Evidence map›Paper›PMID 14668789›Full record

ArticleGenes and immunity2004

Leishmaniasis host response loci (lmr1-3) modify disease severity through a Th1/Th2-independent pathway.

C M Elso, L J Roberts, G K Smyth, R J Thomson, T M Baldwin, S J Foote, E Handman

Abstract readComparative Study
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In one paragraph

Article in Genes and immunity, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 89 papers.

0numbers the graph read from it
0cells of the map it votes in
89citing 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.

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

89 citing papers in PubMed.

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  13. DHFR2 RNA directly regulates dihydrofolate reductase and its expression level impacts folate one carbon metabolism.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
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  17. Review
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  20. Article

29 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

7 authors.

C M ElsoThe Walter and Eliza Hall Institute of Medical Research, Victoria, Australia.
L J Roberts
G K Smyth
R J Thomson
T M Baldwin
S J Foote
E Handman

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The severity of disease caused by infection with Leishmania major depends critically on the genetics of the host. Early induction of T helper (Th)1-type immune responses in the resistant C57BL/6 mice and Th2-type responses in the susceptible BALB/c mice are thought to determine cure or disease, respectively. We have previously mapped three host response loci in a genetic cross between C57BL/6 and BALB/c mice, and here we show definitively the involvement of these loci in disease severity using animals congenic for each of the loci. Surprisingly, in the late stage of infection when the difference in disease severity between congenic and parental mice was most pronounced, their cytokine profile correlated with the genetic background of the mice and not with the severity of disease. This indicates that the loci that we have mapped are acting by a mechanism independent of Th phenotype.

Indexed as

Leishmania majorPhenotypeAnimalsAnimals, CongenicCrosses, GeneticDisease Models, AnimalDNA PrimersFluorescenceGenetic LinkageGenotypeInterferon-gammaInterleukin-4Leishmaniasis, CutaneousMiceMice, Inbred BALB CMice, Inbred C57BLDNA PrimersInterferon-gammaInterleukin-4

Identifiers

What OpenQuestion holds

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Registered trials

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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.