According to a report studied by WHO, 2 billion people are infected with Mycobacterium tuberculosis and 8–12 million new cases occur each year, accounting for 2–3 million deaths annually [1]. Epidemiological studies

indicate that 5–10% of people infected with M. Tuberculosis will develop active tuberculosis [2]. Nowadays, the prevalence of tuberculosis is worse in China owing to the increasing number of mobile population, the aggravating environment and the transformed biology of bacilli. To date, several candidate genes have been associated with the onset of TB [3, 4]. Therefore, the candidate genes such as vitamin D receptor genes and others have provided PLX3397 purchase us the understanding of pulmonary tuberculosis (PTB) infection. Killer cell immunoglobulin-like receptor (KIR), a large group of polymorphic receptor expressed on NK cells and T cells, recognizing human leucocyte antigen (HLA) class I molecules and playing a pivotal

role in immune responses. KIR AZD2281 mouse haplotypes can be simplified into two distinct groups, A and B [5]. Group A haplotype has a fixed number of genes that encode inhibitory receptors with the exception of 2DS4, whereas group B has variable gene content including additional activating receptor genes (KIR2DS1, 2, 3, 5 and KIR3DS1) as well as two inhibitory receptors (KIR2DL2 and KIR2DL5). When this distinction is used, all individuals can be assigned to have 1 of 2 genotypes: A/A, which CYTH4 is homozygous for group A haplotype, or B/x, which includes A/B heterozygotes or B/B homozygotes. HLA class I is the most polymorphic region of the human genome. HLA class I genes are found at the A, B and C loci of chromosome 6 and have been shown to play an important role in controlling of infection [6]. In addition, HLA-C molecules are classified as either C1 group with Ser77Asn80 in the HLA H chain (HLA-Cw*01, HLA-Cw*03, HLA-Cw*07, HLA-Cw*08, HLA-Cw*12, HLA-Cw*14 and HLA-Cw*16) or C2 group with Asn77Lys80 in the H chain (HLA-Cw*02,

HLA-Cw*04, HLA-Cw*05, HLA-Cw*06, HLA-Cw*15, HLA-Cw*16, HLA-Cw*17 and HLA-Cw*18). KIR polymorphisms and allelic variation affect the KIR-HLA binding specificity and are linked to the outcome of diseases [7, 8]. The peptide-binding motif for HLA-Cw*0304 has been formally determined [9]. Recent genome-wide association research has indicated the significant role of HLA-Cw genes [10]. However, HLA-Cw alleles have been less well studied than their HLA-A and HLA-B counterparts. Although some effective measures have been taken to control this disease [11], the incidence of TB has recently re-emerged as a public health problem in many countries. To investigate the influence of KIR and HLA-Cw genes on the risk of PTB development, a case–control study was conducted in patients with PTB and controls by using sequence-specific primer polymerase chain reaction (SSP-PCR) method. Our findings provided a better understanding on the genetic diversity of KIR-HLA across patients with PTB. Patients group.