FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2317233072> ?p ?o ?g. }

• W2317233072 abstract "Objective: To characterize novel mechanisms by which CD4 T cells can injure human oligodendrocytes, and identify these cells in patients with Multiple Sclerosis (MS). Background Destruction of oligodendrocytes is a fundamental hallmark of MS. Although CD4 T cells are considered important contributors to this immunopathology, the mechanisms involved are not completely resolved. In recent years, CD4 T cells that acquire NK-associated markers have been implicated in tissue destruction in other immunopathologies such as Crohns Disease. We investigated whether cytotoxic NKG2+ CD4 T cells were detected in MS patients and whether human adult oligodendrocytes express the recognized ligands. We studied whether these receptors were involved in the immune-mediated injury of oligodendrocytes. Design/Methods: Proportions of NKG2D/C+ CD4 T cells in the blood of MS patients versus healthy donors were analyzed using flow cytometry (FACS). Peripheral blood mononuclear cells (PBMCs) from human donors are activated with the lectin phytohemagglutinin (PHA) and stained for NKG2C, NKG2D, CD4. CD4 T cells isolated from these cultures are incubated with primary cultures of human adult oligodendrocytes, and then analyzed by FACS for effector functions. Immunohistochemistry was done on post-mortem CNS sections of MS patients. Results: Our studies show an increased proportion of cytotoxic NKG2D/C+ CD4 T cells in the blood of MS patients. These CD4 T cells expressed elevated levels of lytic enzymes. We have previously shown that inflamed human oligodendrocytes upregulate NKG2D ligands; we now show that they can also express NKG2C ligand (HLA-E) upon inflammatory conditions mimicking MS lesions. Our functional results show that blocking NKG2C and NKG2D on PHA-activated CD4 T cells decreases their cytotoxicity towards the oligodendrocytes. Our in situ studies show that these cells are detected in post-mortem CNS sections of MS patients. Conclusions: Our results demonstrate that activated human CD4 T cells can mediate injury to oligodendrocytes through acquired cytotoxic NK-associated receptors. Supported by: Multiple Sclerosis Society of Canada (MSSOC). Disclosure: Dr. Zaguia has nothing to disclose. Dr. Antel has received personal compensation for activities with Sanofi-Aventis Pharmaceuticals, Inc., Biogen Idec, Novartis, Serono, Inc., Genzyme Corporation, Teva Neuroscience, and GlaxoSmithKline. Dr. Antel has received personal compensation in an editorial capacity for Multiple Sclerosis. Dr. Antel has received research support from Novartis. Dr. Saikali has nothing to disclose. Dr. Arbour has nothing to disclose." @default.
• W2317233072 created "2016-06-24" @default.
• W2317233072 creator A5001868151 @default.
• W2317233072 creator A5063692826 @default.
• W2317233072 creator A5074910128 @default.
• W2317233072 creator A5090874208 @default.
• W2317233072 date "2012-04-22" @default.
• W2317233072 modified "2023-09-26" @default.
• W2317233072 title "NKG2 Receptors Acquired by Activated Human CD4 T Cells Are Involved in Oligodendrocyte Destruction in the Context of MS (P07.086)" @default.
• W2317233072 doi "https://doi.org/10.1212/wnl.78.1_meetingabstracts.p07.086" @default.
• W2317233072 hasPublicationYear "2012" @default.
• W2317233072 type Work @default.
• W2317233072 sameAs 2317233072 @default.
• W2317233072 citedByCount "0" @default.
• W2317233072 crossrefType "journal-article" @default.
• W2317233072 hasAuthorship W2317233072A5001868151 @default.
• W2317233072 hasAuthorship W2317233072A5063692826 @default.
• W2317233072 hasAuthorship W2317233072A5074910128 @default.
• W2317233072 hasAuthorship W2317233072A5090874208 @default.
• W2317233072 hasConcept C114684123 @default.
• W2317233072 hasConcept C134018914 @default.
• W2317233072 hasConcept C137061746 @default.
