Araştırma Makalesi
BibTex RIS Kaynak Göster

CEREBROSPINAL FLUID (CSF) IL-17A, IL-17F, IL-34 AND CXCL-13 LEVELS IN AMYOTROPHIC LATERAL SCLEROSIS (ALS/MND) PATIENTS

Yıl 2019, Cilt: 14 Sayı: 3, 154 - 162, 08.07.2019

Öz

In this study, our clinic follow-up ALS/MND diagnose the cerebrospinal fluid of patients (CSF), IL-17A, IL-17F, IL-34 cytokines and CXCL-13 chemokine to evaluate the levels. that were determined by ELISA. In our study, significantly higher in the patient group and the proinflammatory cytokine, IL-17A and IL-17F of endothelial cells, fibroblasts and also known to be expressed in neurones. However, CXCL13 level is considered among the patient group and the control group was not statistically significant difference. IL-34 also to be increased when compared to the patient group (n=4) than the control group (n=6), a recently described cytokine due to the IL-34 Th17 with modulating immune pathogenesis and immune with cytokines released from cells in a short time to be involved ALS/MND such as rare as to be made further studies for the diagnosis of a disease to a powerful new biomarker may and science has been suggested to contribute in this respect. 

Kaynakça

  • 1. Shefner, J.M., (2019). Effects of Strength Training in Amyotrophic Lateral Sclerosis: How Much Do We Know? Muscle Nerve, 59(1):6-7.
  • 2. Benjaminsen, E., et al., (2018). Amyotrophic Lateral Sclerosis in Nordland County, Norway, 2000-2015: Prevalence, Incidence, and Clinical Features. Amyotroph Lateral Scler Frontotemporal Degener, pp:1-6.
  • 3. Robberecht, W. and Philips, T., (2013). The Changing Scene of Amyotrophic Lateral Sclerosis. Nat Rev Neurosci, 214(4):248-64.
  • 4. Eisen, A., (2009). Amyotrophic Lateral Sclerosis-Evolutionary and Other Perspectives. Muscle Nerve, 40(2):297-304.
  • 5. Andersen, P.M. and Al-Chalabi, A., (2011). Clinical Genetics of Amyotrophic Lateral Sclerosis: What Do We Really Know? Nat Rev Neurol, 7(11):603-15.
  • 6. Regensburger, M., Weidner, N., and Kohl, Z., (2018). Motor Neuron Diseases: Clinical and Genetic Differential Diagnostics. Nervenarzt, 89(6):658-665.
  • 7. Pansarasa, O., et al., (2018). SOD1 in Amyotrophic Lateral Sclerosis: "Ambivalent" Behavior Connected to the Disease. Int J Mol Sci, 19(5).
  • 8. Cleveland, D.W., et al., (1996). Mechanisms of Selective Motor Neuron Death in Transgenic Mouse Models of Motor Neuron Disease. Neurology, 47(4 Suppl 2):S54-61; discussion S61-2.
  • 9. Ferraiuolo, L., et al., (2011). Molecular Pathways of Motor Neuron Injury in Amyotrophic Lateral Sclerosis. Nat Rev Neurol, 7(11):616-30.
  • 10. Perry, T.L., et al., (1990). Amyotrophic Lateral Sclerosis: Amino Acid Levels in Plasma and Cerebrospinal Fluid. Ann Neurol, 28(1):12-7.
  • 11. Cheah, B.C., et al., (2010). Riluzole, Neuroprotection and Amyotrophic Lateral Sclerosis. Curr Med Chem, 17(18):1942-199.
  • 12. Rothstein, J.D., et al., (1995). Selective Loss of Glial Glutamate Transporter GLT-1 in Amyotrophic Lateral Sclerosis. Ann Neurol, 38(1):73-84.
  • 13. Lattante, S., et al., (2015). Defining the Genetic Connection Linking Amyotrophic Lateral Sclerosis (ALS) With Frontotemporal Dementia (FTD). Trends Genet, 31(5):263-73.
