PECAM-1 Is Down-Regulated in γδT Cells during Remission, but Up-Regulated in Relapse of Multiple Sclerosis

Abstract

Introduction. PECAM-1 and NKRP1A are both involved in the vascular transmigration of T lymphocytes. Vascular transmigration is a crucial process in multiple sclerosis pathogenesis. Methods and aim. The current paper presents an analysis of PECAM-1 and NKRP1A expression on γδ T cells. Expression of PECAM-1 and NKRP1A on subsets of γδ T cells was performed with flow cytometry. Results. Based on the flow cytometry data, PECAM1 was slightly differentially modulated on γδ T cells—it was up-regulated during relapse, but down-regulated during remission. Moreover, a significant downregulation of CD3 expression was noted on γδ T cells from MS patients, most notably during relapse. Conclusions. This may be a sign of the overall activation of γδ T cells in the course of multiple sclerosis.

Elevated Levels of Serum Biomarkers Associated with Damage to the CNS Neurons and Endothelial Cells Are Linked with Changes in Brain Connectivity in Breast Cancer Patients with Vestibulo-Atactic Syndrome

“…Thus, several studies have reported a significant increase in the levels of soluble ICAM-1 molecules in patients with vascular cognitive impairment and Alzheimer’s disease, attributing the marker elevation to neuroinflammation and cerebrovascular dysfunction [ 40 , 41 ]. Another molecule of the immunoglobulin superfamily, PECAM-1, also participates in neuroinflammation, showing its prognostic potential in such clinical conditions as stroke and the relapse of multiple sclerosis [ 42 , 43 , 44 ]. NSE, an isoenzyme of the glycolytic enzyme enolase, can also be employed as a marker for ischemic stroke, intracranial hemorrhage, and traumatic brain injury, indicating changes in neuronal activity [ 45 , 46 ].…”

Multiple Sclerosis: Diagnosis, Management, and Future Opportunities

“…Last but not least, two papers [23,24] in this Special Issue focused on molecular research to better understand the pathogenetic mechanisms of MS. The study designed by Barac and colleagues [23] aimed to assess the potential contribution in MS susceptibility of polymorphisms of IL-27 and IL-23 genes, both modulators of T-helper 17 (Th17) cell activity.…”

“…In contrast, SNPIL-23-R381Q conferred a lower likelihood of MS according to a codominant model of inheritance and the allelic model. Zarobkiewicz et al [24] investigated the role of the platelet endothelial cell-adhesion molecule (PECAM-1/CD31), a protein involved in several mechanisms such as leukocyte transmigration, apoptosis, angiogenesis and many others. In MS patients, the expression of PECAM-1 is up-regulated in serum, plasma and cerebrospinal fluid and may also be involved in stabilizing the blood-brain barrier.…”