Senescence marker killer cell lectin-like receptor G1 (KLRG1) contributes to TNF-α production by interaction with its soluble E-cadherin ligand in chronically inflamed joints

Melis, Lode; Praet, Liesbet Van; Pircher, Hanspeter; Venken, Koen; Elewaut, Dirk

doi:10.1136/annrheumdis-2013-203881

Cited by 33 publications

(27 citation statements)

References 54 publications

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“…At variance, the subset of CD56 dim KLRG1 high NK cells is expanded in the elderly, displaying impaired cytotoxicity and proliferation as well as other features of senescence ( 103 ). Interestingly, KLRG1 or the killer cell lectin-like receptor G1 is also considered a marker for T cell senescence ( 111 , 112 ) like CD57 molecule ( 113 ).…”

Section: Cells and Receptors Involved In Trained Immunity During Aginmentioning

confidence: 99%

Immunobiography and the Heterogeneity of Immune Responses in the Elderly: A Focus on Inflammaging and Trained Immunity

et al. 2017

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Owing to its memory and plasticity, the immune system (IS) is capable of recording all the immunological experiences and stimuli it was exposed to. The combination of type, dose, intensity, and temporal sequence of antigenic stimuli that each individual is exposed to has been named “immunobiography.” This immunological history induces a lifelong continuous adaptation of the IS, which is responsible for the capability to mount strong, weak or no response to specific antigens, thus determining the large heterogeneity of immunological responses. In the last years, it is becoming clear that memory is not solely a feature of adaptive immunity, as it has been observed that also innate immune cells are provided with a sort of memory, dubbed “trained immunity.” In this review, we discuss the main characteristics of trained immunity as a possible contributor to inflammaging within the perspective of immunobiography, with particular attention to the phenotypic changes of the cell populations known to be involved in trained immunity. In conclusion, immunobiography emerges as a pervasive and comprehensive concept that could help in understanding and interpret the individual heterogeneity of immune responses (to infections and vaccinations) that becomes particularly evident at old age and could affect immunosenescence and inflammaging.

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Section: Cells and Receptors Involved In Trained Immunity During Aginmentioning

confidence: 99%

Immunobiography and the Heterogeneity of Immune Responses in the Elderly: A Focus on Inflammaging and Trained Immunity

et al. 2017

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“…Studies have shown that sE‐cad is a ligand of KLRG1. The binding of sE‐cad to KLRG1 on the surface of NK cells and T cells significantly inhibits antigen reactivity, cell proliferation and the production of TNF‐α and other cytokines by effector immune cells in response to antigen stimulation . In the peripheral blood of B‐cell chronic lymphocytic leukemia patients, although both the quantity and ratio of KLRG1 + CD8 effector T cells significantly increased, the high concentration of sE‐cad in patient serum inhibits the above‐mentioned effector T cell function .…”

Section: Se‐cad and Cancer Progressionmentioning

confidence: 99%

Beyond a tumor suppressor: Soluble E‐cadherin promotes the progression of cancer

Kuang

Yang³

et al. 2016

Intl Journal of Cancer

100

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E-cadherin (E-cad) plays important roles in tumorigenesis as well as in tumor progression, invasion and metastasis. This protein exists in two forms: a membrane-tethered form and a soluble form. Full-length E-cad is membrane tethered. As a type I transmembrane glycoprotein, E-cad mainly mediates adherens junctions between cells and is involved in maintaining the normal structure of epithelial tissues. Soluble E-cad (sE-cad) is the extracellular fragment of the protein that is cleaved from the membrane after proteolysis of full-length E-cad. The production of sE-cad undermines adherens junctions, causing a reduction in cell aggregation capacity; furthermore, sE-cad can diffuse into the extracellular environment and the blood. As a paracrine/ autocrine signaling molecule, sE-cad activates or inhibits multiple signaling pathways and participates in the progression of various types of cancer, such as breast cancer, ovarian cancer, and lung cancer, by promoting invasion and metastasis. This article briefly reviews the role of sE-cad in tumorigenesis and tumor progression and its significance in clinical therapeutics.

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“…The killer cell lectin-like G1 (KLRG1) is a marker for T cell senescence as expressing cells have limited proliferative capacity (19,21). However, KLRG1 expressing T cells are not exhausted as they display cytokine production and cytotoxic potential (47). KLRG1 expression is supposed to be limited to tissue-homing and thus T EM and T EMRA cells (8,28,(48)(49)(50).…”

Section: Also the Investigations On Murine Memory T Cells Were Eithementioning

confidence: 99%

Progressive change in expression of killer-like receptorsr and GPR56 expression defines the cytokine production potential of human CD4⁺ T memory cells

Truong

Schlickeiser

Vogt

et al. 2017

Preprint

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Memory T cells mount an accelerated response upon re-challenge but are heterogeneous in phenotype and function. Traditionally memory T cells were classified into central memory, effector memory and terminally differentiated effector memory (T EMRA ) cells based on expression of CCR7 and CD45RA. Functional heterogeneity even within these subsets demonstrated the need for more suitable markers. We applied bulk and single gene expression profiling of human CD4 + memory T cells and identified surface markers, KLRB1, KLRG1, GPR56 and KLRF1, allowing classification into "low", "high" or "exhausted" cytokine producers. In contrast to common understanding KLRG1 expression was not associated with exhaustion and highest production of multiple cytokines was observed in KLRB1 + KLRG1 + GPR56 + T cells. Only additional KLRF1expression was associated with a decline in cytokine production. The superiority of KLRF1 to define exhausted cytokine producers compared to classical T EMRA identification was best exemplified for intrahepatic T cells in patients with inflammatory liver diseases.

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Senescence marker killer cell lectin-like receptor G1 (KLRG1) contributes to TNF-α production by interaction with its soluble E-cadherin ligand in chronically inflamed joints

Abstract: sE-cadherin contributes to the local proinflammatory environment in the joint by favouring TNF-α production by KLRG1(+) CD4(+) T cells. This pathway seems to be operational in both SpA and RA, but not in crystal-induced arthritis.

Cited by 33 publications

References 54 publications

Immunobiography and the Heterogeneity of Immune Responses in the Elderly: A Focus on Inflammaging and Trained Immunity

Immunobiography and the Heterogeneity of Immune Responses in the Elderly: A Focus on Inflammaging and Trained Immunity

Beyond a tumor suppressor: Soluble E‐cadherin promotes the progression of cancer

Progressive change in expression of killer-like receptorsr and GPR56 expression defines the cytokine production potential of human CD4⁺ T memory cells

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Senescence marker killer cell lectin-like receptor G1 (KLRG1) contributes to TNF-α production by interaction with its soluble E-cadherin ligand in chronically inflamed joints

Abstract: sE-cadherin contributes to the local proinflammatory environment in the joint by favouring TNF-α production by KLRG1(+) CD4(+) T cells. This pathway seems to be operational in both SpA and RA, but not in crystal-induced arthritis.

Cited by 33 publications

References 54 publications

Immunobiography and the Heterogeneity of Immune Responses in the Elderly: A Focus on Inflammaging and Trained Immunity

Immunobiography and the Heterogeneity of Immune Responses in the Elderly: A Focus on Inflammaging and Trained Immunity

Beyond a tumor suppressor: Soluble E‐cadherin promotes the progression of cancer

Progressive change in expression of killer-like receptorsr and GPR56 expression defines the cytokine production potential of human CD4+ T memory cells

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Progressive change in expression of killer-like receptorsr and GPR56 expression defines the cytokine production potential of human CD4⁺ T memory cells