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--- group_5_presentation_1_-_multiple_sclerosis [2016/09/25 19:13]
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+++ group_5_presentation_1_-_multiple_sclerosis [2018/01/25 15:18] (current)
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-**Multiple Sclerosis (MS)** is an autoimmune disease affecting the central nervous system. The disease specifically affects the myelin and as a result inflammation occurs and the myelin is damaged. Myelin performs the crucial role of nerve impulse through nerve fibers. If myelin is damaged then there will be a decrease in the transmission of nerve impulses. When the damage is significant then scar tissue will replace the myelin. The symptoms of MS vary for each individual, some include fatigue, pain, bladder problems, walking problems, cognitive difficulties and optic neuritis. Canada currently has the highest rate of MS with approximately 100,000 Canadians currently diagnosed (Multiple Sclerosis Society of Canada,2016).
+**Multiple Sclerosis (MS)** is an autoimmune disease affecting the central nervous system. The disease specifically affects the myelin and as a result inflammation occurs and the myelin is damaged. Myelin performs the crucial role of nerve impulse through nerve fibers. If myelin is damaged then there will be a decrease in the transmission of nerve impulses. When the damage is significant then scar tissue will replace the myelin. The symptoms of MS vary for each individual, some include fatigue, pain, bladder problems, walking problems, cognitive difficulties and optic neuritis. Canada currently has the highest rate of MS with approximately 100,000 Canadians currently diagnosed (Multiple Sclerosis Society of Canada, 2016).
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 ====== Symptoms ======
-MS symptoms vary from person to person.
+MS symptoms vary from person to person (Multiple Sclerosis Clinical Presentation, 2016).
 MS Symptoms include:
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 {{:ms-mri_t1_535x314-01.jpg|}}
-Figure 1: A T1-weighted MRI demonstrating permanent lesions in a MS patient. The dark spots
+**Figure 1**: A T1-weighted MRI demonstrating permanent lesions in a MS patient. The dark spots
 in the scan are the lesions. (Source: Spinms, 2016)
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-The diagnosis of Multiple Sclerosis (MS) can be detected through MRI, lumbar puncture and electroencephalography. MS is difficult to diagnose due to the multiple symptoms associated with the disease, which can vary from person to person. Magnetic resonance imaging (MRI) can be used to reveal areas of lesions. However, MRI has disadvantages as it lacks specificity and many conditions have similar conditions of MS and as a result many false positives occur. It has been determined that 90% of MS patients will display an abnormal MRI scan and thus MRI should be the first diagnostic tool to be used. However, 5% of individuals show no sign of lesions in the brain while using MRI.
+The diagnosis of Multiple Sclerosis (MS) can be detected through MRI, lumbar puncture and electroencephalography. MS is difficult to diagnose due to the multiple symptoms associated with the disease, which can vary from person to person. Magnetic resonance imaging (MRI) can be used to reveal areas of lesions. However, MRI has disadvantages as it lacks specificity and many conditions have similar conditions of MS and as a result many false positives occur. It has been determined that 90% of MS patients will display an abnormal MRI scan and thus MRI should be the first diagnostic tool to be used. However, 5% of individuals show no sign of lesions in the brain while using MRI (Rolak, 2003).
-When there are abnormalities in the cerebrospinal fluid, it can be used to diagnose MS. In the Cerebral spinal fluid (CSF), the white blood cell and spinal fluid proteins are slightly elevated.  An elevated Immunoglobin G level in CSF is the most significant in detecting MS. The Immunoglobin G reflects an autoimmune activation and appears as oligoclonal bands on the electrophoresis performed on the CSF. Oligoclonal bands indicate the presence of immunoglobins, which indicate inflammation in the central nervous system. The oligoclonal bands vary from MS patient, but 90% of MS patients present these bands. A limitation to this method is other diseases produce these bands as well and can lead to misdiagnosis. To obtain the CSF it requires undergoing lumbar puncture, which many patients are unsure of doing.
