RGD Reference Report - Cytokine gene polymorphisms and susceptibility to cutaneous leishmaniasis in Iranian patients. - Rat Genome Database

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Cytokine gene polymorphisms and susceptibility to cutaneous leishmaniasis in Iranian patients.

Authors: Kamali-Sarvestani, E  Rasouli, M  Mortazavi, H  Gharesi-Fard, B 
Citation: Kamali-Sarvestani E, etal., Cytokine. 2006 Aug;35(3-4):159-65. Epub 2006 Sep 6.
RGD ID: 8548800
Pubmed: PMID:16950634   (View Abstract at PubMed)
DOI: DOI:10.1016/j.cyto.2006.07.016   (Journal Full-text)

Cutaneous Leishmaniasis (CL) is one of the most prevalent clinical forms of leishmaniasis. Preliminary data suggest that cytokine gene polymorphisms can contribute to resistance or susceptibility to CL. Therefore, we investigated the association of functional polymorphisms in four cytokine genes with susceptibility to, and clinical outcome of CL. A total of 201 patients with self-healing cutaneous leishmaniasis (SCL) and 92 asymptomatic infected controls (AIC) from Fars province as well as 58 patients with chronic cutaneous leishmaniasis (CCL) and their 688 normal controls (normal Iranian population or NIP) who were collected from the different areas of Iran were included in the study. The allele-specific oligonucleotide polymerase chain reaction (ASO-PCR) or PCR-RFLP (restriction fragment length polymorphism) methods were used for genotyping. The frequency of TNF-alpha -308 G-->A and TNF-beta +252 G-->A gene polymorphisms were not different between studied groups. Distribution of IFN-gamma +874 A-->T and IL-4 -590 C-->T polymorphism were also compared between SCl or CCL patients and their controls. IFN-gamma +874 A-->T polymorphism was less common in CCL patients compared to the NIP (chi(2)=12.53, p=0.0019). Significant differences in frequency of IL-4 -590 C -->T polymorphism were also found between the SCL and AIC (chi(2)=8.64, p=0.003). In conclusion, our results suggest that functional genetic variants in the IL-4 promoter could influence the risk of developing CL while the polymorphism in the first intron of the IFN-gamma gene might influence the progression of disease towards CCL.



RGD Manual Disease Annotations    Click to see Annotation Detail View

  
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
LTAHumancutaneous leishmaniasis no_associationIAGP DNA:SNP:intron:252A>G (human)RGD 
LtaRatcutaneous leishmaniasis no_associationISOLTA (Homo sapiens)DNA:SNP:intron:252A>G (human)RGD 
LtaMousecutaneous leishmaniasis no_associationISOLTA (Homo sapiens)DNA:SNP:intron:252A>G (human)RGD 
TNFHumancutaneous leishmaniasis no_associationIAGP DNA:SNP:promoter:-308G>A (rs1800629) (human)RGD 
TnfRatcutaneous leishmaniasis no_associationISOTNF (Homo sapiens)DNA:SNP:promoter:-308G>A (rs1800629) (human)RGD 
TnfMousecutaneous leishmaniasis no_associationISOTNF (Homo sapiens)DNA:SNP:promoter:-308G>A (rs1800629) (human)RGD 

Objects Annotated

Genes (Rattus norvegicus)
Lta  (lymphotoxin alpha)
Tnf  (tumor necrosis factor)

Genes (Mus musculus)
Lta  (lymphotoxin A)
Tnf  (tumor necrosis factor)

Genes (Homo sapiens)
LTA  (lymphotoxin alpha)
TNF  (tumor necrosis factor)


Additional Information