Card9 controls Dectin‐1‐induced T‐cell cytotoxicity and tumor growth in mice

Haas, Tobias; Heidegger, Simon; Wintges, Alexander; Bscheider, Michael; Bek, Sarah; Fischer, Julius; Eisenkolb, Gabriel; Schmickl, Martina; Spoerl, Silvia; Peschel, Christian; Poeck, Hendrik; Ruland, Jürgen

doi:10.1002/eji.201646775

Cited by 26 publications

(15 citation statements)

References 27 publications

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“…Interestingly, CARD9 as an inflammation-related gene also promote the proliferation and migration of tumor cells, induce cancer, and affect tumor severity and prognosis 81 .…”

Section: Importance Of Card9 In Non-infection-related Inflammationmentioning

confidence: 99%

Molecular and physiological roles of the adaptor protein CARD9 in immunity

et al. 2018

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CARD9 is a caspase recruitment domain-containing signaling protein that plays a critical role in innate and adaptive immunity. It has been widely demonstrated that CARD9 adaptor allows pattern recognition receptors to induce NF-κB and MAPK activation, which initiates a “downstream” inflammation cytokine cascade and provides effective protection against microbial invasion, especially fungal infection. Here our aim is to update existing paradigms and summarize the most recent findings on the CARD9 signaling pathway, revealing significant mechanistic insights into the pathogenesis of CARD9 deficiency. We also discuss the effect of CARD9 genetic mutations on the in vivo immune response, and highlight clinical advances in non-infection inflammation.

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“…Interestingly, CARD9 as an inflammation-related gene also promote the proliferation and migration of tumor cells, induce cancer, and affect tumor severity and prognosis 81 .…”

Section: Importance Of Card9 In Non-infection-related Inflammationmentioning

confidence: 99%

Molecular and physiological roles of the adaptor protein CARD9 in immunity

et al. 2018

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“…For example, administration of β glucans was shown to inhibit tumor growth in murine carcinoma models ( 13 – 15 ), in human melanoma, neuroblastoma, mastocytosis, and lymphoma xenograft models ( 16 , 17 ) and in ovarian ( 18 , 19 ), breast ( 20 ), lung ( 14 , 21 – 23 ), and gastric cancer ( 19 , 24 ). Mechanistically, β glucans were shown to convert immunosuppressive macrophages into an M1-like antitumoral phenotype ( 25 ), to promote NK ( 26 ) and CD8 + T cell cytotoxicity ( 27 ) as well as a decrease in myeloid-derived suppressor cells and regulatory T cells ( 13 , 28 ). Interestingly, Zhao et al recently reported that β glucans upregulate particularly the expression of TNFSF15 and OX40L in DCs in mice, thus promoting efficient Th9 priming and potent anti-melanoma response following vaccination ( 29 ).…”

Section: “(Dectin-1)” Familymentioning

confidence: 99%

C-Type Lectin-Like Receptors As Emerging Orchestrators of Sterile Inflammation Represent Potential Therapeutic Targets

Chiffoleau

2018

Front. Immunol.

121

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Over the last decade, C-type lectin-like receptors (CTLRs), expressed mostly by myeloid cells, have gained increasing attention for their role in the fine tuning of both innate and adaptive immunity. Not only CTLRs recognize pathogen-derived ligands to protect against infection but also endogenous ligands such as self-carbohydrates, proteins, or lipids to control homeostasis and tissue injury. Interestingly, CTLRs act as antigen-uptake receptors via their carbohydrate-recognition domain for internalization and subsequent presentation to T-cells. Furthermore, CTLRs signal through a complex intracellular network leading to the secretion of a particular set of cytokines that differently polarizes downstream effector T-cell responses according to the ligand and pattern recognition receptor co-engagement. Thus, by orchestrating the balance between inflammatory and resolution pathways, CTLRs are now considered as driving players of sterile inflammation whose dysregulation leads to the development of various pathologies such as autoimmune diseases, allergy, or cancer. For examples, the macrophage-inducible C-type lectin (MINCLE), by sensing glycolipids released during cell-damage, promotes skin allergy and the pathogenesis of experimental autoimmune uveoretinitis. Besides, recent studies described that tumors use physiological process of the CTLRs’ dendritic cell-associated C-type lectin-1 (DECTIN-1) and MINCLE to locally suppress myeloid cell activation and promote immune evasion. Therefore, we aim here to overview the current knowledge of the pivotal role of CTLRs in sterile inflammation with special attention given to the “Dectin-1” and “Dectin-2” families. Moreover, we will discuss the potential of these receptors as promising therapeutic targets to treat a wide range of acute and chronic diseases.

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“…Dectin-1 ligation on DCs was further shown to capacitate DCs for priming of cytotoxic CD8 + T cells (63). Dectin-1-activated cross-priming of cytotoxic CD8 + T cells by DCs depends on caspase recruitment domain family member 9 (Card9) but does not depend on the activation of inflammasomes (64). In humans, DECTIN-1 stimulates mast cells to produce leukotrienes (55), which have recently been shown to be involved in the activation of ILCs (65), thereby providing another line of cross-talk between myeloid cells and innate lymphocytes.…”

Section: Hemitam Receptorsmentioning

confidence: 99%