+When there are abnormalities in the cerebrospinal fluid, it can be used to diagnose MS. In the Cerebral spinal fluid (CSF), the white blood cell and spinal fluid proteins are slightly elevated.  An elevated Immunoglobin G level in CSF is the most significant in detecting MS. The Immunoglobin G reflects an autoimmune activation and appears as oligoclonal bands on the electrophoresis performed on the CSF. Oligoclonal bands indicate the presence of immunoglobins, which indicate inflammation in the central nervous system. The oligoclonal bands vary from MS patient, but 90% of MS patients present these bands. A limitation to this method is other diseases produce these bands as well and can lead to misdiagnosis. To obtain the CSF it requires undergoing lumbar puncture, which many patients are unsure of doing (Rolak, 2003).
-Another method that could be used is evoked potential, which is used to measure conduction rates in the CNS pathway though the recording of electroencephalographic response to sensory stimulation.  Slow conduction rates indicate inflammation and demyelination, presenting an MS lesion.
+Another method that could be used is evoked potential, which is used to measure conduction rates in the CNS pathway though the recording of electroencephalographic response to sensory stimulation.  Slow conduction rates indicate inflammation and demyelination, presenting an MS lesion (Rolak, 2003).
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   * Primary progressive (PPMS)
-Clinically Isolated Syndrome refers to a first episode where there is inflammatory demyelination in the CNS. It is not yet considered MS, but could become MS if further activity occurs. In the relapse and remitting stage this indicates good health followed by an immediate change in symptoms. Secondary progressive MS occurs after the relapse and remitting stage. At this point there are more symptoms that are progressively getting worse. Primary progressive MS is the steady development of symptoms that will eventually become worse as the diseases progresses. RRMS, SPMS, and PPMS can be active or not active depending on if there is evidence of relapse or disease activity present.
+Clinically Isolated Syndrome refers to a first episode where there is inflammatory demyelination in the CNS. It is not yet considered MS, but could become MS if further activity occurs. In the relapse and remitting stage this indicates good health followed by an immediate change in symptoms. Secondary progressive MS occurs after the relapse and remitting stage. At this point there are more symptoms that are progressively getting worse. Primary progressive MS is the steady development of symptoms that will eventually become worse as the diseases progresses. RRMS, SPMS, and PPMS can be active or not active depending on if there is evidence of relapse or disease activity present (Hedley, 2012).
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 Initially, for the T cells to cause lesion formation, they need to penetrate the Blood-brain barrier. The Blood-brain barrier consists of endothelial cells, tight junctions and basement membrane (Löscher and Potschka, 2005). The immune system cells travels through blood vessels which also contain endothelial cells. The Blood-brain barrier has selective permeability and prevents the immune system cells from entering the brain (Wingerchuk et al., 2001). However, when triggered by a virus such as Epstein Barr Virus (EBV), the Blood-brain barrier can be penetrated by T cells that can be autoreactive or be programmed to attack myelin protein present on the axons of the neurons (Wu and Alvarez, 2011).
-Inflammation in the area due to a virus or foreign substances causes more T cells and macrophages to be recruited into the Blood-brain barrier due to the help of increased expression of adhesion molecules (Wingerchuk et al., 2001). Then, activated and non-activated T cells can secrete Matrix metalloproteinases (MMPs) which cause the degradation of the extracellular matrix, therefore weakening the Blood-brain barrier and allowing for other leukocytes and macrophages to enter (Wingerchuk et al., 2001). Inside the Central Nervous System, T cells can be activated by Antigen Presenting Cells and antibodies, therefore releasing an increased amount of chemokines and cytokines, which can recruit a much larger inflammatory response and lead to initiation of lesion formation (Wingerchuk et al., 2001).<sup>[X]</sup>.
+Inflammation in the area due to a virus or foreign substances causes more T cells and macrophages to be recruited into the Blood-brain barrier due to the help of increased expression of adhesion molecules (Wingerchuk et al., 2001). Then, activated and non-activated T cells can secrete Matrix metalloproteinases (MMPs) which cause the degradation of the extracellular matrix, therefore weakening the Blood-brain barrier and allowing for other leukocytes and macrophages to enter, as highlighted in //Figure 2// (Wingerchuk et al., 2001). Inside the Central Nervous System, T cells can be activated by Antigen Presenting Cells and antibodies, therefore releasing an increased amount of chemokines and cytokines, which can recruit a much larger inflammatory response and lead to initiation of lesion formation (Wingerchuk et al., 2001).
