Genetic Influence of PTPN22 R620W Polymorphism in Tuberculosis

The PTPN22 gene codes for an intracellular lymphoid-specific phosphatase (Lyp) that has a negative regulatory effect on T-cell activation. Because Lyp is an important molecule involved in the inflammatory response, and its levels are increased in cells that participate in the immune response against...

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Autores:
Tipo de recurso:
Fecha de publicación:
2005
Institución:
Universidad del Rosario
Repositorio:
Repositorio EdocUR - U. Rosario
Idioma:
eng
OAI Identifier:
oai:repository.urosario.edu.co:10336/24216
Acceso en línea:
https://doi.org/10.1016/j.humimm.2005.11.008
https://repository.urosario.edu.co/handle/10336/24216
Palabra clave:
Protein
Protein tyrosine phosphatase nonreceptor 22 protein
Unclassified drug
Protein tyrosine phosphatase
Protein tyrosine phosphatase lyp
Protein-tyrosine phosphatase lyp
Adult
Antigen recognition
Article
Autoimmunity
Confidence interval
Controlled study
Dna polymorphism
Female
Gene frequency
Genetic analysis
Genetic code
Genetic predisposition
Genetic risk
Heredity
Human
Immune system
Lung tuberculosis
Major clinical study
Male
Mycobacterium tuberculosis
Priority journal
Randomization
Risk factor
Tuberculin test
Case control study
Colombia
Genetics
Immunology
Lung tuberculosis
Middle aged
Single nucleotide polymorphism
Adult
Case-control studies
Colombia
Female
Genetic predisposition to disease
Humans
Male
Middle aged
Mycobacterium tuberculosis
Protein-tyrosine-phosphatase
Autoimmunity
Delayed-type hypersensitivity
Ptpn22
Tuberculin skin test
Tuberculosis
pulmonary
single nucleotide
Polymorphism
Tuberculosis
Rights
License
Abierto (Texto Completo)
Description
Summary:The PTPN22 gene codes for an intracellular lymphoid-specific phosphatase (Lyp) that has a negative regulatory effect on T-cell activation. Because Lyp is an important molecule involved in the inflammatory response, and its levels are increased in cells that participate in the immune response against Mycobacterium tuberculosis, we hypothesized that the functional PTPN22 C1858T polymorphism could be a genetic factor predisposing to the development of tuberculosis (TB). Accordingly, we undertook an association study in which 113 patients with pulmonary TB and 161 matched healthy controls stratified by the tuberculin skin test (TST) were examined. Significant skewing was observed when T allele frequencies of patients with TB and all controls were compared (P = 0.04, odds ratio = 0.3; 95% confidence interval = 0.08-1.04) and frequencies of patients with TB and TST+ healthy controls were compared (P = 0.01, odds ratio = 0.2; 95% confidence interval = 0.05-0.79). No stratification was detected between patients and control samples. These results suggest that the T allele may be a factor protecting against development of TB once the immune system recognizes M. tuberculosis (i.e., TST+ individuals), whereas the C allele may be a risk factor for development of overt TB. The results also indicate that an association opposite that between the PTPN22 polymorphism and TB exists between TB and autoimmunity. © 2006 American Society for Histocompatibility and Immunogenetics.