2017
DOI: 10.1016/j.semarthrit.2017.02.005
|View full text |Cite
|
Sign up to set email alerts
|

No detection of varicella-zoster virus in temporal arteries of patients with giant cell arteritis

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
1
1
1
1

Citation Types

0
16
0
1

Year Published

2017
2017
2023
2023

Publication Types

Select...
6
3

Relationship

0
9

Authors

Journals

citations
Cited by 36 publications
(17 citation statements)
references
References 28 publications
0
16
0
1
Order By: Relevance
“… 3 5 , 15 However, with the exception of Mitchell and Font, 16 other investigators have not found substantial VZV in the arterial specimens of biopsy-proven GCA or clinically diagnosed GCA. 17 22 False positive immunohistochemistry from antibody cross-reactivity to shared epitopes between VZV proteins and arterial smooth muscle elements suggest caution when interpreting pathology findings. 23 Gilden and Nagel acknowledge that “the presence of VZV in about 20% of temporal artery biopsies from non-GCA post-mortem controls also suggests that VZV alone is not sufficient to produce disease”.…”
Section: Discussionmentioning
confidence: 99%
“… 3 5 , 15 However, with the exception of Mitchell and Font, 16 other investigators have not found substantial VZV in the arterial specimens of biopsy-proven GCA or clinically diagnosed GCA. 17 22 False positive immunohistochemistry from antibody cross-reactivity to shared epitopes between VZV proteins and arterial smooth muscle elements suggest caution when interpreting pathology findings. 23 Gilden and Nagel acknowledge that “the presence of VZV in about 20% of temporal artery biopsies from non-GCA post-mortem controls also suggests that VZV alone is not sufficient to produce disease”.…”
Section: Discussionmentioning
confidence: 99%
“…Activation of these cells by pathogen‐associated molecular patterns or damage‐associated molecular patterns, including ligands for Toll‐like receptors, may trigger the initial inflammatory response, resulting in chemokine‐mediated migration of immune cells via the vasa vasorum . Although it has been suggested that varicella zoster virus might be directly involved in the development of GCA , a growing number of studies strongly dispute this notion . DCs stimulate T cells with their cognate peptides bound to class II major histocompatibility molecules, costimulatory molecules (i.e., CD80/CD86), and cytokines.…”
Section: Evidence For Distinct Gca Subsets Based On Immunologic Featuresmentioning
confidence: 99%
“…Arch Rheumatol 2018;33(4):494-495. support the hypothesis of the GCA development after VZV reactivation. 4,5 Contrary to these studies, VZV antigen was detected in temporal arteries of patients with GCA in a study. 6 Another study reported that VZV is a risk factor for the development of GCA.…”
Section: Citationmentioning
confidence: 63%