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http://purl.uniprot.org/citations/23638805http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/23638805http://www.w3.org/2000/01/rdf-schema#comment"

Background

The present study sought to investigate the association between HLA-A, HLA-B and HLA-DRB1 genes and susceptibility or resistance to the different clinical manifestations of American cutaneous leishmaniasis (ACL) in southern Brazil.

Methods

The sample consisted of 169 patients with a diagnosis of ACL and 270 healthy subjects for comparison. HLA-A, HLA-B and HLA-DRB1 were typed by PCR-SSO reverse dot blot.

Results

Results showed a trend towards susceptibility to cutaneous lesions for alleles HLA-DRB1*13 (P=0.0228; Pc=0.3420; OR=1.66; 95%CI=1.08 - 2.56), HLA-B*35 (P=0.0218; Pc=0.6758; OR=1.67; 95%CI=1.08 - 2.29) and HLA-B*44 (P=0.0290; Pc=0.8990; OR=1.67; 95%CI=1.05 - 2.64). Subjects with allele HLA-B*27 (P=0.0180; Pc=0.5580; OR=7.1111; 95%CI=1.7850 - 28.3286) tended towards susceptibility to mucocutaneous lesions, those with HLA-B*49 (P=0.0101; Pc=0.3131; OR=6.4000; 95%CI=1.8472 - 22.1743) to recurrent ACL, and HLA-B*52 (P=0.0044; Pc=0.1360; OR=12.61; 95%CI=3.08 - 51.66), to re-infection. Presence of HLA-B*45 (P=0.0107; Pc=0.3317) tended to provide protection against the cutaneous form of ACL. The most frequent haplotypes that may be associated with susceptibility to ACL were A*02 B*44 DRB1*07 (P = 0.0236) and A*24 B*35 DRB1*01 (P = 0.0236).

Conclusion

Some Class I and Class II HLA genes appear to contribute towards susceptibility to and protection against different clinical manifestations of ACL. Other genetic marker studies may contribute toward future prophylactic and therapeutic interventions in ACL."xsd:string
http://purl.uniprot.org/citations/23638805http://purl.org/dc/terms/identifier"doi:10.1186/1471-2334-13-198"xsd:string
http://purl.uniprot.org/citations/23638805http://purl.uniprot.org/core/author"Dos Santos M.C."xsd:string
http://purl.uniprot.org/citations/23638805http://purl.uniprot.org/core/author"Borelli S.D."xsd:string
http://purl.uniprot.org/citations/23638805http://purl.uniprot.org/core/author"Lonardoni M.V."xsd:string
http://purl.uniprot.org/citations/23638805http://purl.uniprot.org/core/author"Ribas A.D."xsd:string
http://purl.uniprot.org/citations/23638805http://purl.uniprot.org/core/author"Ribas-Silva R.C."xsd:string
http://purl.uniprot.org/citations/23638805http://purl.uniprot.org/core/author"Silveira T.G."xsd:string
http://purl.uniprot.org/citations/23638805http://purl.uniprot.org/core/author"da Silva W.V."xsd:string
http://purl.uniprot.org/citations/23638805http://purl.uniprot.org/core/date"2013"xsd:gYear
http://purl.uniprot.org/citations/23638805http://purl.uniprot.org/core/name"BMC Infect Dis"xsd:string
http://purl.uniprot.org/citations/23638805http://purl.uniprot.org/core/pages"198"xsd:string
http://purl.uniprot.org/citations/23638805http://purl.uniprot.org/core/title"Association between HLA genes and American cutaneous leishmaniasis in endemic regions of Southern Brazil."xsd:string
http://purl.uniprot.org/citations/23638805http://purl.uniprot.org/core/volume"13"xsd:string
http://purl.uniprot.org/citations/23638805http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/23638805
http://purl.uniprot.org/citations/23638805http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/23638805
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