Involvement of TL1A and DR3 in induction of pro-inflammatory cytokines and matrix metalloproteinase-9 in atherogenesis

Kang, Younhee; Kim, Wonjung; Bae, Hyung-Uk; Kim, Dong Ik; Park, Yong Bok; Park, Jeong-Euy; Kwon, Byoung S.; Lee, Won‐Ha

doi:10.1016/j.cyto.2004.12.001

Cited by 80 publications

(100 citation statements)

References 31 publications

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“…PBLs and neutrophils cultured with insoluble IC, LPS, or other proinflammatory stimuli were completely unable to release sTL1A or to express mTL1A (P. Scapini, F. Calzetti, and M. A. Cassatella, unpublished observations), further highlighting that monocytes are the major cellular source and insoluble IC the selective stimuli for sTL1A production. In contrast, expression of mTL1A in insoluble IC-stimulated monocytes was minimal, in line with the observations made in LPS-activated monocytes (30). Finally, we have also shown that the molecular interaction between BSA/anti-BSA insoluble IC and monocytes is mainly via Fc␥RII/CD32 (rather than CD64 or CD16), at least under our experimental conditions.…”

Section: Discussionsupporting

confidence: 66%

Soluble TNF-Like Cytokine (TL1A) Production by Immune Complexes Stimulated Monocytes in Rheumatoid Arthritis

Cassatella

Silva

Tinazzi

et al. 2007

The Journal of Immunology

100

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TNF-like cytokine (TL1A) is a newly identified member of the TNF superfamily of ligands that is important for T cell costimulation and Th1 polarization. However, despite increasing information about its functions, very little is known about expression of TL1A in normal or pathological states. In this study, we report that mononuclear phagocytes appear to be a major source of TL1A in rheumatoid arthritis (RA), as revealed by their strong TL1A expression in either synovial fluids or synovial tissue of rheumatoid factor (RF)-seropositive RA patients, but not RF−/RA patients. Accordingly, in vitro experiments revealed that human monocytes express and release significant amounts of soluble TL1A when stimulated with insoluble immune complexes (IC), polyethylene glycol precipitates from the serum of RF+/RA patients, or with insoluble ICs purified from RA synovial fluids. Monocyte-derived soluble TL1A was biologically active as determined by its capacity to induce apoptosis of the human erythroleukemic cell line TF-1, as well as to cooperate with IL-12 and IL-18 in inducing the production of IFN-γ by CD4+ T cells. Because RA is a chronic inflammatory disease with autoimmune etiology, in which ICs, autoantibodies (including RF), and various cytokines contribute to its pathology, our data suggest that TL1A could be involved in its pathogenesis and contribute to the severity of RA disease that is typical of RF+/RA patients.

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Section: Discussionsupporting

confidence: 66%

Soluble TNF-Like Cytokine (TL1A) Production by Immune Complexes Stimulated Monocytes in Rheumatoid Arthritis

Cassatella

Silva

Tinazzi

et al. 2007

The Journal of Immunology

100

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“…An association with rheumatoid arthritis has recently been reported for a destabilizing mutation in the dr3 gene (29). Furthermore, TL1A and DR3 may be involved in the development of atherogenesis through the induction of proinflammatory cytokines and matrix metalloproteinases (30).…”

Section: Discussionmentioning

confidence: 99%

Role of TL1A and its receptor DR3 in two models of chronic murine ileitis

Bamias

Mishina

Nyce

et al. 2006

Proc. Natl. Acad. Sci. U.S.A.

