A literature search of databases (MEDLINE, PUBMED and OVID) between January 1998 and July 2010 was conducted using both MESH terms and the free text words ‘gene’ or ‘P2X7’ in combination with ‘tuberculosis’ in addition to manual searches of citations retrieved from relevant original studies and review articles and correspondence with researchers in this particular field of study. We corresponded with authors whether data on genotype frequencies were not available in their respective articles. For Kinase Inhibitor Library high throughput inclusion in this

analysis, respective studies had to be nonfamilial case–control studies and to provide information regarding the prevalence of P2X7 polymorphisms in tuberculosis patients and control subjects. All control subjects were ethnically matched with case groups. Another prerequisite was that sufficient data be available to calculate odds ratios (OR). HIV-positive patients were excluded

from the metaanalysis. Two investigators (J.X. and L.S) extracted data independently and reached a consensus on all conclusions. For each study, the characteristics of the individual research articles were collected, including author, year of publication, geographic location, gender distribution, mean age, type of tuberculosis, study size, diagnostic methods used to establish tuberculosis Atezolizumab in vivo infection, the techniques used for genotyping variants, DNA extraction methods, the frequency of the genotypes, consistency of genotype frequencies in Hardy–Weinberg equilibrium (HWE) in the control subjects and the source of the control subjects. We evaluated the risk-associated variant allele (1513 C) using the common allele (1513 A) as the reference and the protection-associated variant −762 C allele using the −762 T allele as the reference. Pooled ORs and their corresponding 95% confidence intervals 3-mercaptopyruvate sulfurtransferase (CI) were estimated using the fixed effects model (Mantel–Haenszel). The random effects model (DerSimonian and Laird) was performed when heterogeneity was present.

Because of the limited number of studies published to date, it was not possible to stratify and analyze data for P2X7 polymorphisms according to geographic location, ethnicity and types of tuberculosis, or to analyze publication bias using a funnel plot. We assessed HWE only in controls because cases may not be in HWE if there was an association between genotype and disease outcome. Statistical analysis was performed using revman software, version 5.0 (Cochrane). A P value <0.05 was considered statistically significant. We identified six studies published between 1998 and 2010 that fit our study criteria (Li et al., 2002; Fernando et al., 2007; Niño-Moreno et al., 2007; Mokrousov et al., 2008; Xiao et al., 2009; Sambasivan et al., 2010).