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Raffeiner, Bernd; Dejaco, Christian; Duftner, Christina; Kullich, W.; Goldberger, Christian; Vega, Sandra C; Keller, Michael; Grubeck‐Loebenstein, Beatrix; Schirmer, Michael

doi:10.1186/ar1840

Cited by 44 publications

(23 citation statements)

References 35 publications

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“…Another feature of CD28 − T-cells is their longevity and persistence that can be explained by defects in the apoptotic pathway with upregulation of bcl-2 and Fas-associated death domain like IL-2-converting enzyme-like inhibitory protein (FLIP) (66, 67). Terminally differentiated T-cells also acquire new stimulatory receptors including killer cell immunoglobulin-like receptors (KIRs) and Toll-like receptors (TLRs) (68, 69). Thus, activation of CD4 + CD28 − T-cells no longer depends on professional antigen-presenting cells, rather it is promoted by stress molecules as well as bacterial and/or viral products (65).…”

Section: Development and Cellular Senescence Of Tregsmentioning

confidence: 99%

The Impact of Aging on Regulatory T-Cells

Fessler¹,

Ficjan²,

Duftner³

et al. 2013

Front. Immunol.

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Age-related deviations of the immune system contribute to a higher likelihood of infections, cancer, and autoimmunity in the elderly. Senescence of T-lymphocytes is characterized by phenotypical and functional changes including the loss of characteristic T-cell surface markers, while an increase of stimulatory receptors, cytotoxicity as well as resistance against apoptosis is observed. One of the key mediators of immune regulation are naturally occurring regulatory T-cells (Tregs). Tregs express high levels of CD25 and the intracellular protein forkhead box P3; they exert their suppressive functions in contact-dependent as well as contact-independent manners. Quantitative and qualitative defects of Tregs were observed in patients with autoimmune diseases. Increased Treg activity was shown to suppress anti-tumor and anti-infection immunity. The effect of aging on Tregs, and the possible contribution of age-related changes of the Treg pool to the pathophysiology of diseases in the elderly are still poorly understood. Treg homeostasis depends on an intact thymic function and current data suggest that conversion of non-regulatory T-cells into Tregs as well as peripheral expansion of existing Tregs compensates for thymic involution after puberty to maintain constant Treg numbers. In the conventional T-cell subset, peripheral proliferation of T-cells is associated with replicative senescence leading to phenotypical and functional changes. For Tregs, different developmental stages were also described; however, replicative senescence of Tregs has not been observed yet.

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Section: Development and Cellular Senescence Of Tregsmentioning

confidence: 99%

The Impact of Aging on Regulatory T-Cells

Fessler¹,

Ficjan²,

Duftner³

et al. 2013

Front. Immunol.

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“…TLR5 ligand flagellin and TLR7/8 ligands resiquimod (R-848) also enhance T cell proliferation and IFN-production in human CD45RO+ T cells [114]. Perforin production is stimulated by LPS in TLR4-positive CD28-CD4+ T cells [125]. When stimulated with TLR3 ligand polyI:C and TLR9 ligand CpG DNA, CD4+ T cells survive longer although there is no increase in proliferation [126].…”

Section: Tlr Expression On T Cellsmentioning

confidence: 97%

Role of the Innate Immune System in Autoimmune Inflammatory Demyelination

O’Brien

Fitzgerald²,

Naiken³

et al. 2008

CMC

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Considerable research has been devoted to the role of the adaptive immune system in the pathogenesis of autoimmune inflammatory demyelination (AID). AID is thought to occur spontaneously in patients with multiple sclerosis (MS), a common cause of neurological disability. AID is also observed in the best characterized animal model of MS, experimental autoimmune encephalomyelitis (EAE). The adaptive immune system recognizes and responds to antigens via highly specific T-cell receptors. Myelin-reactive T-cells may initiate pathological immune responses that lead to central nervous system damage in MS and EAE. By contrast, the innate immune system recognizes evolutionarily conserved structures that are common to invading pathogens with high efficiency for rapid recognition and elimination of viruses, bacteria, and fungi. This recognition is mediated by pattern-recognition receptors such as Toll-like receptors (TLRs) expressed on cells of the innate immune system (dendritic cells and CNS-resident cells, such as microglia) that have the potential to activate autoimmune responses by inducing the production of inflammatory cytokines and chemokines. Conversely, the innate immune system can also regulate autoimmune inflammation by inducing the production of immunoregulatory molecules such as type I interferons, which are currently used in the treatment of MS. We review the evidence that TLRs can exacerbate or regulate AID and discuss the therapeutic potential of targeting either process.

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“…Moreover, certain cytokines such as TNF have been shown to increase the expression of TLRs [35]. Indeed, serum and synovial fluid levels of p40 IL-12/IL-23 have been shown to be increased in SpA compared with osteo arthritis patients [36].…”

Section: Consequences Of Tlr Activationmentioning

confidence: 99%

“…showed that this subpopulation of T cells from SpA patients significantly expressed more functionally active TLR4 and 2 compared with controls. These levels decreased significantly with anti-TNF treatment [35]. …”

Section: Consequences Of Tlr Activationmentioning

confidence: 99%

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The potential importance of Toll-like receptors in ankylosing spondylitis

Tan¹,

Farheen²

2011

International Journal of Clinical Rheumatology

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Cells involved in innate immunity scan for pathogens via extracellular and intracellular (endosomal) pattern recognition receptors (PRRs). Engagement of PRRs by a specific ligand results in downstream activation of intracellular inflammatory cascades. There is emerging evidence indicating that one class of PRR, the Toll-like receptor (TLR) plays a potential role in the pathogenesis of spondyloarthropathies. Since certain Gram-negative bacteria are known to act as triggers for reactive arthritis, there has been much interest in studying the role of TLRs in spondyloarthropathies. In this article, we introduce the immunology of TLRs followed by a discussion of their potential role in ankylosing spondylitis.

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Cited by 44 publications

References 35 publications

The Impact of Aging on Regulatory T-Cells

The Impact of Aging on Regulatory T-Cells

Role of the Innate Immune System in Autoimmune Inflammatory Demyelination

The potential importance of Toll-like receptors in ankylosing spondylitis

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