Evidence map›Paper›PMID 31130955›Full record

ReviewFrontiers in immunology2019

Survival of Long-Lived Plasma Cells (LLPC): Piecing Together the Puzzle.

Shivana M Lightman, Adam Utley, Kelvin P Lee

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 130 papers.

0numbers the graph read from it
0cells of the map it votes in
130citing papers in PubMed
8.9field-weighted citation impact, top 2% 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

130 citing papers in PubMed, 196 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Resetting immunometabolic set points in autoimmune disease.Journal of translational autoimmunity · 2026
    Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Transient prophylactic immunosuppression with abatacept or dasatinib prevents immune responses in AAV gene transfer.Molecular therapy : the journal of the American Society of Gene Therapy · 2026
    Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Extending ImmunoSpotVaccines · 2026
    Article
  17. Why are long-lived plasma cells long-lived?Frontiers in immunology · 2026
    Review
  18. Review
  19. Review
  20. Article

70 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

3 authors at 1 institution in 1 country.

Shivana M LightmanDepartment of Immunology, Roswell Park Comprehensive Cancer Center, Buffalo, NY, United States.
Adam UtleyDepartment of Immunology, Roswell Park Comprehensive Cancer Center, Buffalo, NY, United States.
Kelvin P LeeDepartment of Immunology, Roswell Park Comprehensive Cancer Center, Buffalo, NY, United States.
Roswell Park Comprehensive Cancer Center · US

Funding

CD28-mediated Regulation of Multiple Myeloma Cell Proliferation and SurvivalR01CA121044 · NCI · ROSWELL PARK CANCER INSTITUTE CORP · PI LEE, KELVIN P. · 2007 to 2023
$4.8M
MULTIDISCIPLINARY APPROACHES TUMOR IMMUNOLOGYT32CA085183 · NCI · ROSWELL PARK CANCER INSTITUTE CORP · PI Scott I. Abrams · 2001 to 2026
$3.1M
Durable humoral immunity regulated by intrinsic CD28 function in plasma cellsR01AI100157 · NIAID · ROSWELL PARK CANCER INSTITUTE CORP · PI LEE, KELVIN P. · 2013 to 2016
$2.0M
NCI NIH HHS R01 CA121044NCI NIH HHS T32 CA085183NIAID NIH HHS R01 AI100157
6 · The paper itself

Abstract

Durable humoral immunity is dependent upon the generation of antigen-specific antibody titers, produced by non-proliferating bone marrow resident long-lived plasma cells (LLPC). Longevity is the hallmark of LLPC, but why and how they survive and function for years after antigen exposure is only beginning to be understood. LLPC are not intrinsically long-lived; they require continuous signals from the LLPC niche to survive. Signals unique to LLPC survival (vs. PC survival in general) most notably include those that upregulate the anti-apoptotic factor Mcl-1 and activation of the CD28 receptor expressed on LLPC. Other potential factors include expression of BCMA, upregulation of the transcription factor ZBTB20, and upregulation of the enzyme ENPP1. Metabolic fitness is another key component of LLPC longevity, facilitating the diversion of glucose to generate pyruvate during times of stress to facilitate long term survival. A third major component of LLPC survival is the microenvironment/LLPC niche itself. Cellular partners such as stromal cells, dendritic cells, and T regulatory cells establish a niche for LLPC and drive survival signaling by expressing ligands such as CD80/CD86 for CD28 and producing soluble and stromal factors that contribute to LLPC longevity. These findings have led to the current paradigm wherein both intrinsic and extrinsic mechanisms are required for the survival of LLPC. Here we outline this diverse network of signals and highlight the mechanisms thought to regulate and promote the survival of LLPC. Understanding this network of signals has direct implications in increasing our basic understanding of plasma cell biology, but also in vaccine and therapeutic drug development to address the pathologies that can arise from this subset.

Indexed as

AnimalsB-Lymphocyte SubsetsHumansPlasma CellsTranscriptomehumoral responseslong-lived plasma cells (LLPC)plasma cell functionplasma cell nicheplasma cell survival

Identifiers

PMID31130955
PMCPMC6510054
OpenAlexW2943547273

What OpenQuestion 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 OpenQuestion graph.