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-{{:screen_shot_2016-09-23_at_7.57.09_pm.png|Figure X: Illustrates the mechanism used by T cells to penetrate the Blood-brain Barrier.
+{{:screen_shot_2016-09-23_at_7.57.09_pm.png|Figure 2: Illustrates the mechanism used by T cells to penetrate the Blood-brain Barrier.
  (Source: Wingerchuk et al., 2001)}}
-**Figure X**: Illustrates the mechanism used by T cells to penetrate the Blood-brain
+**Figure 2**: Illustrates the mechanism used by T cells to penetrate the Blood-brain.
 Barrier (Source: Wingerchuk et al., 2001).
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 **Lesions:**
 In Multiple Sclerosis, lesions will be formed in the white matter of the brain due to demyelination of neurons in the Central Nervous System. Demyelination or lesion formation can occur in any area, but most often occurs in the periventricular regions, optic nerves, brainstem, cerebellum and spinal cord (Wingerchuk et al., 2001). Demyelination usually occurs due to an autoimmune response by T cells towards myelin protein and oligodendrocytes, which are responsible for synthesizing myelin protein (Wu and Alvarez, 2011).
-<sup>[X]</sup>.
 Different type of lesions: (Wu and Alvarez, 2011)
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   * **Pattern III:** Loss of Oligodendrocytes and myelin glycoprotein
   * **Pattern IV:** Oligodendrocytes dystrophy and absence of remyelination
- <sup>[X]</sup>.
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-{{:screen_shot_2016-09-23_at_7.53.57_pm.png|Figure X: Illustrates the inflammatory response towards myelin protein, thus causing formation of lesions (Source: Luzzio, (n.d.).)}}
+{{:screen_shot_2016-09-23_at_7.53.57_pm.png|Figure 3: Illustrates the inflammatory response towards myelin protein, thus causing formation of lesions (Source: Luzzio, (n.d.).)}}
-**Figure X**: Illustrates the inflammatory response towards myelin
+**Figure 3**: Illustrates the inflammatory response towards myelin
 protein, thus causing formation of lesions (Source: Luzzio, (n.d.)).
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 **Lesion Formation Mechanism: (Brosnan)**
-One of the proposed mechanisms of lesion formation was further examined by Brosnan and Raine (1996). They proposed that CD4 T cells were activated outside the Blood-brain barrier by Antigen presenting cells to either myelin protein or oligodendrocytes. The CD4 T cells would enter the Blood-brain barrier and the  activated CD4 T cells would recognize antigens presented by microglial cells, which are the macrophages in the Blood-brain barrier or B cells antibodies (Brosnan and Raine, 1996). Once the MHC class 2 receptor recognition and costimulation occur, the CD4 T cells can now release cytokines such as TNF-alpha, gamma-IFN and IL-17. Then the activated microglial cell releases free radicals, nitric oxide, proteases which can cause destruction of tissue in Central Nervous System and recruit more of an inflammation response. This can ultimately cause irreversible tissue and axonal damage and therefore leading to the formation of lesions (Brosnan and Raine, 1996).<sup>[X]</sup> [Figure X].
+One of the proposed mechanisms of lesion formation was further examined by Brosnan and Raine (1996) and is illustrated below in //Figure 3//. They proposed that CD4 T cells were activated outside the Blood-brain barrier by Antigen presenting cells to either myelin protein or oligodendrocytes. The CD4 T cells would enter the Blood-brain barrier and the  activated CD4 T cells would recognize antigens presented by microglial cells, which are the macrophages in the Blood-brain barrier or B cells antibodies (Brosnan and Raine, 1996). Once the MHC class 2 receptor recognition and costimulation occur, the CD4 T cells can now release cytokines such as TNF-alpha, gamma-IFN and IL-17. Then the activated microglial cell releases free radicals, nitric oxide, proteases which can cause destruction of tissue in Central Nervous System and recruit more of an inflammation response. This can ultimately cause irreversible tissue and axonal damage and therefore leading to the formation of lesions (Brosnan and Raine, 1996).
