Evidence map›Paper›PMID 26696796›Full record

ReviewTransfusion medicine and hemotherapy : offizielles Organ der Deutschen Gesellschaft fur Transfusionsmedizin und Immunhamatologie2015

New Insights in the Pathogenesis of Autoimmune Hemolytic Anemia.

Wilma Barcellini

Registry-linked trialAbstract readReview
In one paragraph

Review in Transfusion medicine and hemotherapy : offizielles Organ der Deutschen Gesellschaft fur Transfusionsmedizin und Immunhamatologie, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05711264 (Presence of Circulating CD4+CD28 Null T Helper Lymphocytes in Patients With Autoimmune Hemolytic Anemia.), which is not on this map. Cited by 78 papers.

0numbers the graph read from it
0cells of the map it votes in
78citing papers in PubMed
–field-weighted citation impact
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.

NCT05711264 unknown statusnot on this mapstarted 2023, after this paper: background citation

Presence of Circulating CD4+CD28 Null T Helper Lymphocytes in Patients With Autoimmune Hemolytic Anemia.

TypeobservationalSponsorAssiut UniversityRan2023 to 2025Enrolled46ConditionsAutoimmune Hemolytic Anemia
3 · Its place in the literature

Who cites it

78 citing papers in PubMed.

  1. Trial
  2. Trial
  3. Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Observational
  9. Targeting the Neonatal Fc Receptor in Autoimmune Diseases: Pipeline and Progress.BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy · 2025
    Review
  10. Article
  11. Cytopenias in Autoimmune Liver Diseases-A Review.Journal of clinical medicine · 2025
    Review
  12. A case of autoimmune haemolytic anaemia associated with mediastinal teratoma.Indian journal of thoracic and cardiovascular surgery · 2025
    Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. Article

18 more citing papers are in PubMed but not listed here.

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.

Wilma BarcelliniU.O. Oncoematologia, Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico, Milan, Italy.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autoimmune hemolytic anemia (AIHA) is caused by the increased destruction of red blood cells (RBCs) by anti-RBC autoantibodies with or without complement activation. RBC destruction may occur both by a direct lysis through the sequential activation of the final components of the complement cascade (membrane attack complex), or by antibody-dependent cell-mediated cytotoxicity (ADCC). The pathogenic role of autoantibodies depends on their class (the most frequent are IgG and IgM), subclass, thermal amplitude (warm and cold forms),as well as affinity and efficiency in activating complement. Several cytokines and cytotoxic mechanisms (CD8+ T and natural killer cells) are further involved in RBC destruction. Moreover, activated macrophages carrying Fc receptors may recognize and phagocyte erythrocytes opsonized by autoantibodies and complement. Direct complement-mediated lysis takes place mainly in the circulations and liver, whereas ADCC, cytotoxicity, and phagocytosis occur preferentially in the spleen and lymphoid organs. The degree of intravascular hemolysis is 10-fold greater than extravascular one. Finally, the efficacy of the erythroblastic compensatory response can greatly influence the clinical picture of AIHA. The interplay and relative burden of all these pathogenic mechanisms give reason for the great clinical heterogeneity of AIHAs, from fully compensated to rapidly evolving fatal cases.

Indexed as

AutoantibodiesAutoimmune hemolytic anemiaCytokines

Identifiers

PMID26696796
PMCPMC4678320

What OpenQuestion holds

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Read underepoch 390

Registered trials

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.