  • 14. Goetz, C.G., (2000). Amyotrophic Lateral Sclerosis: Early Contributions of Jean‐Martin Charcot. Muscle & Nerve: Official Journal of the American Association of Electrodiagnostic Medicine, 23(3):336-343.
  • 15. Plata-Salaman, C. and Turrin, N., (1999). Cytokine Interactions and Cytokine Balance in the Brain: Relevance to Neurology and Psychiatry. Nature Publishing Group.
  • 16. Gangishetti, U., et al., (2018). CSF Cytokine Profiles Uniquely Identify Different Neurodegenerative Disorders (P4. 175). AAN Enterprises.
  • 17. Kwon, B.K., et al., (2010). Cerebrospinal Fluid Inflammatory Cytokines and Biomarkers of Injury Severity in Acute Human Spinal Cord Injury. Journal of Neurotrauma, 27(4):669-682.
  • 18. Turner, M.D., et al., (2014). Cytokines and Chemokines: at the Crossroads of Cell Signalling and Inflammatory Disease. Biochimica et Biophysica Acta (BBA)-Molecular Cell Research, 1843(11):2563-2582.
  • 19. McCluskey, G., et al., (20159. Idiopathic Intracranial Hypertension in the Northwest of Northern Ireland: Epidemiology and Clinical Management. Neuroepidemiology, 45(1):34-9.
  • 20. Kesler, A., et al., (2014). The Incidence of Idiopathic Intracranial Hypertension in Israel from 2005 to 2007: Results of a Nationwide Survey. Eur J Neurol, 21(8):1055-1059.
  • 21. Dhungana, S., Sharrack, B., and Woodroofe, N., (2009). Cytokines and Chemokines in Idiopathic Intracranial Hypertension. Headache, 49(2):282-5.
  • 22. Edwards, L.J., et al., (2013). Increased Levels of Interleukins 2 and 17 in the Cerebrospinal Fluid of Patients with Idiopathic Intracranial Hypertension. Am J Clin Exp Immunol, 2(3):234-44.
  • 23. Akitsu, A. and Iwakura, Y., (2018). Interleukin-17-Producing Gammadelta T (gammadelta17) Cells in Inflammatory Diseases. Immunology.
  • 24. Kugelberg, E., (2016). Neuroimmunology: IL-17A Mediates a Path to Autism. Nat Rev Immunol, 16(4):205.
  • 25. Miossec, P., (2017). Update on Interleukin-17: a Role in the Pathogenesis of Inflammatory Arthritis and Implication for Clinical Practice. RMD open, 3(1):e000284.
  • 26. Baghdadi, M., et al., (2018). Interleukin-34, a Comprehensive Review. J Leukoc Biol, 104(5):931-951.
  • 27. Huber, A.K. and D.N. Irani, D.N., (2015). Targeting CXCL13 During Neuroinflammation. Adv Neuroimmune Biol, 6(1):1-8.
  • 28. Pietikäinen, A., Oksi, J., and Hytönen, J., (2018). Point-of-Care Testing for CXCL13 in Lyme Neuroborreliosis. Diagnostic Microbiology and Infectious Disease, 91(3):226-228.
  • 29. Philips, T. and Robberecht, W., (2011). Neuroinflammation in Amyotrophic Lateral Sclerosis: Role of Glial Activation in Motor Neuron Disease. The Lancet Neurology, 10(3):53-263.
  • 30. Barschke, P., et al., (2017). Proteomic Studies in the Discovery of Cerebrospinal Fluid Biomarkers for Amyotrophic Lateral Sclerosis. Expert Rev Proteomics, 14(9):769-777.
  • 31. Miller, R.G., Mitchell, J.A., and Moore, D.H., (2012). Riluzole for Amyotrophic Lateral Sclerosis (ALS)/Motor Neuron Disease (MND). Cochrane Database of Systematic Reviews, (3).
  • 32. Al-Chalabi, A., et al., (2014). Analysis of Amyotrophic Lateral Sclerosis as a Multistep Process: a Population-Based Modelling Study. The Lancet Neurology, 13(11):1108-1113.