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-{{:screen_shot_2016-09-23_at_8.10.04_pm.png|Figure X:Demonstrates the location and as well as the immune cells involved in the production of IL-17
+{{:screen_shot_2016-09-23_at_8.10.04_pm.png|Figure 4:Demonstrates the location and as well as the immune cells involved in the production of IL-17
   (Source: Tzartos et al., 2008).}}
-**Figure X**: Demonstrates the location and as well as the immune cells involved
+**Figure 4**: Demonstrates the location and as well as the immune cells involved
 in the production of IL-17 (Source: Tzartos et al., 2008).
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 **Inflammation:**
 The attacks by the T-cells on myelin cause inflammatory processes, triggering other immune cells, cytokines and antibodies. The Blood-brain barrier starts to swell as well as macrophages are activated along with cytokines and other destructive proteins (Wu and Alvarez, 2011).
-<sup>[X]</sup>
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 **Effect of Demyelination:**
 After demyelination, the nerve tissue is damaged and the axons are not able to conduct action potentials effectively due to loss of myelin, which ultimately acts as an insulator. This prevents the body to communicate with the Central Nervous System effectively, therefore causing numbness in certain areas of the body (Smith and McDonald, 1999).
-<sup>[X]</sup>
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-{{:screen_shot_2016-09-23_at_8.03.06_pm.png|Figure X: Illustrates the expression of CD3 T cells and as well as the activity of the CD3 T cells based on IL-17 production in patients with different stages of MS.
+{{:screen_shot_2016-09-23_at_8.03.06_pm.png|Figure 5: Illustrates the expression of CD3 T cells and as well as the activity of the CD3 T cells based on IL-17 production in patients with different stages of MS.
 (Source: Tzartos et al., 2008)}}
-**Figure X:** Illustrates the expression
+**Figure 5:** Illustrates the expression
 of CD3 T cells and as well as the
@@ Line 187: / Line 187: @@
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 **Evidence Supporting Immune-mediated Pathophysiology:**
-In an experiment conducted by Tzartos et al. (2008), they wanted to explore specifically which immune system factors and cells were involved in demyelination as well as the  role of Interleukin-17 in demyelination (Tzartos et al., 2008). Initially, they wanted to determine whether T cells, astrocytes, microglia/macrophages, oligodendrocytes were able to produce IL-17, since there were earlier reports that IL-17 is present in higher concentrations in MS tissues. They used in situ hybridization and immunofluorescent-labelled IL-17 mRNA (Tzartos et al., 2008). In addition, they also labelled the interested cells and used an overlap imaging technique to show where IL-17 was present and therefore indicating its production . Astrocytes, T cells, oligodendrocytes all overlapped with IL-17 expression while microglia/macrophages did not (Tzartos et al., 2008). ( Fig X- T cells showed the largest expression, while astrocytes and oligodendrocytes showed small amount). In another experiment, they then wanted to see whether there was an increase of activity of CD3 T cell involved ( Th17 cells) in lesions/plaques and compare this to normal nerve tissue. They also looked at IL-17 to assess the activity of the activated Th17 cells (Tzartos et al., 2008). Using tissue samples from the perivascular areas of acute lesions, active borders of chronic active lesions, inactive lesions, inactive areas of chronic active lesions and as well as NAWM in MS patients(normal appearing white matter), they observed that there was increased amount of IL-17 cytokine and CD3 T cells in MS patient tissues samples compared to the non MS brain (control variable) . This indicated that IL-17 is largely involved in the inflammatory response in MS (Tzartos et al., 2008). In addition, they looked at alternative method to quantify the presence of IL-17 in MS patient brain sample. They compared the densities and were able to conclude the similar results as previously reported. Therefore, demonstrating that  IL-17 and CD3 T cells were involved in carrying out an inflammatory response leading to demyelination of neurons (Tzartos et al., 2008).  Fig <sup>[X]</sup>
