Activated platelet–T-cell conjugates in peripheral blood of patients with HIV infection

Green, Samantha A.; Smith, Mindy; Hasley, Rebecca B.; Stephany, David; Harned, Adam; Nagashima, Kunio; Abdullah, Shahed; Pittaluga, Stefania; Imamichi, Tomozumi; Qin, Jing; Rupert, Adam; Ober, Alex; Lane, H. Clifford; Catálfamo, Marta

doi:10.1097/qad.0000000000000701

Cited by 47 publications

(75 citation statements)

References 45 publications

(47 reference statements)

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“…Furthermore, CX3CR1 + CD8 + T cells were able to form complexes with activated platelets in the presence of thrombin. Higher frequencies of circulating CD8 + T-cell-platelet conjugates have been found in fresh blood samples obtained from ART recipients [14]. Notably, it is unlikely that platelets exert a substantial effect on CD8 + T cells globally, as only a small fraction of CD8 + T cells are found to be complexed with platelets in circulation, and it is unknown how stable these interactions are in vivo.…”

Section: Discussionmentioning

confidence: 99%

“…Platelets are critical mediators of hemostasis, coagulation, and wound healing and can form conjugates with CD8 + T cells or other leukocytes [14]. Increased frequencies of platelet/leukocyte complexes have been observed in the peripheral blood of HIV-infected ART recipients, as well as in the blood of patients with CVD, type I diabetes, or systemic lupus erythematosus [14][15][16][17], yet the biological significance of these interactions, or the cross-talk that occurs among these cell types, remains to be determined.…”

Section: Human Immunodeficiency Virus (Hiv) Infection Results In a Mamentioning

confidence: 99%

“…However, given that plasma levels of the coagulation marker D-dimer correlate with frequencies of circulating CD8 + Tcell-platelet conjugates in HIV-infected ART recipients [14], it is conceivable that coagulation can influence these interactions, which, in turn, could affect CD8 + T-cell function in some meaningful way. Local effects of CD8 + T-cell-platelet complexes may be particularly important at sites of vascular inflammation and injury, where cross-talk with platelets could limit CD8 + T-cell effector function and regulate inflammation at the site of clot formation.…”

Section: Discussionmentioning

confidence: 99%

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Inflammatory Function of CX3CR1⁺CD8⁺T Cells in Treated HIV Infection Is Modulated by Platelet Interactions

et al. 2016

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Increases in inflammation, coagulation, and CD8 + T-cell numbers are associated with an elevated cardiovascular disease (CVD) risk in human immunodeficiency virus (HIV)-infected antiretroviral therapy (ART) recipients. Circulating memory CD8 + T cells that express the vascular endothelium-homing receptor CX3CR1 (fractalkine receptor) are enriched in HIV-infected ART recipients. Thrombin-activated receptor (PAR-1) expression is increased in HIV-infected ART recipients and is particularly elevated on CX3CR1 + CD8 + T cells, suggesting that these cells could interact with coagulation elements. Indeed, thrombin directly enhanced T-cell receptor-mediated interferon γ production by purified CD8 + T cells but was attenuated by thrombin-induced release of transforming growth factor β by platelets. We have therefore identified a population of circulating memory CD8 + T cells in HIV infection that may home to endothelium, can be activated by clot-forming elements, and are susceptible to platelet-mediated regulation. Complex interactions between inflammatory elements and coagulation at endothelial surfaces may play an important role in CVD risk in HIV-infected ART recipients.

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Section: Discussionmentioning

confidence: 99%

Section: Human Immunodeficiency Virus (Hiv) Infection Results In a Mamentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Inflammatory Function of CX3CR1⁺CD8⁺T Cells in Treated HIV Infection Is Modulated by Platelet Interactions

et al. 2016

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“…In murine models, CD62P-positive platelets mediate adhesion of leukocytes into endothelium leading to the recruitment of T-cells to the place of inflammation/ injury. 22 Individual leukocyte subpopulation demonstrates different affinity for CD62P present on platelets surface. From all leukocytes, monocytes show the greatest affinity for platelet CD62P, and thus to the formation of plateletleukocyte aggregates.…”

Section: Interactions Between Platelets and Leukocytes In Inflammationmentioning

confidence: 99%

Interactions between platelets and leukocytes in pathogenesis of multiple sclerosis