  • 33. Al-Chalabi, A. and Hardiman, O., (2013). The Epidemiology of ALS: a Conspiracy of Genes, Environment and Time. Nature Reviews Neurology, 9(11):617.
  • 34. A McCombe, P. and R. D Henderson,R.D., (2011). The Role of Immune and Inflammatory Mechanisms in ALS. Current Molecular Medicine, 11(3):246-254.
  • 35. Zotova, E., et al., (2010). Inflammation in Alzheimer's Disease: Relevance to Pathogenesis and Therapy. Alzheimers Res Ther, 2(1):1.
  • 36. Tufekci, K.U., et al., (2012). Inflammation in Parkinson's Disease, in Advances in Protein Chemistry and Structural Biology. Elsevier. 69-132.
  • 37. Filippi, M. and Agosta, F., (2016). Does Neuroinflammation Sustain Neurodegeneration in ALS? AAN Enterprises.
  • 38. Hooten, K.G., et al., (2015). Protective and Toxic Neuroinflammation in Amyotrophic Lateral Sclerosis. Neurotherapeutics, 12(2):364-375.
  • 39. Thonhoff, J.R., Simpson, E.P., and Appel, S.H., (2018). Neuroinflammatory Mechanisms in Amyotrophic Lateral Sclerosis Pathogenesis. Curr Opin Neurol, 31(5):635-639.
  • 40. D'Ambrosi, N., Cozzolino, M., and Carrì, M.T., (2018). Neuroinflammation in Amyotrophic Lateral Sclerosis: Role of Redox (dys) Regulation. Antioxidants & Redox signaling, 29(1):15-36.
  • 41. Miller, R.G., et al., (2015). Randomized Phase 2 Trial of NP001, a Novel Immune Regulator: Safety and Early Efficacy in ALS. Neurology-Neuroimmunology Neuroinflammation, 2(3):e100.
  • 42. Guo, H., Callaway, J.B., and Ting, J.P., (2015). Inflammasomes: Mechanism of Action, Role in Disease, and Therapeutics. Nature Medicine, 21(7):677.
  • 43. Moisse, K. and Strong, M.J., (2006). Innate Immunity in Amyotrophic Lateral Sclerosis. Biochimica et Biophysica Acta (BBA)-Molecular Basis of Disease, 1762(11-12):1083-1093.
  • 44. Vilček, J. and Feldmann, M., (2004). Historical Review: Cytokines as Therapeutics and Targets of Therapeutics. Trends in Pharmacological Sciences, 25(4):201-209.
  • 45. Spangler, J.B., et al., (2015). Insights into Cytokine–Receptor Interactions from Cytokine Engineering. Annual Review of Immunology, 33:139-167.
  • 46. Fiala, M., et al., (2010). IL-17A is Increased in the Serum and in Spinal Cord CD8 and Mast Cells of ALS Patients. Journal of Neuroinflammation, 7(1):76.
  • 47. Cheng, Y., et al., (2018). Cerebrospinal Fluid Inflammatory Cytokine Aberrations in Alzheimer’s Disease, Parkinson’s Disease and Amyotrophic Lateral Sclerosis: a Systematic Review and Meta-analysis. Frontiers in Immunology, 9:2122.
  • 48. Moling, O., et al., (2014). Increased IL-17, a Pathogenic Link Between Hepatosplenic Schistosomiasis and Amyotrophic Lateral Sclerosis: A Hypothesis. Case Reports in Immunology.
  • 49. Agah, E., et al., (2018). CSF and Blood Biomarkers in Amyotrophic Lateral Sclerosis: Protocol for a Systematic Review and Meta-Analysis. Systematic Reviews, 7(1):237.
  • 50. Celeste, D.B. and M.S. Miller, M.S., (2018). Reviewing the Evidence for Viruses as Environmental Risk Factors for ALS: A New Perspective. Cytokine, 108:173-178.
  • 51. Fredi, M., et al., (2019). C9orf72 Intermediate Alleles in Patients with Amyotrophic Lateral Sclerosis, Systemic Lupus Erythematosus, and Rheumatoid Arthritis. Neuromolecular Medicine, 1-10.

