title: Study of KIR expression and HLA ligands in CD56+ lymphocytes of drug resistant tuberculosis patients.
abstract: Analysis of receptor-ligand interactions in the context of diseases necessitates to understand how HLA-KIR genotypes function in diseases. Although CD56+ lymphocytes are derived from multiple lineages, they share a functional association with immunosurviellance and antimicrobial responses. The present study aimed to determine whether KIR phenotype in CD56 lymphocytes and corresponding HLA-class 1 ligands are associated with multidrug resistance tuberculosis (MDR-TB). We compared the frequencies of HLA-C and HLA-BW4 genes, the expression of KIRs 2DL1/2DS1, 2DL2/2DL3, 3DL1, and 2DS4 and the combinations of HLA/KIR in 32 Nifamycin and Isoniazid-resistant TB with those in 68 drug non resistant (NR) sputum smear positive pulmonary TB patients. PCR-SSP and flow cytometry were performed for HLA and KIRs typing, respectively. We showed no significant differences between inhibitory or activating KIRs as well as HLA ligands in MDR TB patients compared with NR-TB . The combinations of inhibitory KIR-HLA ligands in MDR-TB were much more prevalent, but not statistically significant than in NR patients (p=0.07). The frequency of MDR patients with all HLA-C and HLA-BW4 ligands was higher than NR-TB (p<0.009). Conversely, the percentage of MDR patients having only one kind of HLA gene was significantly lower than NR-TB (p<0.01). We conclude that the expression of inhibitory KIRs with corresponding HLA ligands genes, and/or co-existence of three HLA class 1 ligands for inhibitory KIRs may be associated with drug resistance in pulmonary tuberculosis.
authors: Department of Immunology, Tehran University of Medical Sciences, Tehran, Iran. tshabestari@sina.tums.ac.ir
authors: Tahereh
authors: T
authors: Mousavi
authors: Farhad
authors: F
authors: Shahsavar
authors: Parisa
authors: P
authors: Farnia
authors: Nader
authors: N
authors: Tajik
authors: Mahbubeh
authors: M
authors: Soofi
mesh_terms: D019002:CD56 Antigen / Q000276:immunology / Q000378:metabolism; D005434:Flow Cytometry; D020022:Genetic Predisposition to Disease / Q000235:genetics*; D006680:HLA Antigens / Q000235:genetics* / Q000276:immunology; D006801:Humans; D007694:Killer Cells, Natural / Q000276:immunology* / Q000378:metabolism; D008024:Ligands; D055611:Natural Killer T-Cells / Q000276:immunology / Q000378:metabolism; D054340:Receptors, KIR / Q000096:biosynthesis / Q000235:genetics* / Q000276:immunology; D018088:Tuberculosis, Multidrug-Resistant / Q000235:genetics* / Q000276:immunology / Q000378:metabolism
chemical_list: D019002:CD56 Antigen; D006680:HLA Antigens; D008024:Ligands; D054340:Receptors, KIR