Evidence map›Paper›PMID 18188454›Full record

ArticleThe Journal of clinical investigation2008

Pathogen-imposed skewing of mouse chemokine and cytokine expression at the infected tissue site.

Shoshana D Katzman, Deborah J Fowell

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

27 citing papers in PubMed, 47 citations in OpenAlex.

  1. More than malaria: ExploringCurrent research in parasitology & vector-borne diseases · 2026
    Review
  2. Review
  3. Article
  4. CXCL10Cell reports · 2021
    Article
  5. In-situ immune profile of polymorphic vs. macular Indian Post Kala-azar dermal leishmaniasis.International journal for parasitology. Drugs and drug resistance · 2019
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. Article
  16. Mechanisms of immune evasion in leishmaniasis.Advances in applied microbiology · 2013
    Article
  17. Article
  18. Article
  19. Article
  20. 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

2 authors at 1 institution in 2 countries.

Shoshana D KatzmanDavid H. Smith Center for Vaccine Biology and Immunology, Aab Institute of Biomedical Sciences, Department of Microbiology and Immunology, University of Rochester, Rochester, New York 14642, USA.
Deborah J Fowell
Institute of Biomedical Science · GB

Funding

The T32 Predoctoral Training Program in Immunology (PTPI)T32AI007285 · NIAID · UNIVERSITY OF ROCHESTER · PI Scott Andrew Gerber, JACQUES Robert · 1986 to 2026
$7.6M
Remodeling of Lymph Node-Derived Cytokine Responses at the Infected Tissue SiteR01AI072690 · NIAID · UNIVERSITY OF ROCHESTER · PI FOWELL, DEBORAH J · 2008 to 2020
$3.6M
The Role of Itk in Th DifferentiationR01AI050201 · NIAID · UNIVERSITY OF ROCHESTER · PI FOWELL, DEBORAH J · 2001 to 2005
$1.6M
NIAID NIH HHS R01 AI050201NIAID NIH HHS R01-AI50201NIAID NIH HHS T32-AI07285
6 · The paper itself

Abstract

Compartmentalization of immunity ensures tight regulation of T cell activation in the LN and precise effector T cell delivery to inflamed sites. Herein we show that the tissue-specific accumulation of effector T cells can be subverted by a pathogen at the infection site. Using the Leishmania major mouse model of dermal infection, we observed a restricted chemokine profile at the infection site, i.e., the expression of Th2 cell-attracting CCL7 but not of Th1 cell-attracting chemokines. Consistent with these chemokine expression data, recruitment of cytokine-producing T cells to the infection site was also selective. Both IL-4- and IFN-gamma-producing effector T cells homed to inflamed OVA/CFA-immunized dermis, but only IL-4-producing cells homed to L. major-infected dermis. The narrowing of the cytokine repertoire at the site of infection with L. major was driven, in part, by pathogen-induced CCL7. Inflammatory signals failed to disrupt the early restrictive L. major infection site, which suggests that L. major dominantly modifies the local milieu. We have highlighted an emerging principle in pathogen-host interactions: that the cytokine repertoire at the infection site and the LN draining the infection site can be different because of the ability of the pathogen to modify the chemokine profile at the infection site. Thus, pathogens may edit the LN cytokine repertoire through differential recruitment of cytokine-producing cells.

Indexed as

Leishmania majorAnimalsChemokinesCytokinesDisease Models, AnimalHost-Pathogen InteractionsLeishmaniasis, CutaneousLymph NodesMiceMice, Inbred StrainsTh1 CellsTh2 CellsChemokinesCytokines

Identifiers

PMID18188454
PMCPMC2176190
OpenAlexW1989356573

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.