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Warrington, Kenneth J.; Kent, Peter D.; Frye, Robert L.; Lymp, James; Kopecky, Stephen L.; Goronzy, Jörg J.; Weyand, Cornelia M.

doi:10.1186/ar1775

Cited by 123 publications

(22 citation statements)

References 38 publications

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“…A greater percentage of CD4+CD28– lymphocytes in this condition was accompanied by a faster pace of atherosclerosis. Concurrently, the risk of acute vascular episodes in such patients is now acknowledged to be higher [29, 30]. …”

Section: Discussionmentioning

confidence: 99%

Can We Talk about CD4+CD28– Lymphocytes as a Risk Factor for Ischemic Stroke?

Nowik

Nowacki²,

Grabarek³

et al. 2007

Eur Neurol

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Background: CD4+CD28– lymphocytes are implicated in the destabilization of atheromatous plaque, leading to acute coronary episodes. One may ask whether these cells play a similar role in ischemic stroke pathogenesis with an atherosclerotic background. Methods: Flow cytometry was applied to determine the percentage of CD4+CD28– lymphocytes in the peripheral blood of patients during the acute phase of their first ischemic stroke (group I) and in patients without a history of stroke but with two of the most important risk factors (hypertension, diabetes) for atherosclerosis-related ischemic stroke (group II). The results were compared with healthy controls. Results: The median percentages of CD4+CD28– lymphocytes in groups I and II did not differ significantly, but for each of these groups the percentage was higher than in the control group. The time of blood sampling from onset of stroke, presence of the ischemic focus in the CT brain scan and severity of neurological deficits did not correlate with the percentage of CD4+CD28– lymphocytes. Conclusions: We conclude that CD4+CD28– lymphocytes are implicated in mechanisms enhancing the risk of acute ischemic stroke and not a consequence of stroke.

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Section: Discussionmentioning

confidence: 99%

Can We Talk about CD4+CD28– Lymphocytes as a Risk Factor for Ischemic Stroke?

Nowik

Nowacki²,

Grabarek³

et al. 2007

Eur Neurol

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“…Similar to Th1 cells, an unusual subset of T cells that lack CD28 and secrete high levels of IFN-γ and TNF were suggested to modulate atherosclerosis in humans. [37][38][39] Unfortunately, CD4 + CD28 null T cells are not present in mice, and their contribution to disease cannot, therefore, be assessed by depletion or genetic experiments.…”

Section: Role Of Different T-cell Subtypes In Atherosclerosismentioning

confidence: 99%

Adaptive Response of T and B Cells in Atherosclerosis

Ketelhuth

Hansson

2016

Circulation Research

224

191

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“…Warrington and Coll consider RA as an independent risk of CV diseases mostly when seen at the coronary level. [14]. In Park study regarding 53 RA women patients without any prior CV conditions et 53 control case of the same age, exists a significative IMT increase in the PR group [15].…”

Section: Discussionmentioning

confidence: 99%

Accelerated Atherosclerosis in Takayasu Disease: Case-Control Study

Hatri¹,

Guermaz²,

Laroche³

et al. 2017

OJIM

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Aim: The aim of our study was to evaluate the atherosclerosis prevalence in Takayasu's disease. Patients We performed a measurement of the intima-media thickness (IMT) in carotid level and we looked for the presence of carotid, aortic and femoral atheroma. Results: We found more plaques of atheroma in the Takayasu group; the carotid intima-media thickness was significantly higher in the Takayasu group and the RA group compared with the control group. The mean IMT of the Takayasu group was 0.91 mm [±0.368]. It was 0.76 mm [±0.151] for the RA group. And 0.71 mm [±0.141] for the controls. (P: 0.000). CRP > 12 mg was identified as the most strongly associated with the development of accelerated atherosclerosis in Takayasu's disease and RA (p: 0.002) with an odds ratio of 14.5 (IC: 95%). Conclusion: The high prevalence of atherosclerosis discovered in Takayasu's disease is not explained by the traditional vascular risk factors. It is not also explained by the corticoids and immuno-suppression treatments. The systemic inflammation associated with parietal local inflammation, observed in Takayasu arteritis appears to be responsible of premature and accelerated atherosclerosis.

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Untitled

Cited by 123 publications

References 38 publications

Can We Talk about CD4+CD28– Lymphocytes as a Risk Factor for Ischemic Stroke?

Can We Talk about CD4+CD28– Lymphocytes as a Risk Factor for Ischemic Stroke?

Adaptive Response of T and B Cells in Atherosclerosis

Accelerated Atherosclerosis in Takayasu Disease: Case-Control Study

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