148

164

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TL1A is a TNF-like cytokine that binds to the death-domain receptor (DR)3 and provides costimulatory signals to activated lymphocytes. Through this interaction, TL1A induces secretion of IFN-␥ and may, therefore, participate in the development of T helper-1-type effector responses. In this study, we investigated whether interactions between TL1A and DR3 are involved in the pathogenesis of chronic murine ileitis. We demonstrate that alternative splicing of DR3 mRNA takes place during the activation of lymphocytes, which results in up-regulation of the complete͞transmembrane (tm) form of DR3. Using two immunogenetically distinct animal models of Crohn's disease, we demonstrate that induction of intestinal inflammation is associated with significant up-regulation of TL1A and tm DR3 in the inflamed mucosa. In addition, within isolated lamina propria mononuclear cells from mice with inflammation, TL1A is primarily expressed on CD11c high dendritic cells. We also report that TL1A acts preferentially on memory CD4 ؉ ͞CD45RB lo murine lymphocytes by significantly inducing their proliferation, whereas it does not affect the proliferation of the naïve CD4 ؉ ͞ CD45RB hi T helper cell subpopulation. Finally, we demonstrate that TL1A synergizes with both the cytokine-dependent IL-12͞IL-18 pathway and with low-dose stimulation of the T cell receptor to significantly induce the secretion of IFN-␥ via an IL-18-independent pathway. Our results raise the possibility that interaction(s) between TL1A expressed on antigen-presenting cells and tm DR3 on lymphocytes may be of particular importance for the pathogenesis of chronic inflammatory conditions that depend on IFN-␥ secretion, including inflammatory bowel disease. Blockade of the TL1A͞DR3 pathway may, therefore, offer therapeutic opportunities in Crohn's disease.Crohn's disease ͉ cytokines ͉ mucosal inflammation T he differentiation of naïve CD4 ϩ lymphocytes into IFN-␥-secreting Th1 ''effector'' cells is a multistep process that involves several cell types, costimulatory molecules, transcription factors, and secreted cytokines (1). Antigen-presenting cell (APC)-derived IL-12 is essential for the induction of IFN-␥, an effect that is greatly enhanced by IL-18 (2). IL-12 up-regulates T-bet, a transcription factor that is critical for the stabilization of a T helper (Th)1-polarized phenotype (3). Recently, additional cytokines that play prominent roles during Th1 responses have been described, such as IL-27 and IL-23 (4). Engagement of the T cell receptor (TCR) provides further signals for the induction of IFN-␥, both in parallel to and independently of cytokinemediated pathways (1).Members of the TNF and TNF-receptor superfamilies of proteins (TNFSFPs and TNFRSFPs, respectively) are abundantly expressed in the immune system, and are critically involved in the differentiation, proliferation, and apoptosis of immune cells (5). Several members of these families induce secretion of IFN-␥ upon ligand͞receptor binding, thereby enhancing Th1-type responses (6-8). TL1A (TNFSPF15) is a r...

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“…Most of the studies have been related to DR3 involvement in immune system modulation due to its frequent expression on lymphoid tissues such as the spleen, thymus, and peripheral blood lymphocytes [131]. The role of DR3 in the development of some human malignancies has also been enlightened.…”

Section: Death Receptormentioning

confidence: 99%

Major apoptotic mechanisms and genes involved in apoptosis

et al. 2016

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As much as the cellular viability is important for the living organisms, the elimination of unnecessary or damaged cells has the opposite necessity for the maintenance of homeostasis in tissues, organs and the whole organism. Apoptosis, a type of cell death mechanism, is controlled by the interactions between several molecules and responsible for the elimination of unwanted cells from the body. Apoptosis can be triggered by intrinsically or extrinsically through death signals from the outside of the cell. Any abnormality in apoptosis process can cause various types of diseases from cancer to auto-immune diseases. Different gene families such as caspases, inhibitor of apoptosis proteins, B cell lymphoma (Bcl)-2 family of genes, tumor necrosis factor (TNF) receptor gene superfamily, or p53 gene are involved and/or collaborate in the process of apoptosis. In this review, we discuss the basic features of apoptosis and have focused on the gene families playing critical roles, activation/inactivation mechanisms, upstream/downstream effectors, and signaling pathways in apoptosis on the basis of cancer studies. In addition, novel apoptotic players such as miRNAs and sphingolipid family members in various kind of cancer are discussed.

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Involvement of TL1A and DR3 in induction of pro-inflammatory cytokines and matrix metalloproteinase-9 in atherogenesis

Cited by 80 publications

References 31 publications

Soluble TNF-Like Cytokine (TL1A) Production by Immune Complexes Stimulated Monocytes in Rheumatoid Arthritis

Soluble TNF-Like Cytokine (TL1A) Production by Immune Complexes Stimulated Monocytes in Rheumatoid Arthritis

Role of TL1A and its receptor DR3 in two models of chronic murine ileitis

Major apoptotic mechanisms and genes involved in apoptosis

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