Identification of CD245 as myosin 18A, a receptor for surfactant A: A novel pathway for activating human NK lymphocytes

Masson, Annie; Giustiniani, Jérôme; Marie‐Cardine, Anne; Bouaziz, J.‐D.; Dulphy, Nicolas; Gossot, Dominique; Validire, Pierre; Tazi, Abdellatif; Garbar, Christian; Bagot, Martine; Merrouche, Yacine; Bensussan, Armand

doi:10.1080/2162402x.2015.1127493

Cited by 16 publications

(26 citation statements)

References 46 publications

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“…Emerging evidence indicated that resting NK cell functional priming is stringently controlled by the integration of various immune modulators [10]. Recent studies demonstrated that SP-D could bind to NK cells and modulate their function [36,37]. Additionally, a previous study found that ficolin-1 could attach to the NK cell surface via the pathogen recognition domain of ficolin-1, although whether this interaction might affect NK cell function was still unclear [38].…”

Section: Mediators Of Inflammationmentioning

confidence: 99%

Mannan-Binding Lectin Regulates Inflammatory Cytokine Production, Proliferation, and Cytotoxicity of Human Peripheral Natural Killer Cells

Zhou

et al. 2019

Mediators of Inflammation

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Natural killer (NK) cells represent the founding members of innate lymphoid cells (ILC) and play critical roles in inflammation and the immune response. NK cell effector functions are regulated and fine-tuned by various immune modulators. Mannan (or mannose)-binding lectin (MBL), a soluble C-type lectin, is traditionally recognized as an initiator of the complement pathway. Recently, it is also considered as an immunomodulator by its interaction with kinds of immune cells. However, the effect of MBL on NK cell function remains unexplored. In this study, we found that human plasma MBL could interact directly with peripheral NK cells partially via its collagen-like region (CLR). This MBL binding markedly suppressed the interleukin-2- (IL-2-) induced inflammatory cytokine tumor necrosis factor-alpha (TNF-α) and interferon-gamma (IFN-γ) production but increased the IL-10 production in NK cells. In addition, the expression of activation surface markers such as CD25 and CD69 declined after MBL treatment. Also, MBL impaired the proliferation and lymphokine-activated killing (LAK) of NK cells. Moreover, we demonstrated that MBL inhibited IL-2-induced signal transducers and activators of transcription 5 (STAT5) activation in NK cells. In conclusion, we have uncovered a far unknown regulatory role of MBL on NK cells, a new clue that could be important in the immunomodulatory networks of immune responses.

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Section: Mediators Of Inflammationmentioning

confidence: 99%

Mannan-Binding Lectin Regulates Inflammatory Cytokine Production, Proliferation, and Cytotoxicity of Human Peripheral Natural Killer Cells

Zhou

et al. 2019

Mediators of Inflammation

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“…Additionally, the interaction between myosin-18A and SP-A was also found to be important for macrophage activation ( Yang et al, 2015 ). Besides, CD245, a highly conserved motor enzyme reported as a receptor for SP-A, has also been identified as myosin-18A ( De Masson et al, 2016 ). Certainly, these studies shed light on the new feature of myosin-18A function.…”

Section: Introductionmentioning

confidence: 99%

Multifaceted Function of Myosin-18, an Unconventional Class of the Myosin Superfamily

Ouyang

Zhao

Yao

et al. 2021

Front. Cell Dev. Biol.

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Myosin is a diverse superfamily of motor proteins responsible for actin-based motility and contractility in eukaryotic cells. Myosin-18 family, including myosin-18A and myosin-18B, belongs to an unconventional class of myosin, which lacks ATPase motor activity, and the investigations on their functions and molecular mechanisms in vertebrate development and diseases have just been initiated in recent years. Myosin-18A is ubiquitously expressed in mammalian cells, whereas myosin-18B shows strong enrichment in striated muscles. Myosin-18 family is important for cell motility, sarcomere formation, and mechanosensing, mostly by interacting with other cytoskeletal proteins and cellular apparatus. Myosin-18A participates in several intracellular transport processes, such as Golgi trafficking, and has multiple roles in focal adhesions, stress fibers, and lamellipodia formation. Myosin-18B, on the other hand, participates in actomyosin alignment and sarcomere assembly, thus relating to cell migration and muscle contractility. Mutations of either Myo18a or Myo18b cause cardiac developmental defects in mouse, emphasizing their crucial role in muscle development and cardiac diseases. In this review, we revisit the discovery history of myosin-18s and summarize the evolving understanding of the molecular functions of myosin-18A and myosin-18B, with an emphasis on their separate yet closely related functions in cell motility and contraction. Moreover, we discuss the diseases tightly associated with myosin-18s, especially cardiovascular defects and cancer, as well as highlight the unanswered questions and potential future research perspectives on myosin-18s.

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“…S6C) aMϕs. Myo18A is an unconventional myosin that does not operate as a traditional molecular motor, having both intracellular and cell-surface locations (14), and was recently defined as CD245 (15). Immune activation results in Myo18A localization on the cell surface, where it binds to the collagen-like domain of SP-A (6, 16) and we confirmed that an intact collagen-like domain is required to enhance IL-4-mediated type 2 responses (Fig.…”

mentioning

confidence: 99%

Local amplifiers of IL-4Rα–mediated macrophage activation promote repair in lung and liver

Minutti

Jackson-Jones

García-Fojeda

et al. 2017

Science

171

170

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The type 2 immune response controls helminth infection and maintains tissue homeostasis but can lead to allergy and fibrosis when improperly controlled. We reveal the existence of local tissue-specific enhancers of type 2 mediated-macrophage activation. In the lung, surfactant protein A (SP-A) enhanced IL-4-dependent proliferation and activation of alveolar macrophages, accelerating parasite clearance and reducing pulmonary injury following infection with a lung-migrating helminth. In the peritoneal cavity and liver, C1q enhancement of type 2 macrophage activation was required for liver repair following bacterial infection, but resulted in tissue fibrosis following peritoneal dialysis. Both SP-A and C1q generated their effects on macrophages via the unconventional myosin18A that acts as a cell surface receptor. We conclude that the structurally related defense collagens SP-A and C1q are tissue-specific factors that act through myosin18A to license local type 2 responses with consequences for parasite control, tissue repair, and fibrosis.

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Identification of CD245 as myosin 18A, a receptor for surfactant A: A novel pathway for activating human NK lymphocytes

Cited by 16 publications

References 46 publications

Mannan-Binding Lectin Regulates Inflammatory Cytokine Production, Proliferation, and Cytotoxicity of Human Peripheral Natural Killer Cells

Mannan-Binding Lectin Regulates Inflammatory Cytokine Production, Proliferation, and Cytotoxicity of Human Peripheral Natural Killer Cells

Multifaceted Function of Myosin-18, an Unconventional Class of the Myosin Superfamily

Local amplifiers of IL-4Rα–mediated macrophage activation promote repair in lung and liver

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