Dziedzic¹,

Bijak²

2019

Adv Clin Exp Med

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Neurodegenerative diseases are an increasing problem in the modern world. Multiple sclerosis (MS) is a major human demyelinating and degenerative disease of the central nervous system (CNS). There are many reports that point to the significant role of platelet-leukocyte interaction in neurodegenerative diseases and cardiovascular disturbances. Epidemiological studies confirm the high risk of cardiovascular diseases in patients with MS. The pathophysiology mechanisms of this multi-component disease are very complex and involve various types of cells. There is increasing evidence that some co-stimulatory pathways affect the function of inflammatory cells, both in the periphery and in the CNS. Interactions of leukocytes and endothelial cells (ECs) could be significantly modulated in the presence of activated blood platelets. The supposed role of activated platelets in the development of vessel inflammatory response is due to their ability to adhere to inflamed ECs or proteins included in the subendothelial layer of the blood vessel wall, as well as to the ability of platelets to form aggregates with leukocytes. Blood platelets are able to directly activate leukocytes through a receptor-dependent mechanism or, indirectly, by biologically active compounds secreted from their granules. Cell-cell interactions provide critical mechanisms by which platelets link thrombosis, inflammation and related processes, such as diapedesis and leukocyte infiltration, to the affected vessel. Determining the relationship between platelet-leukocyte interactions and the development of neuroinflammation in the course of MS may provide new therapeutic targets in the future.

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“…Conversely, coagulation factors and products (thrombin and fibrin) can also activate inflammation. 71,72 The proinflammatory state in HIV-infected patients, with upregulated cytokines and other inflammatory molecules present in the blood, [73][74][75][76][77][78][79][80][81][82][83][84] is therefore strongly associated with DVT formation. However, the medical treatment of DVT remains the same for HIV-infected and HIV-negative patients.…”

Section: Hiv the Accompanying Proinflammatory State And The Developmmentioning

confidence: 99%

Pathological Clotting and Deep Vein Thrombosis in Patients with HIV

Jackson

Pretorius

2018

Semin Thromb Hemost

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The number of people infected with human immunodeficiency virus (HIV) is rapidly increasing and the majority of those infected are living in sub-Saharan Africa. Some hallmarks of HIV are inflammation and upregulation of inflammatory markers. A pathological coagulation system may accompany these inflammatory changes and potentially result in venous thromboembolism such as a deep vein thrombosis (DVT). In this review, the authors describe the inflammatory profile in HIV, the treatment regimens currently in place in South Africa, and in particular how HIV affects the hematological system, with specific focus on platelets, red blood cells (RBCs; erythrocytes), and fibrin(ogen). They also discuss the presence of DVT in HIV, focus on screening tests, and suggest a more proactive approach to track the inflammatory profile of HIV patients, by specifically using parameters that might point to pathological coagulation; these should involve platelet, RBC, and fibrin(ogen) analysis. They conclude by suggesting that including coagulation function tests to study the effect of treatment interventions would improve outcomes in these individuals, as it could help in the diagnosis of thromboembolic disease. Furthermore, this approach could streamline treatment strategies due to improved monitoring. A better understanding of hypercoagulability of HIV-infected patients is therefore urgently needed. In conclusion, the authors suggest a panel of pathology tests that should be considered as standard procedures when HIV is present.

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Activated platelet–T-cell conjugates in peripheral blood of patients with HIV infection

Cited by 47 publications

References 45 publications

Inflammatory Function of CX3CR1⁺CD8⁺T Cells in Treated HIV Infection Is Modulated by Platelet Interactions

Inflammatory Function of CX3CR1⁺CD8⁺T Cells in Treated HIV Infection Is Modulated by Platelet Interactions

Interactions between platelets and leukocytes in pathogenesis of multiple sclerosis

Pathological Clotting and Deep Vein Thrombosis in Patients with HIV

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Activated platelet–T-cell conjugates in peripheral blood of patients with HIV infection

Cited by 47 publications

References 45 publications

Inflammatory Function of CX3CR1+CD8+T Cells in Treated HIV Infection Is Modulated by Platelet Interactions

Inflammatory Function of CX3CR1+CD8+T Cells in Treated HIV Infection Is Modulated by Platelet Interactions

Interactions between platelets and leukocytes in pathogenesis of multiple sclerosis

Pathological Clotting and Deep Vein Thrombosis in Patients with HIV

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Product

Resources

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Inflammatory Function of CX3CR1⁺CD8⁺T Cells in Treated HIV Infection Is Modulated by Platelet Interactions

Inflammatory Function of CX3CR1⁺CD8⁺T Cells in Treated HIV Infection Is Modulated by Platelet Interactions