Evidence map›Paper›PMID 20083664›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2010

Cyclophosphamide induces dynamic alterations in the host microenvironments resulting in a Flt3 ligand-dependent expansion of dendritic cells.

Mohamed L Salem, Amir A Al-Khami, Sabry A El-Naggar, C Marcela Díaz-Montero, Yian Chen, David J Cole

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
3.3field-weighted citation impact, top 7% 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

36 citing papers in PubMed, 63 citations in OpenAlex.

  1. Trial
  2. Article
  3. Review
  4. Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Ferulic Acid against Cyclophosphamide-Induced Heart Toxicity in Mice by Inhibiting NF-κB Pathway.Evidence-based complementary and alternative medicine : eCAM · 2016
    Article
  16. Article
  17. Article
  18. Review
  19. Chemoimmunotherapy: reengineering tumor immunity.Cancer immunology, immunotherapy : CII · 2013
    Review
  20. Article
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

6 authors at 3 institutions in 2 countries.

Mohamed L SalemDepartment of Surgery, Hollings Cancer Center, Medical University of South Carolina, Charleston, SC 29425, USA. salemm@musc.edu
Amir A Al-Khami
Sabry A El-Naggar
C Marcela Díaz-Montero
Yian Chen
David J Cole
Medical University of South Carolina · USTanta University · EGUniversity of Miami · US

Funding

Targeting Early Activated T cells for Adoptive TherapyR01CA083672 · NCI · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI COLE, DAVID J · 2001 to 2010
$2.8M
NCI NIH HHS 1 R01 CA94856-01NCI NIH HHS R01 CA083672
6 · The paper itself

Abstract

Preconditioning a recipient host with lymphodepletion can markedly augment adoptive T cell therapy. However, the precise mechanisms involved are poorly understood. In a recent study, we observed a significant increase in the circulating levels of dendritic cells (DCs; CD11c(+)CD11b(+)) during the recovery from cyclophosphamide (CTX)-induced lymphodepletion. Herein, we demonstrate that the CTX-induced DC expansion was not altered by adjuvant chemotherapy or tumor burden but was augmented by coadministration of granulocyte-colony stimulating factor. Although the increase in the number of DCs was preceded by a systemic expansion of a population expressing the phenotype of myeloid-derived suppressor cells (Gr-1(+)CD11b(+)), depletion of these Gr-1(+) cells had no effect on the noted expansion. Moreover, when Gr-1(high)CD11b(high) cells were sorted from CTX-treated mice and adoptively transferred into control or CTX-treated recipients, they did not differentiate into DCs. Post-CTX expansion of DCs was associated with proliferation of DCs in bone marrow (BM) during the lymphopenic phase and in the blood and spleen during the recovery phase. Furthermore, adoptive transfer of BM cells from CTX-treated mice produced equal numbers of DCs in the blood of either CTX-treated or untreated recipients. CTX induced a dynamic surge in the expression of growth factors and chemokines in BM, where CCR2 and Flt3 signaling pathways were critical for DC expansion. In sum, our data suggest that CTX induces proliferation of DCs in BM prior to their expansion in the periphery. Targeting DCs at these phases would significantly improve their contribution to the clinical application of lymphodepletion to adoptive immunotherapy.

Indexed as

Cell ProliferationAdoptive TransferAnimalsCD11b AntigenCell Line, TumorCyclophosphamideDendritic CellsLeukopeniaLigandsLymphocyte DepletionMelanoma, ExperimentalMembrane ProteinsMiceMice, Inbred BALB CMice, Inbred C57BLMice, KnockoutCD11b AntigenCyclophosphamideflt3 ligand proteinGr-1 protein, mouseLigandsMembrane ProteinsReceptors, Chemokine

Identifiers

PMID20083664
PMCPMC3066076
OpenAlexW2140723264

What OpenQuestion holds

Textmetadata
LicenceTDM
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.