Publications by authors named "Negar Farzam-Kia"
Human monocytes and macrophages are two major myeloid cell subsets with similar and distinct functions in tissue homeostasis and immune responses. GM-CSF plays a fundamental role in myeloid cell differentiation and activation. Hence, we compared the effects of GM-CSF on the expression of several immune mediators by human monocytes and monocyte-derived macrophages obtained from healthy donors.
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- - The study investigates changes in T lymphocytes related to multiple sclerosis (MS) and focuses on the NKG2D pathway, which is crucial for CD4 and CD8 T cell activation, revealing that its activity varies across different forms of MS (RRMS, SPMS, and PPMS).
- - Using flow cytometry and microscopy, researchers found that NKG2D T lymphocytes are less abundant in RRMS patients compared to healthy controls, and their proportion decreases with age in PPMS patients due to reduced γδ and αβ CD4CD8 populations.
- - Blocking NKG2D in co-cultured CD8 T lymphocytes and astrocytes resulted in increased mobility and a shift from long-lasting
Article Synopsis
- GM-CSF plays a significant role in chronic inflammatory diseases like multiple sclerosis (MS) by affecting myeloid cell functions, specifically monocyte-derived macrophages (MDMs) and microglia.
- The study found that GM-CSF increases IL-15 expression in MDMs from both healthy individuals and MS patients, as well as in human microglia, which may enhance the immune response against MS.
- Notably, while GM-CSF-stimulated MDMs elevate CD8 T lymphocytes' production of effector molecules, this enhancement occurs independently of IL-15, suggesting that GM-CSF influences myeloid cells through multiple pathways.
Article Synopsis
- Interleukin-27 (IL-27) can cause both pro-inflammatory and anti-inflammatory effects and is found at higher levels in the central nervous system of multiple sclerosis (MS) patients, but its specific role in neuroinflammation is not fully understood.
- * The study investigates how astrocytes respond to IL-27 and how this affects their interaction with activated T lymphocytes under both inflamed and non-inflamed conditions.
- * Results show that IL-27 exposure leads to increased immune-related gene expression in astrocytes, enhances the secretion of certain chemokines, and alters the activation status and motility of CD8 T lymphocytes, suggesting more dynamic interactions between these cells in the context of inflammation.
Article Synopsis
- Multiple sclerosis (MS) involves damage to myelin and oligodendrocytes (cells that produce myelin) in the central nervous system, with Th17 cells being particularly harmful to these OLs.
- Research utilized live imaging and single-cell RNA sequencing to show that Th17 cells interact more aggressively with OLs than Th2 cells, leading to the production of pro-inflammatory molecules and increased cell death.
- The study confirmed that granzyme B, which is secreted by Th17 cells during direct contact, contributes to oligodendrocyte death, illustrating a critical mechanism in MS progression.
Stress Signal ULBP4, an NKG2D Ligand, Is Upregulated in Multiple Sclerosis and Shapes CD8 T-Cell Behaviors.
Neurol Neuroimmunol Neuroinflamm
January 2022
Background And Objectives: We posit the involvement of the natural killer group 2D (NKG2D) pathway in multiple sclerosis (MS) pathology via the presence of specific NKG2D ligands (NKG2DLs). We aim to evaluate the expression of NKG2DLs in the CNS and CSF of patients with MS and to identify cellular stressors inducing the expression of UL16-binding protein 4 (ULBP4), the only detectable NKG2DL. Finally, we evaluate the impact of ULBP4 on functions such as cytokine production and motility by CD8 T lymphocytes, a subset largely expressing NKG2D, the cognate receptor.
View Article and Find Full Text PDFTo fully perform their functions, T lymphocytes migrate within organs' parenchyma and interact with local cells. Infiltration of T lymphocytes within the central nervous system (CNS) is associated with numerous neurodegenerative disorders. Nevertheless, how these immune cells communicate and respond to neural cells remains unresolved.
View Article and Find Full Text PDFObjectives: Pro- and anti-inflammatory properties have been attributed to interleukin-27 (IL-27). Nevertheless, the impact of this cytokine on chronic inflammatory diseases such as multiple sclerosis (MS) remains ill-defined. We investigated the biology of IL-27 and its specific receptor IL-27Rα in MS patients.
View Article and Find Full Text PDFBackground: The symptoms of multiple sclerosis (MS) can be diverse, complex, and progressive, creating a need for frequent and long-standing health care services. The purpose of this scoping review was to identify the barriers people with MS encounter when attempting to access multidisciplinary health services and the reported facilitators for better access to health services.
Methods: The MEDLINE, Embase, and CINAHL databases were searched, without date or geographic restrictions, using the following terms: and .
Dysregulated immune profiles have been described in symptomatic patients infected with SARS-CoV-2. Whether the reported immune alterations are specific to SARS-CoV-2 infection or also triggered by other acute illnesses remains unclear. We performed flow cytometry analysis on fresh peripheral blood from a consecutive cohort of (a) patients hospitalized with acute SARS-CoV-2 infection, (b) patients of comparable age and sex hospitalized for another acute disease (SARS-CoV-2 negative), and (c) healthy controls.
View Article and Find Full Text PDFInterleukin-15 enhances proinflammatory T-cell responses in patients with MS and EAE.
Neurol Neuroimmunol Neuroinflamm
January 2021
Objective: We posit that interleukin-15 (IL-15) is a relevant contributor to MS pathobiology as this cytokine is elevated in the CNS and periphery of patients with MS. We aim to investigate (1) the impact of IL-15 on T lymphocytes from patients with MS and (2) the in vivo role of IL-15 using the experimental autoimmune encephalomyelitis (EAE) mouse model.
Methods: We compared the impact of IL-15 on T lymphocytes obtained from untreated patients with MS (relapsing-remitting, secondary progressive, and primary progressive) to cells from age/sex-matched healthy controls (HCs) using multiparametric flow cytometry and in vitro assays.