Evidence map›Paper›PMID 35967436›Full record

ReviewFrontiers in immunology2022

TCR-like antibodies targeting autoantigen-mhc complexes: a mini-review.

Ying Li, Wei Jiang, Elizabeth D Mellins

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
2.7field-weighted citation impact, top 10% 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

20 citing papers in PubMed, 1 synthesis or guideline pooled it, 20 citations in OpenAlex.

  1. Pooled it
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  6. Review
  7. Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. A general platform for targeting MHC-II antigens via a single loop.bioRxiv : the preprint server for biology · 2024
    Article
  13. Review
  14. Article
  15. Article
  16. Human leukocyte antigen and tumor immunotherapy (Review).International journal of oncology · 2023
    Review
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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

3 authors at 1 institution in 1 country.

Ying LiDepartment of Pediatrics, Divisions of Human Gene Therapy and Allergy, Immunology & Rheumatology, Stanford University School of Medicine, Stanford, CA, United States.
Wei JiangDepartment of Pediatrics, Divisions of Human Gene Therapy and Allergy, Immunology & Rheumatology, Stanford University School of Medicine, Stanford, CA, United States.
Elizabeth D MellinsDepartment of Pediatrics, Divisions of Human Gene Therapy and Allergy, Immunology & Rheumatology, Stanford University School of Medicine, Stanford, CA, United States.
Stanford University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

T cell receptors (TCRs) recognize peptide antigens bound to major histocompatibility complex (MHC) molecules (p/MHC) that are expressed on cell surfaces; while B cell-derived antibodies (Abs) recognize soluble or cell surface native antigens of various types (proteins, carbohydrates, etc.). Immune surveillance by T and B cells thus inspects almost all formats of antigens to mount adaptive immune responses against cancer cells, infectious organisms and other foreign insults, while maintaining tolerance to self-tissues. With contributions from environmental triggers, the development of autoimmune disease is thought to be due to the expression of MHC risk alleles by antigen-presenting cells (APCs) presenting self-antigen (autoantigen), breaking through self-tolerance and activating autoreactive T cells, which orchestrate downstream pathologic events. Investigating and treating autoimmune diseases have been challenging, both because of the intrinsic complexity of these diseases and the need for tools targeting T cell epitopes (autoantigen-MHC). Naturally occurring TCRs with relatively low (micromolar) affinities to p/MHC are suboptimal for autoantigen-MHC targeting, whereas the use of engineered TCRs and their derivatives (e.g., TCR multimers and TCR-engineered T cells) are limited by unpredictable cross-reactivity. As Abs generally have nanomolar affinity, recent advances in engineering TCR-like (TCRL) Abs promise advantages over their TCR counterparts for autoantigen-MHC targeting. Here, we compare the p/MHC binding by TCRs and TCRL Abs, review the strategies for generation of TCRL Abs, highlight their application for identification of autoantigen-presenting APCs, and discuss future directions and limitations of TCRL Abs as immunotherapy for autoimmune diseases.

Indexed as

AutoantigensAutoimmune DiseasesAntibodiesHistocompatibility AntigensHumansMajor Histocompatibility ComplexReceptors, Antigen, T-CellAntibodiesAutoantigensHistocompatibility AntigensReceptors, Antigen, T-Cellantigen-specific therapyautoantigen presentationautoimmune diseasesimmunotherapyTCR-like antibodies

Identifiers

PMID35967436
PMCPMC9363607
OpenAlexW4288034012

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.