IL-6 and activates transcription by binding to NFκB

Unphosphorylated STAT3 accumulates in response to IL-6 and activates transcription by binding to NFκB

CXCL12 is essential for migration of activated Langerhans cells from epidermis to dermis

Immunopathological mechanisms in dogs with rupture of the cranial cruciate ligament

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