Evidence map›Paper›PMID 19300567›Full record

ArticleNeuropsychiatric disease and treatment2007

Mechanisms of over-activated innate immune system regulation in autoimmune and neurodegenerative disorders.

Zofia Blach-Olszewska, Jerzy Leszek

Open access · greenAbstract read
In one paragraph

Article in Neuropsychiatric disease and treatment, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
1.1field-weighted citation impact, top 20% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

28 citing papers in PubMed, 55 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Zofia Blach-OlszewskaInstitute of Immunology and Experimental Therapy Polish Academy of Sciences, Wrocław, Poland.
Jerzy Leszek
Ludwik Hirszfeld Institute of Immunology and Experimental Therapy · PL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Reactions of innate immunity include phagocytosis, the production and activity of cytokines, chemokines, and adhesion molecules, the killing of infected or changed cells by NK cells and complement activated by natural lectins, and the cytokine-dependent resistance of leukocytes to viral infection. All these mechanisms maintain innate immunity. Deficiency in this immunity is sometimes accompanied by frequent bacterial and viral infections. When innate immunity is permanently stimulated and the intensity of the reactions is stronger, these mechanisms may be directed against the host and subsequently stimulate acquired immunity (antibody and cellular immunity). A higher production of cytokines, oxidative stress, and a high production of NO accompany autoimmunity and neurodegeneration. The possible participation of innate immune receptors, cytokines, and other factors in the development of autoimmune and neurodegenerative diseases is discussed. The importance and possible role of blood-derived microglial cells in the prevention or elimination of amyloid deposits and plaque formation is described. A possible regulatory system, based on the presence of suppressors of cytokine signaling (SOCS), receptors of the Tyro-3 family, adenosine and adenosine phosphates, and IL-10, is reviewed. This review presents the mechanisms involved in the control of the innate immune response by microglia in the development of neurodegenerative disorders.

Indexed as

deficiency of innate immunityinnate immune reactionsneurodegenerative disordersover-stimulationregulation system

Identifiers

PMID19300567
PMCPMC2654796
OpenAlexW148096308

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.