Research Article The -938C>A Polymorphism in MYD88 Is Associated with Susceptibility to Tuberculosis: A Pilot Study Kalliopi Aggelou, 1,2 Elena Konstantina Siapati, 2 Irini Gerogianni, 1 Zoe Daniil, 1 Konstantinos Gourgoulianis, 1 Ioannis Ntanos, 2 Emmanouel Simantirakis, 3 Elias Zintzaras, 4 Vassiliki Mollaki, 5,6 and George Vassilopoulos 3,7 1 Department of Respiratory Medicine, University of Tessaly Medical School, Larissa, Greece 2 9th Department for Chest Diseases, “Sotiria” Hospital, Athens, Greece 3 Cell and Gene Terapy Laboratory, Center for Basic Research II, Biomedical Research Foundation of the Academy of Athens, Athens, Greece 4 Department of Biomathematics, University of Tessaly School of Medicine, Larissa, Greece 5 Hellenic National Bioethics Committee, Athens, Greece 6 Department of Medical Laboratories, Faculty of Health and Caring Professions, Technological Educational Institution of Athens, Athens, Greece 7 Division of Haematology, University of Tessaly Medical School, Larissa, Greece Correspondence should be addressed to George Vassilopoulos; gvasilop@bioacademy.gr Received 1 September 2016; Revised 11 November 2016; Accepted 23 November 2016 Academic Editor: Marco E. M. Peluso Copyright © 2016 Kalliopi Aggelou et al. Tis is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Introduction. Tuberculosis (TB) is a major disease worldwide, caused by Mycobacterium tuberculosis (MTB) infection. Te Toll- Like Receptor (TLR) pathway plays a crucial role in the recognition of MTB. Aim. Te present study aimed to investigate the involvement of myeloid diferentiation primary response protein 88 (MYD88) gene polymorphisms in TB. Materials and Methods. A total of 103 TB cases and 92 control subjects were genotyped for the MYD88 -938C>A (rs4988453) and 1944C>G (rs4988457) polymorphisms. Results. Te MYD88 -938CA and -938AA genotypes were associated with an increased risk for tuberculosis with odds ratio (OR) of 5.71 (95% confdence intervals [CIs] 2.89–11.28,  = 0.01). Conclusions. Te MYD88 -938C>A genetic polymorphism is associated with increased susceptibility to TB and may serve as a marker to screen individuals who are at risk. 1. Introduction Tuberculosis (TB) is a chronic, usually airborne, infectious disease caused mainly by Mycobacterium tuberculosis, Mtb. TB is responsible for approximately 1.5 million deaths per year [1]. Afer inhalation of infected aerosols into the host lungs, mycobacteria frst encounter the alveolar macrophages and get phagocytosed. Mycobacteria that escape the ini- tial intracellular destruction can multiply and disrupt the macrophage. Tis results in further chemokine release and recruitment of monocytes and other infammatory cells to the site. However, Mtb inhibit phagosome maturation in macrophages and, along with lysosomal fusion, they can survive intracellularly [2]. Two to three weeks afer infection, antigen-specifc T lymphocytes are recruited at the early lesions (tubercles) and release proinfammatory cytokines such as interferon- (IFN-), in a second attempt to activate macrophages and kill the intracellular mycobacteria. Tis results in the formation of a granuloma which is a structure consisting of macrophages, epithelioid cells (diferentiated macrophages), and multinucleated giant cells (also known as Langerhans giant cells), surrounded by T lymphocytes. Te granuloma provides the Mtb with a long-term survival shelter where the microorganisms are protected from the immune response [3]. Finally, another defense mechanism for the con- trol of intracellular pathogens is autophagy; in macrophages, Hindawi Publishing Corporation Disease Markers Volume 2016, Article ID 4961086, 5 pages http://dx.doi.org/10.1155/2016/4961086