Genetic Influence of PTPN22 R620W Polymorphism in Tuberculosis

Luis M. Gomez, Juan Manuel Anaya, Javier Martin

Resultado de la investigación: Contribución a RevistaArtículo

49 Citas (Scopus)

Resumen

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.
Idioma originalEnglish (US)
Páginas (desde-hasta)1242-1247
Número de páginas6
PublicaciónHuman Immunology
DOI
EstadoPublished - dic 1 2005

Huella dactilar

Tuberculosis
Tuberculin Test
Non-Receptor Type 22 Protein Tyrosine Phosphatase
Skin Tests
Mycobacterium tuberculosis
Alleles
Odds Ratio
Confidence Intervals
Autoimmunity
Pulmonary Tuberculosis
Gene Frequency
Causality
Immune System
T-Lymphocytes
Genes

Citar esto

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title = "Genetic Influence of PTPN22 R620W Polymorphism in Tuberculosis",
abstract = "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. {\circledC} 2006 American Society for Histocompatibility and Immunogenetics.",
author = "Gomez, {Luis M.} and Anaya, {Juan Manuel} and Javier Martin",
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Genetic Influence of PTPN22 R620W Polymorphism in Tuberculosis. / Gomez, Luis M.; Anaya, Juan Manuel; Martin, Javier.

En: Human Immunology, 01.12.2005, p. 1242-1247.

Resultado de la investigación: Contribución a RevistaArtículo

TY - JOUR

T1 - Genetic Influence of PTPN22 R620W Polymorphism in Tuberculosis

AU - Gomez, Luis M.

AU - Anaya, Juan Manuel

AU - Martin, Javier

PY - 2005/12/1

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N2 - 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.

AB - 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.

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