Cerebrospinal Fluid (CSF) IL-17A, IL-17F, IL-34 and CXCL-13 Levels in Amyotrophic Lateral Sclerosis (ALS/MND) Patients

Yıl 2019, Cilt: 14 Sayı: 3, 154 - 162, 08.07.2019

Öz

     In this study, our clinic follow-up ALS/MND diagnose
the cerebrospinal fluid of patients (CSF), IL-17A, IL-17F, IL-34 cytokines and
CXCL-13 chemokine to evaluate the levels. that were determined by ELISA. In our
study, significantly higher in the patient group and the proinflammatory
cytokine, IL-17A and IL-17F of endothelial cells, fibroblasts and also known to
be expressed in neurones. However, CXCL-13 level is considered among the
patient group and the control group was not statistically significant difference.
IL-34 also to be increased when compared to the patient group (n=4) than the
control group (n=6), a recently described cytokine due to the IL-34 Th17 with
modulating immune pathogenesis and immune with cytokines released from cells in
a short time to be involved ALS/MND such as rare as to be made further studies
for the diagnosis of a disease to a powerful new biomarker may and science has
been suggested to contribute in this respect.


Kaynakça

  • 1. Shefner, J.M., (2019). Effects of Strength Training in Amyotrophic Lateral Sclerosis: How Much Do We Know? Muscle Nerve, 59(1):6-7.
  • 2. Benjaminsen, E., et al., (2018). Amyotrophic Lateral Sclerosis in Nordland County, Norway, 2000-2015: Prevalence, Incidence, and Clinical Features. Amyotroph Lateral Scler Frontotemporal Degener, pp:1-6.
  • 3. Robberecht, W. and Philips, T., (2013). The Changing Scene of Amyotrophic Lateral Sclerosis. Nat Rev Neurosci, 214(4):248-64.
  • 4. Eisen, A., (2009). Amyotrophic Lateral Sclerosis-Evolutionary and Other Perspectives. Muscle Nerve, 40(2):297-304.
  • 5. Andersen, P.M. and Al-Chalabi, A., (2011). Clinical Genetics of Amyotrophic Lateral Sclerosis: What Do We Really Know? Nat Rev Neurol, 7(11):603-15.
  • 6. Regensburger, M., Weidner, N., and Kohl, Z., (2018). Motor Neuron Diseases: Clinical and Genetic Differential Diagnostics. Nervenarzt, 89(6):658-665.
  • 7. Pansarasa, O., et al., (2018). SOD1 in Amyotrophic Lateral Sclerosis: "Ambivalent" Behavior Connected to the Disease. Int J Mol Sci, 19(5).
  • 8. Cleveland, D.W., et al., (1996). Mechanisms of Selective Motor Neuron Death in Transgenic Mouse Models of Motor Neuron Disease. Neurology, 47(4 Suppl 2):S54-61; discussion S61-2.
  • 9. Ferraiuolo, L., et al., (2011). Molecular Pathways of Motor Neuron Injury in Amyotrophic Lateral Sclerosis. Nat Rev Neurol, 7(11):616-30.
  • 10. Perry, T.L., et al., (1990). Amyotrophic Lateral Sclerosis: Amino Acid Levels in Plasma and Cerebrospinal Fluid. Ann Neurol, 28(1):12-7.
  • 11. Cheah, B.C., et al., (2010). Riluzole, Neuroprotection and Amyotrophic Lateral Sclerosis. Curr Med Chem, 17(18):1942-199.
  • 12. Rothstein, J.D., et al., (1995). Selective Loss of Glial Glutamate Transporter GLT-1 in Amyotrophic Lateral Sclerosis. Ann Neurol, 38(1):73-84.
  • 13. Lattante, S., et al., (2015). Defining the Genetic Connection Linking Amyotrophic Lateral Sclerosis (ALS) With Frontotemporal Dementia (FTD). Trends Genet, 31(5):263-73.
