Mouse T cells receive costimulatory signals from LIGHT, a TNF family member

Shi, Guixiu; Luo, Hongyu; Wan, Xiaochun; Salcedo, Theodora W.; Zhang, Jun; Wu, Jiangping

doi:10.1182/blood-2002-05-1404

Cited by 74 publications

(78 citation statements)

References 34 publications

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“…However, the interaction of HVEM-Ig with membrane-anchored or soluble LIGHT might elicit other effects than the interaction with LT␤R-Ig. Since LIGHT itself is a costimulatory receptor expressed on T cells that transmits reverse signals after ligation with HVEM (20,21), the HVEM-Ig fusion protein could specifically costimulate T cells in CIA (Fig. 8B, ᮍ b ).…”

Section: Discussionmentioning

confidence: 99%

Herpesvirus Entry Mediator-Ig Treatment during Immunization Aggravates Rheumatoid Arthritis in the Collagen-Induced Arthritis Model

Pierer¹,

Schulz²,

Rossol³

et al. 2009

The Journal of Immunology

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Section: Discussionmentioning

confidence: 99%

Herpesvirus Entry Mediator-Ig Treatment during Immunization Aggravates Rheumatoid Arthritis in the Collagen-Induced Arthritis Model

Pierer¹,

Schulz²,

Rossol³

et al. 2009

The Journal of Immunology

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“…One is the signal transduced through the T cell receptor (TCR), and the other is the costimulation signal transduced through CD28 or other costimulatory molecules. A number of T cell surface molecules with costimulatory activity have been reported recently, including tumor necrosis factor (TNF)-related apoptosisinducing ligand (TRAIL) (5)(6)(7)(8)(9)(10)(11)(12)(13). The significance of these newly defined costimulatory molecules in T cell activation is still not clear.…”

Section: Conclusion Trail Engagement Induces Costimulation Of Human mentioning

confidence: 99%

Induction of costimulation of human CD4 T cells by tumor necrosis factor–related apoptosis‐inducing ligand: Possible role in T cell activation in systemic lupus erythematosus

Tsai¹,

Lai²,

Chou³

et al. 2004

Arthritis & Rheumatism

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Objective. Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) has recently been shown to induce costimulation of mouse T cells in conjunction with signals from the T cell receptor. This study was undertaken to investigate TRAIL-induced costimulation of human T cells in order to determine the role of TRAIL-induced T cell activation in human systemic lupus erythematosus (SLE).Methods. An in vitro T cell stimulation system with immobilized anti-CD3 and recombinant TRAIL receptor DR4-Fc proteins was used to activate human T cells purified from healthy individuals and from patients with SLE. The T cells were stimulated in vitro to assay their proliferation response by 3 H-thymidine incorporation, and their cytokine production by enzymelinked immunosorbent assay. Activation of p38 MAPK after TRAIL stimulation was detected with specific anti-phospho-p38 MAPK monoclonal antibodies in Western blots. Results. Enhanced T cell proliferation and increased interleukin-2 and interferon-␥ (IFN␥) production were demonstrated in human T cells after stimulation with immobilized DR4-Fc and anti-CD3 in vitro. TRAIL engagement selectively activated human CD4, rather than CD8, T cells and augmented IFN␥ production. Activation of p38 MAPK was detected after TRAILinduced T cell activation. T cells isolated from patientswith SLE demonstrated a stronger response to TRAILinduced costimulation, in terms of proliferation and increased up-regulation of CD25 after activation, when compared with T cells from healthy subjects.Conclusion. TRAIL engagement induces costimulation of human CD4 T cells via a p38 MAPKdependent pathway. The results suggest that enhanced reactivity of T cells to autoantigens as a result of TRAIL-induced costimulation may play a role in the development of human autoimmune diseases.

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“…Because of such a high frequency of L d -specific precursors, this assay has high sensitivity and a high signal versus noise ratio and was routinely used to assess CTL activity in our laboratory (17,19,21). 2C spleen cells (0.4 ϫ 10 6 cells/well) were stimulated with an equal amount of mitomycin C-treated BALB/c mouse spleen cells (H-2 d ) in flat-bottomed 96-well plates, which were pre-coated with EFNB1-Fc or normal human IgG (both at 10 g/ml).…”

Section: Methodsmentioning

confidence: 99%

EphrinB1 Is Essential in T-cell-T-cell Co-operation during T-cell Activation

Luo

et al. 2004

Journal of Biological Chemistry

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Eph kinases are the largest family of receptor tyrosine kinases, and their ligands are ephrins (EFNs), which are also cell surface molecules. We have very limited knowledge about the expression and function of these kinases and their ligands in the immune system. In this study we investigated the effect of EFNB1 on mouse T-cells. EFNB1 and the Eph kinases it interacts with (collectively called EFNB1 receptors (EFNB1R)) were expressed on T-cells, B cells, and monocytes/macrophages. Some T-cells were double positive for EFNB1 and EFBB1R. Solid phase EFNB1 in the presence of suboptimal TCR ligation augmented T-cell responses in terms interferon-␥ secretion, proliferation, and cytotoxic T lymphocyte activity but not interleukin-2 production. After T-cell receptor (TCR) ligation, EFNB1R congregated to TCR caps, and then both of them translocated to raft caps. This provides a morphological basis for EFNB1R to enhance TCR signaling. Further downstream of the signaling pathway, EFNB1R stimulation led to increased LAT (linker for activation of T-cells) phosphorylation and p44/42 and p38 MAPK activation. Similar to CD28 costimulation, EFNB1R costimulation was insensitive to cyclosporin A inhibition. On the other hand, unlike the former, EFNB1R costimulation failed to activate Akt, which is essential in triggering interleukin-2 production. Our study suggests that EFNB1 is pivotal in T-cell-T-cell costimulation and in reducing T-cell response threshold to antigen stimulation.

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Mouse T cells receive costimulatory signals from LIGHT, a TNF family member

Abstract: LIGHT is a tumor necrosis factor (TNF)family

Cited by 74 publications

References 34 publications

Herpesvirus Entry Mediator-Ig Treatment during Immunization Aggravates Rheumatoid Arthritis in the Collagen-Induced Arthritis Model

Herpesvirus Entry Mediator-Ig Treatment during Immunization Aggravates Rheumatoid Arthritis in the Collagen-Induced Arthritis Model

Induction of costimulation of human CD4 T cells by tumor necrosis factor–related apoptosis‐inducing ligand: Possible role in T cell activation in systemic lupus erythematosus

EphrinB1 Is Essential in T-cell-T-cell Co-operation during T-cell Activation

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