STUDI LITERATR REVIEW: ASOSIASI POLIMORFISME GEN INTERFERON GAMMA +874 A/T TERHADAP PASIEN SKIZOFRENIA

Agnes Felicia Lubis; Eddy Mart Salim; Abdullah Sahab; Zen Hafy

doi:10.30649/obj.v5i2.86

Penulis

Agnes Felicia Lubis Universitas Sriwijaya
Eddy Mart Salim Universitas Sriwijaya
Abdullah Sahab Universitas Sriwijaya
Zen Hafy Universitas Sriwijaya

DOI:

https://doi.org/10.30649/obj.v5i2.86

Kata Kunci:

skizofrenia, polimorfisme, gen interferon gamma, sitokin, genetika

Abstrak

Skizofrenia adalah psikiater akut dan kronis dengan banyak faktor penentu lingkungan dan genetik. Beberapa laporan menunjukkan bahwa itu memainkan peran penting dalam regulasi sistem kekebalan dalam penyebab skizofrenia. Bukti yang dikumpulkan menunjukkan hubungan antara skizofrenia dan psikopatologi dan penurunan produksi sitokin. Polimorfisme gen Interferon gamma +874 A/T yang terletak pada pasang basa ke +874. Tujuan: Literature review ini bertujuan untuk mengidentifikasi polimorfisme gen Interferon Gamma +874 A/T pada pasien Skizofrenia. Metode: Desain penelitian adalah literature review. Pencarian literature dilakukan dengan melakukan penelusuran jurnal internasional dan nasional. Hasil pencarian artikel pada database ditemukan sebanyak 32 artikel. Jumlah artikel yang sesuai kriteria inklusi adalah sebanyak 28 artikel. Hasil literatur review didapatkan 5 jurnal yang membahas polimorfisme gen Interferon Gamma +874 A/T pada pasein skizofrenia. 5 jurnal tersebut merupakan penelitian studi kasus. Hasil: Dari artikel yang telah dibahas, dapat disimpulkan bahwa 874+ polimorfisme intron pertama gen interferon gamma berhubungan dengan produksi senyawa ini. Kehadiran genotipe AA dikaitkan dengan penurunan produksi sitokin, dan genotipe AT dikaitkan dengan produksi selulosa sedang dan TT serta produksi sel yang tinggi.

Referensi

Kemenkes RI. Riset kesehatan dasar. Jakarta : Kementrian Kesehatan Republik Indonesia; 2018.

Owen MJ, Sawa A, Mortensen PB. Schizophrenia. The Lancet. 2016;388(10039):86-97. doi:10.1016/s0140-6736(15)01121-6

Kirkpatrick BW, Morris CA. 2015. A major gene for bovine ovulation rate. PLoS One 2015:10; e0129025:1-13.

Khandaker, M. M., Boyce, A. N., Osman, N. Dan Hossain, ABM. S.: Physiochemical and Phytochemical Properties of Wax Apple (Syzygium samarangense [Blume] Merrill & L. M. Perry var. Jambu Madu) As Affected by Growth Regulator Application. The Scientific World Journa 2012, 20, 11-12.

Kronfol Z, Remick DG. Sitokin dan otak: implikasi untuk psikiatri klinis. Am J Psikiatri.

; 157 (5): 683 - 94.

Maes M, Stevens WJ, Declerck LS, et al. Significantly increased expression of T-cell activation markers (interleukin-2 and HLA-DR) in depression: Further evidence for an inflamatory process during that illness. Progress in Neuro-Psychopharmacology and Biological Psychiatry. 1993;17(2):241-255. doi:10.1016/0278-5846(93)90045-t

Fineberg AM, Ellman LM. Inflammatory Cytokines and Neurological and Neurocognitive Alterations in the Course of Schizophrenia. Biological Psychiatry. 2013;73(10):951-966. doi:10.1016/j.biopsych.2013.01.001.

Kim H-J, Eom C-Y, Kwon J, et al. Roles of interferon-gamma and its target genes in schizophrenia: Proteomics-based reverse genetics from mouse to human. PROTEOMICS. 2012;12(11):1815-1829. doi:10.1002/pmic.201100184.

Orgogozo V, Morizot B, Martin A. The differential view of genotype-phenotype relationships. Front Genet. 2015;6:179. https://doi.org/10.3389/fgene.2015.00179.

Srinivas L, Vellichirammal NN, Alex AM, Nair C, Nair IV, Banerjee M. Pro-inflammatory cytokines and their epistatic interactions in genetic susceptibility to schizophrenia. Journal of Neuroinflammation. 2016;13(1). doi:10.1186/s12974-016-0569-8.

Zhang, XY, Zhou, DF, Cao, LY, Zhang, PY dkk., Menurun produksi interleukin-2 (IL- 2), sel yang mensekresi IL-2 dan sel CD4 + pada pasien skizofrenia bebas pengobatan. J. Psikiater. Res. 2002, 36, 331–336.