  • 14. Goetz, C.G., (2000). Amyotrophic Lateral Sclerosis: Early Contributions of Jean‐Martin Charcot. Muscle & Nerve: Official Journal of the American Association of Electrodiagnostic Medicine, 23(3):336-343.
  • 15. Plata-Salaman, C. and Turrin, N., (1999). Cytokine Interactions and Cytokine Balance in the Brain: Relevance to Neurology and Psychiatry. Nature Publishing Group.
  • 16. Gangishetti, U., et al., (2018). CSF Cytokine Profiles Uniquely Identify Different Neurodegenerative Disorders (P4. 175). AAN Enterprises.
  • 17. Kwon, B.K., et al., (2010). Cerebrospinal Fluid Inflammatory Cytokines and Biomarkers of Injury Severity in Acute Human Spinal Cord Injury. Journal of Neurotrauma, 27(4):669-682.
  • 18. Turner, M.D., et al., (2014). Cytokines and Chemokines: at the Crossroads of Cell Signalling and Inflammatory Disease. Biochimica et Biophysica Acta (BBA)-Molecular Cell Research, 1843(11):2563-2582.
  • 19. McCluskey, G., et al., (20159. Idiopathic Intracranial Hypertension in the Northwest of Northern Ireland: Epidemiology and Clinical Management. Neuroepidemiology, 45(1):34-9.
  • 20. Kesler, A., et al., (2014). The Incidence of Idiopathic Intracranial Hypertension in Israel from 2005 to 2007: Results of a Nationwide Survey. Eur J Neurol, 21(8):1055-1059.
  • 21. Dhungana, S., Sharrack, B., and Woodroofe, N., (2009). Cytokines and Chemokines in Idiopathic Intracranial Hypertension. Headache, 49(2):282-5.
  • 22. Edwards, L.J., et al., (2013). Increased Levels of Interleukins 2 and 17 in the Cerebrospinal Fluid of Patients with Idiopathic Intracranial Hypertension. Am J Clin Exp Immunol, 2(3):234-44.
  • 23. Akitsu, A. and Iwakura, Y., (2018). Interleukin-17-Producing Gammadelta T (gammadelta17) Cells in Inflammatory Diseases. Immunology.
  • 24. Kugelberg, E., (2016). Neuroimmunology: IL-17A Mediates a Path to Autism. Nat Rev Immunol, 16(4):205.
  • 25. Miossec, P., (2017). Update on Interleukin-17: a Role in the Pathogenesis of Inflammatory Arthritis and Implication for Clinical Practice. RMD open, 3(1):e000284.
  • 26. Baghdadi, M., et al., (2018). Interleukin-34, a Comprehensive Review. J Leukoc Biol, 104(5):931-951.
  • 27. Huber, A.K. and D.N. Irani, D.N., (2015). Targeting CXCL13 During Neuroinflammation. Adv Neuroimmune Biol, 6(1):1-8.
  • 28. Pietikäinen, A., Oksi, J., and Hytönen, J., (2018). Point-of-Care Testing for CXCL13 in Lyme Neuroborreliosis. Diagnostic Microbiology and Infectious Disease, 91(3):226-228.
  • 29. Philips, T. and Robberecht, W., (2011). Neuroinflammation in Amyotrophic Lateral Sclerosis: Role of Glial Activation in Motor Neuron Disease. The Lancet Neurology, 10(3):53-263.
  • 30. Barschke, P., et al., (2017). Proteomic Studies in the Discovery of Cerebrospinal Fluid Biomarkers for Amyotrophic Lateral Sclerosis. Expert Rev Proteomics, 14(9):769-777.
  • 31. Miller, R.G., Mitchell, J.A., and Moore, D.H., (2012). Riluzole for Amyotrophic Lateral Sclerosis (ALS)/Motor Neuron Disease (MND). Cochrane Database of Systematic Reviews, (3).
  • 32. Al-Chalabi, A., et al., (2014). Analysis of Amyotrophic Lateral Sclerosis as a Multistep Process: a Population-Based Modelling Study. The Lancet Neurology, 13(11):1108-1113.