+In an experiment conducted by Tzartos et al. (2008), they wanted to explore specifically which immune system factors and cells were involved in demyelination as well as the  role of Interleukin-17 in demyelination (Tzartos et al., 2008). Initially, they wanted to determine whether T cells, astrocytes, microglia/macrophages, oligodendrocytes were able to produce IL-17, since there were earlier reports that IL-17 is present in higher concentrations in MS tissues. They used in situ hybridization and immunofluorescent-labelled IL-17 mRNA (Tzartos et al., 2008). In addition, they also labelled the interested cells and used an overlap imaging technique to show where IL-17 was present and therefore indicating its production . Astrocytes, T cells, oligodendrocytes all overlapped with IL-17 expression while microglia/macrophages did not, as shown in //Figure 4// (Tzartos et al., 2008). In another experiment, they then wanted to see whether there was an increase of activity of CD3 T cell involved ( Th17 cells) in lesions and compare this to normal nerve tissue. They also looked at IL-17 to assess the activity of the activated Th17 cells (Tzartos et al., 2008). Using tissue samples from the perivascular areas of acute lesions, active borders of chronic active lesions, inactive lesions, inactive areas of chronic active lesions and as well as NAWM in MS patients(normal appearing white matter), they observed that there was increased amount of IL-17 cytokine and CD3 T cells in MS patient tissues samples compared to the non MS brain (control variable), highlighted in //Figure 5// below. This indicated that IL-17 is largely involved in the inflammatory response in MS (Tzartos et al., 2008). In addition, they looked at alternative method to quantify the presence of IL-17 in MS patient brain sample. They compared the densities from //Figure 6// and were able to conclude the similar results as previously reported. Therefore, demonstrating that  IL-17 and CD3 T cells were involved in carrying out an inflammatory response leading to demyelination of neurons (Tzartos et al., 2008).
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-{{:zjh0010875050004.jpg|Figure X:Illustrates the observed expression as a density for both CD3 T cells and IL-17 based on the different stages of MS (Source: Tzartos et al., 2008).}}
+{{:zjh0010875050004.jpg|Figure 6:Illustrates the observed expression as a density for both CD3 T cells and IL-17 based on the different stages of MS (Source: Tzartos et al., 2008).}}
-**Figure X:** Illustrates the observed expression as a density for both CD3 T cells and
+**Figure 6:** Illustrates the observed expression as a density for both CD3 T cells and
 IL-17 based on the different stages of MS (Source: Tzartos et al., 2008).
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 >Glatiramer acetate is thought to alter the immune processes believed to be responsible for the pathogenesis of MS, however its mechanism is not fully known. (Hedley, 2012) Studies have shown that there is delay of progression from CIS to “clinically definite MS” in MS patients for up to three years with use of glatiramer acetate. (Hedley, 2012) This treatment reduces the number and severity of relapses, and the formation of new lesions on a brain MRI, however its effects on long-term progression are not clear. (Hedley, 2012) Adverse effects of glatiramer acetate minor and mainly consist of injection site reactions, seen in 70% of patients. (Hedley, 2012) Other less common side effects include lipoatrophy, flushing, shortness of breath, chest tightness, and palpitations. (Hillman, 2014)
-Deciding on which treatment to use (interferon beta or glatiramer acetate) depends on patient preference in type and frequency of injection. (See Figure **X**)
+Deciding on which treatment to use (interferon beta or glatiramer acetate) depends on patient preference in type and frequency of injection. (See Figure 7)
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@@ Line 250: / Line 250: @@
 {{:table_01.png|}}
-&nbsp;**Figure X**: The dosing, frequency, and route of administration for the ACB-R therapies. (Source: Hillman & Khorassani, 2014)
+&nbsp;**Figure 7**: The dosing, frequency, and route of administration for the ACB-R therapies. (Source: Hillman & Khorassani, 2014)
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@@ Line 296: / Line 296: @@
 {{:treadmill_training.jpg|}}
-**Figure X**: Body weight assisted treadmill training. There is physical assistance for each
