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. 2018 May 3:9:974.
doi: 10.3389/fimmu.2018.00974. eCollection 2018.

T Cell Co-Stimulation: Inhibition of Immunosuppression?

Karl-Gösta Sundqvist  1
Affiliations

T Cell Co-Stimulation: Inhibition of Immunosuppression?

Karl-Gösta Sundqvist. Front Immunol. .
No abstract available

Keywords: adhesion molecules; cell surface receptor; co-stimulatory molecules; motility; shedding.

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Figures

Figure 1
Figure 1
Behavior of low-density lipoprotein receptor-related protein 1 (LRP1) in the absence (A) and presence (B) of co-stimulation through different receptors and its possible impact on cell signaling through the multiple molecular interactions and connections of LRP1 and its ligand thrombospondin-1 (TSP-1). The constitutive shedding-dependent low cell surface LRP1 as shown in a favors motility, whereas the upregulated level induced by co-receptor ligation by B7, integrin ligands, and CXCL12 also may trigger activating signals through LRP1-dependent expression of signaling and metabolic receptors as well as LRP1-associated TSP-1. TSP-1 binds to cell surface receptors, components of the extracellular matrix, other matricellular proteins, growth factors, cytokines, and proteases (25). Besides its interactions with signaling molecules, as mentioned in the text, LRP1 can interact with multiple different exogenous ligands including α-2-macroglobulin, tissue plasminogen activator, plasminogen activator inhibitor, and apolipoprotein E. Apolipoprotein E is involved in fat metabolism and is produced by macrophages pointing to a possible influence on antigen presentation. It is conceivable that LRP1 and associated TSP-1 in collaboration can communicate with other cell surface receptors besides connecting to or integrating vital pathways for cell signaling or cell metabolism.
See this image and copyright information in PMC

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