• W2317233072 hasConcept C153911025 @default.
• W2317233072 hasConcept C154317977 @default.
• W2317233072 hasConcept C167672396 @default.
• W2317233072 hasConcept C170493617 @default.
• W2317233072 hasConcept C202751555 @default.
• W2317233072 hasConcept C203014093 @default.
• W2317233072 hasConcept C2776985911 @default.
• W2317233072 hasConcept C2778609137 @default.
• W2317233072 hasConcept C2778867473 @default.
• W2317233072 hasConcept C2780640218 @default.
• W2317233072 hasConcept C2781462264 @default.
• W2317233072 hasConcept C529278444 @default.
• W2317233072 hasConcept C553184892 @default.
• W2317233072 hasConcept C55493867 @default.
• W2317233072 hasConcept C86803240 @default.
• W2317233072 hasConcept C8891405 @default.
• W2317233072 hasConcept C95444343 @default.
• W2317233072 hasConceptScore W2317233072C114684123 @default.
• W2317233072 hasConceptScore W2317233072C134018914 @default.
• W2317233072 hasConceptScore W2317233072C137061746 @default.
• W2317233072 hasConceptScore W2317233072C153911025 @default.
• W2317233072 hasConceptScore W2317233072C154317977 @default.
• W2317233072 hasConceptScore W2317233072C167672396 @default.
• W2317233072 hasConceptScore W2317233072C170493617 @default.
• W2317233072 hasConceptScore W2317233072C202751555 @default.
• W2317233072 hasConceptScore W2317233072C203014093 @default.
• W2317233072 hasConceptScore W2317233072C2776985911 @default.
• W2317233072 hasConceptScore W2317233072C2778609137 @default.
• W2317233072 hasConceptScore W2317233072C2778867473 @default.
• W2317233072 hasConceptScore W2317233072C2780640218 @default.
• W2317233072 hasConceptScore W2317233072C2781462264 @default.
• W2317233072 hasConceptScore W2317233072C529278444 @default.
• W2317233072 hasConceptScore W2317233072C553184892 @default.
• W2317233072 hasConceptScore W2317233072C55493867 @default.
• W2317233072 hasConceptScore W2317233072C86803240 @default.
• W2317233072 hasConceptScore W2317233072C8891405 @default.
• W2317233072 hasConceptScore W2317233072C95444343 @default.
• W2317233072 hasLocation W23172330721 @default.
• W2317233072 hasOpenAccess W2317233072 @default.
• W2317233072 hasPrimaryLocation W23172330721 @default.
• W2317233072 hasRelatedWork W1743472435 @default.
• W2317233072 hasRelatedWork W1983431609 @default.
• W2317233072 hasRelatedWork W1990869196 @default.
• W2317233072 hasRelatedWork W1994417017 @default.
• W2317233072 hasRelatedWork W2003670951 @default.
• W2317233072 hasRelatedWork W2015852374 @default.
• W2317233072 hasRelatedWork W2053228376 @default.
• W2317233072 hasRelatedWork W2082205336 @default.
• W2317233072 hasRelatedWork W2083233431 @default.
• W2317233072 hasRelatedWork W2092987441 @default.
• W2317233072 hasRelatedWork W2103249039 @default.
• W2317233072 hasRelatedWork W2135150353 @default.
• W2317233072 hasRelatedWork W2346692422 @default.
• W2317233072 hasRelatedWork W2379236828 @default.
• W2317233072 hasRelatedWork W2522102096 @default.
• W2317233072 hasRelatedWork W2587507365 @default.
• W2317233072 hasRelatedWork W2930525306 @default.
• W2317233072 hasRelatedWork W3097362772 @default.
• W2317233072 hasRelatedWork W3182167158 @default.
• W2317233072 hasRelatedWork W629276613 @default.
• W2317233072 isParatext "false" @default.
• W2317233072 isRetracted "false" @default.
• W2317233072 magId "2317233072" @default.
• W2317233072 workType "article" @default.