Evidence map›Paper›PMID 24595881›Full record

ReviewClinical reviews in allergy & immunology2014

Unmet needs in autoimmunity and potential new tools.

Qianjin Lu

Abstract readReview
PubMed Publisher
In one paragraph

Review in Clinical reviews in allergy & immunology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.0field-weighted citation impact, top 23% 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

6 citing papers in PubMed, 12 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. The Inflammatory Response in Psoriasis: a Comprehensive Review.Clinical reviews in allergy & immunology · 2016
    Review
  5. Review
  6. Review
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

1 author at 1 institution in 1 country.

Qianjin LuDepartment of Dermatology, Hunan Key Laboratory of Medical Epigenetics, Second Xiangya Hospital, Central South University, #139 Renmin Middle Rd, Changsha, Hunan, 410011, People's Republic of China, qianlu5860@gmail.com.
Second Xiangya Hospital of Central South University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The term "autoimmunity" refers to a pathological condition in which the immunological tolerance of self-antigens is broken through, cross-reactive T cells are activated, and autoantibodies are produced by B cells. The intricate interplay among those aberrantly activated immune cells as well as inflammatory cytokines secreted by them contributes to the development of proinflammatory cascade which eventually leads to the occurrence of autoimmune diseases (AIDs) and organ damage. Autoimmune diseases occupy a broad spectrum of human diseases with more than 70 different disorders and afflict approximately 5-8 % of the world's population. AIDs can be categorized into organ-specific and systemic. Although the exact mechanism of AIDs remains elusive, it is generally believed that both genetic polymorphism and environmental exposure are involved in the development of AIDs. Aberrant epigenetic marks are also identified in patients with AIDs. In addition, dysregulation of innate immune system and molecular mimicry are indicated to play important roles in the initiation and maintenance of autoreactive inflammation. Based on the progress made in elucidating molecular mechanisms underlying AIDs, novel biomarkers for prediction, early diagnosis, prognosis and treatment response, and therapeutic strategies are proposed, which represents a promising future in the battle against AIDs. However, challenges remain regarding the clinical application of these potential new tools.

Indexed as

Autoimmune DiseasesAutoimmunityBiomarkersB-LymphocytesCytokinesEpigenesis, GeneticHistocompatibility Antigens Class IHistocompatibility Antigens Class IIHLA AntigensHumansImmune ToleranceImmunity, InnateImmunologic FactorsMolecular MimicryPolymorphism, GeneticT-LymphocytesBiomarkersCytokinesHistocompatibility Antigens Class IHistocompatibility Antigens Class IIHLA AntigensImmunologic Factors

Identifiers

PMID24595881
OpenAlexW2069234369

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.