Results 71 to 80 of about 1,284,834 (277)
ABSTRACT Objective To identify inflammatory analytes in cerebrospinal fluid (CSF) and plasma associated with cognitive decline in cognitively normal (CN) older adults at risk for Alzheimer's disease (AD). Methods In a longitudinal study of 118 CN older adults (65–80 years, 54% APOE ε4, 26% preclinical AD), 1331 CSF and 1501 plasma analytes were ...
Jagan A. Pillai +13 more
wiley +1 more source
The human natural killer cell immune synapse [PDF]
Inhibitory killer Ig-like receptors (KIR) at the surface of natural killer (NK) cells induced clustering of HLA-C at the contacting surface of target cells. In this manner, inhibitory immune synapses were formed as human NK cells surveyed target cells. At target/NK cell synapses, HLA-C/KIR distributed into rings around central patches of intercellular ...
Davis, Daniel M. +5 more
openaire +2 more sources
The role of complement in synaptic degeneration
Synapse loss is an early event of many neurodegenerative diseases including Alzheimer?s disease and Parkinson?s disease. The causes and mechanisms that underpin synapse dysfunction and degeneration are poorly understood.
Malfa, Katya
core +1 more source
CD28, CTLA-4 and PD-L1, the three identified ligands for CD80/86, are pivotal positive and negative costimulatory molecules that, among other functions, control T cell motility and formation of immune synapse between T cells and antigen-presenting cells (
Nahzli Dilek +9 more
doaj +1 more source
Copine‐4 Paraneoplastic Autoimmune Encephalitis
ABSTRACT We characterize copine‐4 (CPNE4)‐IgG and report clinical associations. Among 844 samples with unclassified neural IgGs identified by mouse‐brain indirect immunofluorescence assay over 2 years, 5 samples (serum, 3; CSF, 2) from 3 patients produced a distinctive cerebrum‐restricted synaptic pattern.
Mimi S. Fang +12 more
wiley +1 more source
Tumours can escape immune destruction through the development of antigen loss variants and loss of antigen processing/presentation pathways thereby rendering them invisible to T cells.
Marian eNassef Kadry Naguib Roufaiel +2 more
doaj +1 more source
Investigation of Complement Activation and Cytokine Signatures in AQP4+ NMOSD, MOGAD, and MS
ABSTRACT Objective Aquaporin‐4‐IgG seropositive neuromyelitis optica spectrum disorder (AQP4+ NMOSD), myelin oligodendrocyte glycoprotein antibody‐associated disease (MOGAD), and multiple sclerosis (MS) are pathophysiologically distinct neuroinflammatory disorders. Complement activation is a major mechanism of injury in AQP4+ NMOSD, whereas its role in
Angeliki G. Filippatou +23 more
wiley +1 more source
Visualizing the Immune Synapse
T cells that interact with antigen-specific APCs an mount a wide spectrum of responses that range rom induction of cytokine production and proliferaion to induction of anergy, as defined by lack of roliferation and IL-2 secretion [1-3], and even to riggering programmed cell death [4-8].
openaire +1 more source
Investigative and clinical applications of synthetic immune synapses [PDF]
Abstract The immune synapse (IS) has emerged as a compelling model of cell–cell communication. This interface between a T cell and antigen‐presenting cell (APC) serves as a key point in coordinating the immune response.
Michael C, Milone, Lance C, Kam
openaire +2 more sources
Acute Endocrine Alterations After Traumatic Brain Injury and 6‐Month Functional Outcome
ABSTRACT Objective Acute multi‐axis endocrine alterations after traumatic brain injury (TBI) remain incompletely characterized. This study aimed to examine their temporal patterns and explore their associations with 6‐month functional outcome and early inflammatory markers.
Biao Xu +9 more
wiley +1 more source