+**Figure 8**: Body weight assisted treadmill training. There is physical assistance for each
 leg due to impaired walking ability. (Source: http://agelessphysio.com)
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 __Walking Ability__
-> A common symptom of MS is impaired walking ability. Dalfampridine (Fampyra or Ampyra) can be used to improve walking ability. Dalfampridine is a potassium channel blocker that enhances conduction along demyelinated nerve fibres. (Hillman, 2014) In phase 3 clinical trials, walking speed was increased by about 25% within weeks in MS patients. (Hedley, 2012) There are, however, side effects such as a greater risk of seizures, anxiety, insomnia, dizziness, and tremor. (Hedley, 2012) In terms of physical therapy, exercise through treadmill training has been shown to improve walking endurance and velocity. (Amato & Portaccio, 2012) (See Figure **X**)
+> A common symptom of MS is impaired walking ability. Dalfampridine (Fampyra or Ampyra) can be used to improve walking ability. Dalfampridine is a potassium channel blocker that enhances conduction along demyelinated nerve fibres. (Hillman, 2014) In phase 3 clinical trials, walking speed was increased by about 25% within weeks in MS patients. (Hedley, 2012) There are, however, side effects such as a greater risk of seizures, anxiety, insomnia, dizziness, and tremor. (Hedley, 2012) In terms of physical therapy, exercise through treadmill training has been shown to improve walking endurance and velocity. (Amato & Portaccio, 2012) (See Figure 8)
 __Depression__
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 </HTML>
+====== Conclusion ======
+Multiple Sclerosis is an inflammatory, autoimmune disease which disrupts the neurons’ ability to trigger action potentials. As of today, the pathophysiology of this disease is not fully understood, however, considerable advances have been made in understanding the factors behind this disease. It is evident that further research needs to be conducted to figure out the precise mechanism of the demyelination and remyelination process. The findings of this research will lead to more efficient treatment mechanisms and may even lead to a cure for Multiple Sclerosis.
+<HTML>
+<br>
+</HTML>
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 Amato, M. P. & Portaccio, E. (2012). Management options in multiple sclerosis-associated fatigue. Expert Opinion on Pharmacotherapy, 13(2), 207-216
+Ascherio A, Munger KL (April 2007). "Environmental risk factors for multiple sclerosis. Part I: the role of infection". Annals of Neurology. 61 (4): 288–99.
 Brosnan, C. F., & Raine, C. S. (1996). Mechanisms of immune injury in multiple sclerosis. Brain Pathology, 6(3), 243-257.
+Compston A, Coles A (October 2008). "Multiple sclerosis". Lancet. 372 (9648): 1502–17
 de la Fuente AG et al. Vitamin D receptor-retinoid X receptor heterodimer signaling regulates oligodendrocyte progenitor cell differentiation. J Cell Biol. 2015; 211(5):975-85.
 Multiple Sclerosis Clinical Presentation. (2016). Retrieved September 18, 2016, from http://emedicine.medscape.com/article/1146199-clinical
+Dyment DA, Ebers GC, Sadovnick AD (February 2004). "Genetics of multiple sclerosis".Lancet Neurol. 3 (92): 104–10
 Fowler, C. J., Panicker, J. N., Drake, N., Harris, C., Harrison, S. C. W., Kirby, M., Lucas, M., Macleod, N., Mangnall, J., North, A., et al. (2009). A UK consensus on the management of the bladder in multiple sclerosis. Postgraduate Medical Journal. 85, 552-559.
+Gilden DH (March 2005). "Infectious causes of multiple sclerosis". The Lancet Neurology. 4 (3): 195–202
 Hedley, L. (2012). Multiple sclerosis treatment options. The Pharmaceutical Journal. 288, 247-250.
@@ Line 348: / Line 366: @@
 Löscher, W., & Potschka, H. (2005). Blood-brain barrier active efflux transporters: ATP-binding cassette gene family. NeuroRx, 2(1), 86-98.
+Multiple Sclerosis Clinical Presentation. (2016). Retrieved September 18, 2016, from http://emedicine.medscape.com/article/1146199-clinical
 Multiple Sclerosis Society of Canada. (2016). Retrieved September 18, 2016, from https://mssociety.ca/about-ms/what-is-ms
@@ Line 365: / Line 385: @@
 Wucherpfennig, K. W., & Strominger, J. L. (1995). Molecular mimicry in T cell-mediated autoimmunity: viral peptides activate human T cell clones specific for myelin basic protein. Cell, 80(5), 695-705.

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