  • 33. Al-Chalabi, A. and Hardiman, O., (2013). The Epidemiology of ALS: a Conspiracy of Genes, Environment and Time. Nature Reviews Neurology, 9(11):617.
  • 34. A McCombe, P. and R. D Henderson,R.D., (2011). The Role of Immune and Inflammatory Mechanisms in ALS. Current Molecular Medicine, 11(3):246-254.
  • 35. Zotova, E., et al., (2010). Inflammation in Alzheimer's Disease: Relevance to Pathogenesis and Therapy. Alzheimers Res Ther, 2(1):1.
  • 36. Tufekci, K.U., et al., (2012). Inflammation in Parkinson's Disease, in Advances in Protein Chemistry and Structural Biology. Elsevier. 69-132.
  • 37. Filippi, M. and Agosta, F., (2016). Does Neuroinflammation Sustain Neurodegeneration in ALS? AAN Enterprises.
  • 38. Hooten, K.G., et al., (2015). Protective and Toxic Neuroinflammation in Amyotrophic Lateral Sclerosis. Neurotherapeutics, 12(2):364-375.
  • 39. Thonhoff, J.R., Simpson, E.P., and Appel, S.H., (2018). Neuroinflammatory Mechanisms in Amyotrophic Lateral Sclerosis Pathogenesis. Curr Opin Neurol, 31(5):635-639.
  • 40. D'Ambrosi, N., Cozzolino, M., and Carrì, M.T., (2018). Neuroinflammation in Amyotrophic Lateral Sclerosis: Role of Redox (dys) Regulation. Antioxidants & Redox signaling, 29(1):15-36.
  • 41. Miller, R.G., et al., (2015). Randomized Phase 2 Trial of NP001, a Novel Immune Regulator: Safety and Early Efficacy in ALS. Neurology-Neuroimmunology Neuroinflammation, 2(3):e100.
  • 42. Guo, H., Callaway, J.B., and Ting, J.P., (2015). Inflammasomes: Mechanism of Action, Role in Disease, and Therapeutics. Nature Medicine, 21(7):677.
  • 43. Moisse, K. and Strong, M.J., (2006). Innate Immunity in Amyotrophic Lateral Sclerosis. Biochimica et Biophysica Acta (BBA)-Molecular Basis of Disease, 1762(11-12):1083-1093.
  • 44. Vilček, J. and Feldmann, M., (2004). Historical Review: Cytokines as Therapeutics and Targets of Therapeutics. Trends in Pharmacological Sciences, 25(4):201-209.
  • 45. Spangler, J.B., et al., (2015). Insights into Cytokine–Receptor Interactions from Cytokine Engineering. Annual Review of Immunology, 33:139-167.
  • 46. Fiala, M., et al., (2010). IL-17A is Increased in the Serum and in Spinal Cord CD8 and Mast Cells of ALS Patients. Journal of Neuroinflammation, 7(1):76.
  • 47. Cheng, Y., et al., (2018). Cerebrospinal Fluid Inflammatory Cytokine Aberrations in Alzheimer’s Disease, Parkinson’s Disease and Amyotrophic Lateral Sclerosis: a Systematic Review and Meta-analysis. Frontiers in Immunology, 9:2122.
  • 48. Moling, O., et al., (2014). Increased IL-17, a Pathogenic Link Between Hepatosplenic Schistosomiasis and Amyotrophic Lateral Sclerosis: A Hypothesis. Case Reports in Immunology.
  • 49. Agah, E., et al., (2018). CSF and Blood Biomarkers in Amyotrophic Lateral Sclerosis: Protocol for a Systematic Review and Meta-Analysis. Systematic Reviews, 7(1):237.
  • 50. Celeste, D.B. and M.S. Miller, M.S., (2018). Reviewing the Evidence for Viruses as Environmental Risk Factors for ALS: A New Perspective. Cytokine, 108:173-178.
  • 51. Fredi, M., et al., (2019). C9orf72 Intermediate Alleles in Patients with Amyotrophic Lateral Sclerosis, Systemic Lupus Erythematosus, and Rheumatoid Arthritis. Neuromolecular Medicine, 1-10.
Toplam 51 adet kaynakça vardır.

