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1.
Figure 1

Figure 1. From: Herpesvirus Exploitation of Host Immune Inhibitory Pathways.

PD-1, BTLA and their mammalian and herpesvirus ligands. Left: T cell-expressed PD-1 and BTLA induce inhibitory signalling following binding of their respective mammalian and viral ligands. BTLA binding to T cell-expressed HVEM elicits NFκB‑induced pro-inflammatory/pro-survival signalling. Middle: Up-regulation of PD-1 expression by monocytes is observed in HIV infection and PD-1 ligation induces monocyte secretion of IL-10. Right: PD-L1 expressed by tumour cells induces anti-apoptotic signalling.

Gabrielle Stack, et al. Viruses. 2012 August;4(8):1182-1201.
2.
Figure 2

Figure 2. From: Herpesvirus Exploitation of Host Immune Inhibitory Pathways.

Determined structures of cellular CD200 and CD200 homologues encoded by human and rat herpesviruses. ‘V’ denotes a conserved variable-like Ig domain and ‘C’ denotes a conserved constant-like Ig domain. These domains are formed by disulfide binds which are denoted by a red broken line. Light blue portions of the intracellular domain of CD200R denotes tyrosine residues which can be phosphorylated during intracellular signalling. Dashed lines between receptor/ligands represent known interaction as detected in biochemical binding assays. Blue = structure known, Green = predicted structure based on homology to cellular CD200. Structural data was obtained from [112].

Gabrielle Stack, et al. Viruses. 2012 August;4(8):1182-1201.

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