Abstract
Infectious, genetic factors, and autoimmunity have been considered as potential causes of sarcoidosis (SA). Pathological similarities between SA and tuberculosis (TB) suggest M. tuberculosis antigen(s) as causative agent(s). Our published comparative analysis of the human leukocyte antigens (HLA) system in patients with SA or TB in the same ethnic group revealed that some antigens were connected with high risk of developing of SA or TB, but other were comparable in both patient populations. Is it possible that the predominating occurrence of HLA antigens characteristic for TB may cause tuberculosis in patients with SA? To answer this question we evaluated the HLA class I and II alleles frequency by PCR amplification with sequence-specific primers in three women with histopathologically proven pulmonary SA, who developed bacteriologically confirmed TB on a corticosteroids (CS) therapy. Analysis of HLA in every case separately revealed a trend for higher occurrence of both alleles predisposing and protecting from TB than SA, in comparison with healthy individuals in our previously mentioned HLA genotyping study. Overall, the number of alleles predisposing to TB was statistically greater than the number of alleles connected with a high risk of developing SA. Also, the frequency of protecting alleles was statistically higher for TB than for SA. Therefore, SA in these patients developed at first, and the presence of additional environmental factors, e.g., age, CS might decrease an immune response and provoked TB. There is a possibility that the occurrence of HLA antigen more associated with high risk of developing TB than SA causes the development of tuberculosis in our patients with sarcoidosis.
Access this chapter
Tax calculation will be finalised at checkout
Purchases are for personal use only
References
American Thoracic Society. (1999). Statement on sarcoidosis. American Journal of Respiratory and Critical Care Medicine, 160, 736–755.
Dubaniewicz, A. (2010). Mycobacterium tuberculosis heat shock proteins and autoimmunity in sarcoidosis. Autoimmunity Reviews, 9(6), 419–424.
Dubaniewicz, A., & Dubaniewicz, A. (2005). Human Leukocyte antigens class I and class II: Associations and distribution in different ethnic groups of patients with pulmonary tuberculosis. Current Respiratory Medicine Reviews, 1(2), 117–121.
Dubaniewicz, A., Szczerkowska, Z., & Hoppe, A. (2003). Comparative analysis of HLA class I antigens in pulmonary sarcoidosis and tuberculosis in the same ethnic group. Mayo Clinic Proceedings, 78(4), 436–442.
Dubaniewicz, A., Moszkowska, G., & Szczerkowska, Z. (2005). Frequency of DRB1-DQB1 two-locus haplotypes in tuberculosis: Preliminary report. Tuberculosis (Edinburgh, Scotland), 85, 259–267.
Dubaniewicz, A., Dubaniewicz-Wybieralska, M., Moszkowska, G., Sternau, A., & Dubaniewicz, A. (2006). Comparative analysis of DR and DQ alleles occurrence in sarcoidosis and tuberculosis in the same ethnic group: Preliminary study. Sarcoidosis, Vasculitis, and Diffuse Lung Diseases, 23(3), 180–189.
Goljan, A., Puscinska, E., Sankowska, M., & Zielinski, J. (2000). Polymorphism of histocompatibility class II antigens coded with the DRB gene in familial sarcoidosis in Poland. Pneumonologia i Alergologia Polska, 68(11–12), 533–544.
Grosser, M., Luther, T., Fuessel, M., Bickhardt, J., Magdolen, V., & Baretton, G. (2005). Clinical course of sarcoidosis in dependence on HLA-DRB1 allele frequencies, inflammatory markers, and the presence of M. tuberculosis DNA fragments. Sarcoidosis, Vasculitis, and Lung Diseases, 22(1), 66–74.
Idali, F., Wiken, M., Wahlstrom, J., Mellstedt, H., Eklund, A., Rabbani, H., & Grunewald, J. (2006). Reduced Th1 response in the lungs of HLA-DRB1*0301 patients with pulmonary sarcoidosis. European Respiratory Journal, 27(3), 451–459.
Khomenko, A. G., Litvinova, V. I., Chukanovaa, V. P., & Pospelova, L. E. (1990). Tuberculosis in patients with various HLA phenotypes. Tubercle, 71(3), 187–192.
Kurian, S. M., Selvaraj, P., Reetha, A. M., Charles, N., & Narayanan, P. R. (2004). HLA-DR phenotypes and lymphocyte response to M. tuberculosis antigens in cures spinal tuberculosis patients and their contacts. The Indian Journal of Tuberculosis, 51, 71–75.
Livnat, S., Madden, K. S., Felten, D. L., & Felten, S. Y. (1987). Regulation of the immune system by sympathetic neural mechanisms. Progress in Neuro-Psychopharmacology & Biological Psychiatry, 11(2–3), 145–152.
Mach, F. (2002). Immunosuppressive effects of statins. Atherosclerosis Supplements, 3(1), 17–20.