Ayrıntılar

Birincil Dil İngilizce
Konular Sağlık Kurumları Yönetimi
Bölüm Makaleler
Yazarlar

Hayriye Orallar Bu kişi benim 0000-0002-0000-3768

Şeyda Karabörk Bu kişi benim 0000-0002-9026-4485

Bihter Gökçe Bozat Bu kişi benim 0000-0002-6793-6888

Şule Aydın Türkoğlu 0000-0001-8616-832X

Yayımlanma Tarihi 8 Temmuz 2019
Yayımlandığı Sayı Yıl 2019 Cilt: 14 Sayı: 3

Kaynak Göster

APA Orallar, H., Karabörk, Ş., Bozat, B. G., Aydın Türkoğlu, Ş. (2019). CEREBROSPINAL FLUID (CSF) IL-17A, IL-17F, IL-34 AND CXCL-13 LEVELS IN AMYOTROPHIC LATERAL SCLEROSIS (ALS/MND) PATIENTS. Medical Sciences, 14(3), 154-162.
AMA Orallar H, Karabörk Ş, Bozat BG, Aydın Türkoğlu Ş. CEREBROSPINAL FLUID (CSF) IL-17A, IL-17F, IL-34 AND CXCL-13 LEVELS IN AMYOTROPHIC LATERAL SCLEROSIS (ALS/MND) PATIENTS. Medical Sciences. Temmuz 2019;14(3):154-162.
Chicago Orallar, Hayriye, Şeyda Karabörk, Bihter Gökçe Bozat, ve Şule Aydın Türkoğlu. “CEREBROSPINAL FLUID (CSF) IL-17A, IL-17F, IL-34 AND CXCL-13 LEVELS IN AMYOTROPHIC LATERAL SCLEROSIS (ALS/MND) PATIENTS”. Medical Sciences 14, sy. 3 (Temmuz 2019): 154-62.
EndNote Orallar H, Karabörk Ş, Bozat BG, Aydın Türkoğlu Ş (01 Temmuz 2019) CEREBROSPINAL FLUID (CSF) IL-17A, IL-17F, IL-34 AND CXCL-13 LEVELS IN AMYOTROPHIC LATERAL SCLEROSIS (ALS/MND) PATIENTS. Medical Sciences 14 3 154–162.
IEEE H. Orallar, Ş. Karabörk, B. G. Bozat, ve Ş. Aydın Türkoğlu, “CEREBROSPINAL FLUID (CSF) IL-17A, IL-17F, IL-34 AND CXCL-13 LEVELS IN AMYOTROPHIC LATERAL SCLEROSIS (ALS/MND) PATIENTS”, Medical Sciences, c. 14, sy. 3, ss. 154–162, 2019.
ISNAD Orallar, Hayriye vd. “CEREBROSPINAL FLUID (CSF) IL-17A, IL-17F, IL-34 AND CXCL-13 LEVELS IN AMYOTROPHIC LATERAL SCLEROSIS (ALS/MND) PATIENTS”. Medical Sciences 14/3 (Temmuz 2019), 154-162.
JAMA Orallar H, Karabörk Ş, Bozat BG, Aydın Türkoğlu Ş. CEREBROSPINAL FLUID (CSF) IL-17A, IL-17F, IL-34 AND CXCL-13 LEVELS IN AMYOTROPHIC LATERAL SCLEROSIS (ALS/MND) PATIENTS. Medical Sciences. 2019;14:154–162.
MLA Orallar, Hayriye vd. “CEREBROSPINAL FLUID (CSF) IL-17A, IL-17F, IL-34 AND CXCL-13 LEVELS IN AMYOTROPHIC LATERAL SCLEROSIS (ALS/MND) PATIENTS”. Medical Sciences, c. 14, sy. 3, 2019, ss. 154-62.
Vancouver Orallar H, Karabörk Ş, Bozat BG, Aydın Türkoğlu Ş. CEREBROSPINAL FLUID (CSF) IL-17A, IL-17F, IL-34 AND CXCL-13 LEVELS IN AMYOTROPHIC LATERAL SCLEROSIS (ALS/MND) PATIENTS. Medical Sciences. 2019;14(3):154-62.