Impaired Natural Killer Cell Function in Multiple Sclerosis and Association With the Hla System

Benczúr, M.; Gyódi, É; Petrányi, G; Hollán, Susan R.; Pálffy, G; Tálas, Margarita; Stöger, I; Földeş, I

doi:10.1016/b978-0-12-341360-4.50181-5

Cited by 4 publications

(3 citation statements)

References 23 publications

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“…This effect was found mainly to occur in men, who had an inverse relationship between measures of natural killer activity and depression severity ( Evans et al, 1992 ). Diminished natural killer activity has also been observed in studies of cells from multiple sclerosis patients, with men having more reduced activity than women ( Benczur et al, 1980 ). Patients with multiple sclerosis are two to five times more likely to develop depression than someone without ( Feinstein et al, 2014 ).…”

Section: How Does the Innate Immune Response Contribute To Sex Differ...mentioning

confidence: 93%

Sex differences in depression: An immunological perspective

Kropp

Hodes

2023

Brain Research Bulletin

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Section: How Does the Innate Immune Response Contribute To Sex Differ...mentioning

confidence: 93%

Sex differences in depression: An immunological perspective

Kropp

Hodes

2023

Brain Research Bulletin

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“…These (5,26). It is interesting to note in this regard that impaired NK activity has been associated with several human neurological disorders, such as multiple sclerosis (29) and Alzheimer disease (30). Shared …”

Section: Resultsmentioning

confidence: 99%

Involvement of brain opiate receptors in the immune-suppressive effect of morphine.

Shavit¹,

Depaulis²,

Martin³

et al. 1986

Proc. Natl. Acad. Sci. U.S.A.

181

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We previously reported that a single systemic injection of a high dose of morphine (-20 mg/kg) transiently suppresses splenic natural killer cell cytotoxicity in rats. The present study examined the possibility that the immunesuppressive effect of morphine is mediated by opiate receptors in the brain. Supporting this hypothesis, we found that morphine (20 or 40 Ag) injected into the lateral ventricle suppressed natural killer cell activity to the same degree as a systemic dose higher by three orders of magnitude. This effect was blocked by an opiate antagonist, naltrexone. Natural killer cell activity was unaffected by systemic administration of N-methylmorphine, a morphine analogue that does not cross the blood-brain barrier. These data implicate opiate receptors in the brain in morphine-induced suppression of natural killer cell cytotoxicity. 7114The publication costs of this article were defrayed in part by page charge payment. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. §1734 solely to indicate this fact.

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“…52 Decreased numbers of NK cells with reduced cytotoxic function and increased capacity to produce IFN-g are found in blood from patients with active autoimmune diseases. [53][54][55][56] Yet, NK cells comprise one of the most prominent populations found in inflamed joints of patients with rheumatoid arthritis (RA), colocalizing with monocytes, DCs, and T cells. 10,57,58 Through the production of GM-CSF, the CD56 bright NK-cell subset derived from patients' synovial fluid is capable to trigger and maintain the in vitro differentiation of CD14 1 monocytes into "DC-like" cells.…”

Section: Discussionmentioning

confidence: 99%

Human NK cells prime inflammatory DC precursors to induce Tc17 differentiation

et al. 2020

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Adaptive immune responses are acknowledged to evolve from innate immunity. However, limited information exists regarding whether encounters between innate cells direct the generation of specialized T-cell subsets. We aim to understand how natural killer (NK) cells modulate cell-mediated immunity in humans. We found that human CD14+CD16− monocytes that differentiate into inflammatory dendritic cells (DCs) are shaped at the early stages of differentiation by cell-to-cell interactions with NK cells. Although a fraction of monocytes is eliminated by NK-cell–mediated cytotoxicity, the polarization of interferon-γ (IFN-γ) at the NKp30-stabilized synapses triggers a stable IFN-γ signature in surviving monocytes that persists after their differentiation into DCs. Notably, NK-cell–instructed DCs drive the priming of type 17 CD8+ T cells (Tc17) with the capacity to produce IFN-γ and interleukin-17A. Compared with healthy donors, this cellular network is impaired in patients with classical NK-cell deficiency driven by mutations in the GATA2 gene. Our findings reveal a previously unrecognized connection by which Tc17-mediated immunity might be regulated by NK-cell–mediated tuning of antigen-presenting cells.

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Impaired Natural Killer Cell Function in Multiple Sclerosis and Association With the Hla System

Cited by 4 publications

References 23 publications

Sex differences in depression: An immunological perspective

Sex differences in depression: An immunological perspective

Involvement of brain opiate receptors in the immune-suppressive effect of morphine.

Human NK cells prime inflammatory DC precursors to induce Tc17 differentiation

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