Messerli, F. H., & Grossman, E. (1998). The calcium antagonist controversy: A posthumous commentary. The American Journal of Cardiology, 82(9B), 35R–39R.
Moller, D. R. (2007). Potential etiologic agents in sarcoidosis. Proceedings of the American Thoracic Society, 4(5), 465–468.
Morgenthau, A. S., & Iannuzzi, M. C. (2011). Recent advances in sarcoidosis. Chest, 139(1), 174–182.
Mrazek, F., Holla, L. I., Hutyrova, B., Znojil, V., Vasku, A., Kolek, V., Welsh, K. I., Vacha, J., du Bois, R. M., & Petrek, M. (2005). Association of tumor necrosis factor-α, lymphotoxin-α and HLA-DRB1 gene polymorphisms with Löfgren’s syndrome in Czech patients with sarcoidosis. Tissue Antigens, 65(2), 163–171.
Olerup, O., & Zetterquist, H. (1991). HLA-DRB1*01 subtyping by allele-specific PCR amplification: A sensitive, specific and rapid technique. Tissue Antigens, 37(5), 197–204.
Papadopoulos, K. I., Wassmuth, R., Sponsel, T., Sjöberg, K., & Hallengren, B. (2006). Sarcoidosis and autoimmunity: Evidence of differential associations with HLA class II markers. International Journal of Endocrinology and Metabolism, 4, 13–18.
Plesner, A., Greenbaum, C. J., Gaur, L. K., Ernst, R. K., & Lernmark, A. (2002). Macrophages from high-risk HLA-DQB1*0201/*0302 type 1 diabetes mellitus patients are hypersensitive to lipopolysacharide stimulation. Scandinavian Journal of Immunology, 56(5), 522–529.
Price, P., Witt, C., Allcock, R., Sayer, D., Garlepp, M., Kok, C. C., French, M., Mallal, S., & Christiansen, F. (1999). The genetic basis for the association of the 8.1 ancestral haplotype (A1,B8,DR3) with multiple immunopathological diseases. Immunology Reviews, 167, 257–274.
Sato, H., Woodhead, F. A., Ahmad, T., Grutters, J. C., Spagnolo, P., van den Bosch, J. M., Maier, L. A., Newman, L. S., Nagai, S., Izumi, T., Wells, A. U., du Bois, R. M., & Welsh, K. I. (2010). Sarcoidosis HLA class II genotyping distinguishes differences of clinical phenotype across ethnic groups. Human Molecular Genetics, 19(20), 4100–4111.
Sidney, J., del Guercio, M. F., Southwood, S., & Sette, A. (2002). The HLA molecules DQA1*0501/B1*0201 and DQA1*0301/B1*0302 share an extensive overlap in peptide binding specificity. Journal of Immunology, 169(9), 5098–5108.
Steffens, S., & Mach, F. (2004). Anti-inflammatory properties of statins. Seminars in Vascular Medicine, 4(4), 417–422.
Swider, C., Schnittger, L., Bogunia-Kubik, K., Gerdes, J., Flad, H.-D., Lange, A., & Seitze, U. (1999). TNF-alpha and HLA-DR genotyping as potential prognostic markers in pulmonary sarcoidosis. European Cytokine Network, 10(2), 143–146.
Wahlstrom, J., Katchar, K., Wigzell, H., Olerup, O., Eklund, A., & Grunewald, J. (2001). Analysis of intracellular cytokines in CD4+ and CD8+ lung and blood T cells in sarcoidosis. American Journal of Respiratory and Critical Care Medicine, 163(1), 115–121.
Walzl, G., Ronacher, K., Hanekom, W., Scriba, T. J., & Zumla, A. (2011). Immunological biomarkers of tuberculosis. Nature Reviews Immunology, 11(5), 343–354.
Yim, J. J., & Selvaraj, P. (2010). Genetic susceptibility in tuberculosis. Respirology, 15(2), 241–256.
Author information
Authors and Affiliations
Corresponding author
Editor information
Editors and Affiliations
Additional information
Conflicts of interest: The authors declare no conflicts of interest in relation to this article.
Rights and permissions
Copyright information
© 2013 Springer Science+Business Media Dordrecht
About this paper
Cite this paper
Dubaniewicz, A. et al. (2013). Sarcoidosis and Tuberculosis: A Connection to the Human Leukocyte Antigen System. In: Pokorski, M. (eds) Respiratory Regulation - The Molecular Approach. Advances in Experimental Medicine and Biology, vol 756. Springer, Dordrecht. https://doi.org/10.1007/978-94-007-4549-0_29
Download citation
DOI: https://doi.org/10.1007/978-94-007-4549-0_29
Published:
Publisher Name: Springer, Dordrecht
Print ISBN: 978-94-007-4548-3
Online ISBN: 978-94-007-4549-0
eBook Packages: Biomedical and Life SciencesBiomedical and Life Sciences (R0)