Penner JD, Brown AS. Faktor infeksi dan nutrisi prenatal dan risiko Skizofrenia dewasa. Ahli Rev Neurother. 2007; 7 (7): 797 - 805.

Kinney DK, Hintz K, Shearer EM, et al. A unifying hypothesis ofschizophrenia: abnormal immune system development may help explainroles of prenatal hazards, post-pubertal onset, stress, genes, climate,infections, and brain dysfunction. Med Hypotheses. 2011;74(3):555– 63.9.

Watanabe Y, Someya T, Nawa H. Cytokine hypothesis of schizophreniapathogenesis: evidence from human studies and animal models. PsychiatryClin Neurosci. 2012;64(3):217– 30.

Wang, H., Yang, H., Shivalila, C.S., Dawlaty, M.M., Cheng, A.W., Zhang, F.,and Jaenisch,

R. (2013). One-step generation of mice carrying mutations inmultiple genes by CRISPR/Cas- mediated genome engineering. Cell153,910–918.

Steiner, J., Bogerts, B., Sarnyai, Z., Walter, M., Gos, T., Bernstein, H.G., Myint, A.M., 2011a. Bridging the gap between the immune and glutamate hypotheses of schizophrenia and major depression: potential role of glial NMDA receptor modulators and impaired blood– brain barrier integrity. World J Biol. Psychiatry, in press.

Myint, A.M., 2012. Kynurenines: from the perspective of major psychiatric disorders. FEBS

J. 279, 1375–1385.

Doorduin, J., de Vries, E.F., Willemsen, A.T., de Groot, J.C., Dierckx, R.A., Klein, H.C., 2009. Neuroinflammation in schizophrenia-related psychosis: a PET study. J. Nucl. Med. 50, 1801–1807.

Van Berckel, B.N., Bossong, M.G., Boellaard, R., Kloet, R., Schuitemaker, A., Caspers, E., Luurtsema, G., Windhorst, A.D., Cahn, W., Lammertsma, A.A., Kahn, R.S., 2008. Microglia activation in recent-onset schizophrenia: a quantitative (R)-[11C]PK11195 positron emission tomography study. Biol. Psychiatry 64, 820–822.

Takano, A., Arakawa, R., Ito, H., Tateno, A., Takahashi, H., Matsumoto, R., Okubo, Y., Suhara, T., 2010. Peripheral benzodiazepine receptors in patients with chronic schizophrenia: a PET study with [11C]DAA1106. Int. J. Neuropsychopharmacol. 13, 943–950.

Zhang JM, An J. Cytokines, inflammation and pain. Int anesthesiol clin. 2007;45(2): 27-37.

Kontsek P, Kontsekova E. Forty years of interferon. Acta virologica. 1997; 41: 349-353.

Kronfol Z, Remick DG. Cytokines and the brain: implications for clinical psychiatry. Am J Psychiatry. 2000;157(5):683–94.

Müller N, Ackenheil M. Psychoneuroimmunology and the cytokine action in the CNS: implications for psychiatric disorders. Prog Neuropsychopharmacol Biol Psychiatry. 1998;22(1):1–33.

Zhang XY, Zhou DF, Zhang PY, et al. Elevated interleukin-2, interleukin-6 and interleukin-

serum levels in neuroleptic-free schizophrenia: association with psychopathology.

Schizophr Res. 2002;57(2):247–58.

Strous RD, Shoenfeld Y. Schizophrenia, autoimmunity and immune system dysregulation: a comprehensive model updated and revisited. J Autoimmun. 2006;27(2):71–80.

Boehm U, Klamp T, Groot M, Howard JC. Respons seluler terhadap interferon-gamma. Annu Rev Immunol 199; 15: 749–95.

Pravica V, Asderakis A, Perrey C, Hajeer A, Sinnott PJ, Hutchinson IV. In vitro produksi IFN-gamma berkorelasi dengan polimorfisme ulangan CA dalam gen IFN-gamma manusia. Eur J Immunogenet 199; 26: 1–3.

Damanik R, Effendy E, Husada MS. The Relation of Gene Polymorphism Interferon Gamma+874 A/T and Schizophrenia Occurred in Batak Ethnicity. Open Access Macedonian Journal of Medical Sciences. 2020;8(A):70-75. doi:10.3889/oamjms.2020.3975

Samojedny MP, Owezarek A, Suchanek R, Kowalezyk M, Danilow AF, Norkowska P et al. Association study of Interferon gamma (IFN-γ) ++874 T/A gene polymorphisms with paranoid shcizophrenia. J mol neurosci 2011; 43: 309-315

Tamandani DMK, Najafi M, Mojahed A, Shahraki A. Analysis of IFN-γ (++874 A/T) and IL-10 (-1082 G/A) genes polymorphisms with risk of schizophrenia. Jorrnal of cell and molecular research 2014;6(2): 64-68.

Jemli A, Eshili A, Trifa F, Mechri A, Zaafrane F, Gaha L, et al. Association of the IFN-γ (++874 A/T) genetic polymorphism with paranoid schizophrenia in tunisian population. 15 Immunological investigation 2016;13.