Platelets Enhance Dendritic Cell Responses against Staphylococcus aureus through CD40-CD40L

Nishat, Sharmeen; Wuescher, Leah M.; Worth, Randall G.

doi:10.1128/iai.00186-18

Cited by 31 publications

(26 citation statements)

References 56 publications

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“…Expression of CD40L on platelets has been shown to affect dendritic cells as well as B and T lymphocytes, suggesting that it provides a communicative link between innate and adaptive immunity [ 44 – 46 ]. For example, platelets inhibit dendritic cells differentiation in a CD40L-dependent manner and significantly suppress the proinflammatory cytokines production [ 47 ].…”

Section: Platelet Cd40l (Cd154)mentioning

confidence: 99%

Role of platelet biomarkers in inflammatory response

et al. 2020

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Beyond hemostasis, thrombosis and wound healing, it is becoming increasingly clear that platelets play an integral role in inflammatory response and immune regulation. Platelets recognize pathogenic microorganisms and secrete various immunoregulatory cytokines and chemokines, thus facilitating a variety of immune effects and regulatory functions. In this review, we discuss recent advances in signaling of platelet activation-related biomarkers in inflammatory settings and application prospects to apply for disease diagnosis and treatment.

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Section: Platelet Cd40l (Cd154)mentioning

confidence: 99%

Role of platelet biomarkers in inflammatory response

et al. 2020

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“…In addition, IL-27 from APCs reduces the pH of phagolysosomes which boosts the ability of DCs to kill intracellular bacteria [ 32 ]. Moreover, activated platelets can stimulate DCs via CD40L production and improve their maturation, increasing cytokine secretion as well as antigen presentation in case of S. aureus infection [ 33 ].…”

Section: Dendritic Cellsmentioning

confidence: 99%

Messing with the Sentinels—The Interaction of Staphylococcus aureus with Dendritic Cells

et al. 2018

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Staphylococcus aureus (S. aureus) is a dangerous pathogen as well as a frequent colonizer, threatening human health worldwide. Protection against S. aureus infection is challenging, as the bacteria have sophisticated strategies to escape the host immune response. To maintain equilibrium with S. aureus, both innate and adaptive immune effector mechanisms are required. Dendritic cells (DCs) are critical players at the interface between the two arms of the immune system, indispensable for inducing specific T cell responses. In this review, we highlight the importance of DCs in mounting innate as well as adaptive immune responses against S. aureus with emphasis on their role in S. aureus-induced respiratory diseases. We also review what is known about mechanisms that S. aureus has adopted to evade DCs or manipulate these cells to its advantage.

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“…For example, platelet CD40L induces production of IL-6 and IL-12 from DCs as well as increasing their expression of CD80, CD86 and ICAM-1 [ 7 ]. It has also been demonstrated that platelet-CD40L can enhance DC maturation and their ability to directly kill Staphylococcus aureus which leads to efficient adaptive immunity against the bacterium [ 111 ]. Furthermore, platelet CD40L can induce isotype switching in B-cells and augments CD8+ T-cell responses; hence, functioning as a bridge to the adaptive immune system [ 7 ].…”

Section: Introductionmentioning

confidence: 99%

“…Platelets can directly interact with DC via CD62P/CD162 and this influences DC maturation and enhances their production of the Th2 helper chemokine CCL17 [ 139 , 140 ]. Alternatively, direct CD40/CD40L-dependent interactions between platelets and DC increases the latter’s ability to uptake and kill bacteria [ 111 ]. In addition, firm adhesion of platelets to DCs through MAC-1 (integrin alfaMbeta2, CD11b/CD18,) and Junctional Adhesion Molecule-C (JAM-C) leads to enhanced phagocytosis [ 141 , 142 ].…”

Section: Introductionmentioning

confidence: 99%

The Immune Nature of Platelets Revisited

Maouia

Rebetz

Kapur

et al. 2020

Transfusion Medicine Reviews

142

136

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Platelets are the primary cellular mediators of hemostasis and this function firmly acquaints them with a variety of inflammatory processes. For example, platelets can act as circulating sentinels by expressing Toll-like receptors (TLR) that bind pathogens and this allows platelets to effectively kill them or present them to cells of the immune system. Furthermore, activated platelets secrete and express many pro- and anti-inflammatory molecules that attract and capture circulating leukocytes and direct them to inflamed tissues. In addition, platelets can directly influence adaptive immune responses via secretion of, for example, CD40 and CD40L molecules. Platelets are also the source of most of the microvesicles in the circulation and these miniscule elements further enhance the platelet’s ability to communicate with the immune system. More recently, it has been demonstrated that platelets and their parent cells, the MK, can also uptake, process and present both foreign and self-antigens to CD8+ T-cells conferring on them the ability to directly alter adaptive immune responses. This review will highlight several of the non-hemostatic attributes of platelets that clearly and rightfully place them as integral players in immune reactions.

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Platelets Enhance Dendritic Cell Responses against Staphylococcus aureus through CD40-CD40L

Cited by 31 publications

References 56 publications

Role of platelet biomarkers in inflammatory response

Role of platelet biomarkers in inflammatory response

Messing with the Sentinels—The Interaction of Staphylococcus aureus with Dendritic Cells

The Immune Nature of Platelets Revisited

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