All patients with pattern II (= 10), but none with pattern I (= 3) or pattern III (= 6), achieved moderate to substantial functional neurological improvement after PLEX ( 0

All patients with pattern II (= 10), but none with pattern I (= 3) or pattern III (= 6), achieved moderate to substantial functional neurological improvement after PLEX ( 0.0001) [29]. cause of nontraumatic disability among young adults and has great socioeconomic impact in developed countries [6]. Based on the epidemiological studies, approximately 400,000 people have MS in the United States, with 200 new cases added every week. The pathogenesis of MS remains elusive and there were no definitive cause and no effective remedy. Therefore, MS can be classified as an episodic demyelinating disease of the central nervous system. Disease pathophysiology is usually complex and entails genetic susceptibility, environmental factors, and development of a pathologic immune-mediated response leading to focal myelin destruction, axonal loss, and focal inflammatory infiltrates. The pathophysiology of MS is usually further fraught with confusion as researchers struggle to classify the disease as either pathological [7] or clinical [8]. Investigators and clinicians who have studied MS agree that the immune system plays a critical role in the development of lesions, especially during the acute early phases of the disease characterized by relapses. Relapses are fundamentally a manifestation of an inflammatory response occurring mostly in the white matter of the nervous system but also within myelin tracts in the gray matter. This results in focal demyelination with relative axonal sparing. The best evidence for inflammation-induced relapses comes from work in MRI, which demonstrates the association of relapses with gadolinium enhancement that is disruption of the blood brain barrier. The main pathologic hallmark of MS is the demyelinated plaque, which has specific histological and immunocytological characteristics depending on the activity of ZJ 43 the disease [9C12]. Histologically, an MS plaque is ZJ 43 usually characterized by marked predominance of CD8+ T cells and a relative lack of CD4+ T cells (ratios of 100?:?1 to 50?:?1). In addition, there is a sea of macrophages, which may have a primary role in engulfing myelin debris. Whether they are also main effectors in the disease process is usually unknown. Another important immunopathological feature is usually continuous synthesis of immunoglobulins (oligoclonal IgG’s) in cerebrospinal fluid (CSF). The evidence associating antibodies with MS derives from studies such as by Kabat et al., who explained increased levels Rabbit polyclonal to c-Kit of immunoglobulin (Ig) in the cerebrospinal fluid (CSF) [13]. CSF IgG and oligoclonal bands remain the most predictive ZJ 43 immunological test for the diagnosis of MS. All immunoglobulin subtypes ZJ 43 have been implicated in MS. The underlying immunological abnormalities lead to presentation of ZJ 43 different autoimmune manifestations. 2. Is usually MS an Autoimmune Disease? From most recommendations gleaned in the literature, MS is usually boldly stated as an autoimmune disorder. However, the evidence for such a statement is usually poor and circumstantial. We have updated and revised criteria for determining whether a disease is usually autoimmune in nature [14]. The main criterion of a given autoimmune disease is usually that a precise autoantigen be present in all patients with the disease. Despite multiple attempts to identify numerous proteins, lipids, and gangliosides in myelin as potential MS antigens, none have been confirmed or confirmed. Secondly, administration of autoantibody or T cells induces autoimmune disease in normal animals. These approaches have been attempted in animal models of MS with contrasting results [15, 16]. A third criterion is the ability to induce lesions by immunizing animals with relevant autoantigen. This had been partially achieved but with problems. The fact that multiple different antigens can induce the disease process in animal models without one specific antigen being superior to the other makes the results ambiguous from your standpoint of identifying the relevant antigen. The fourth criterion is the ability to isolate autoantibody or autoreactive T cells from your lesion or from serum. Many investigators have suggested a higher precursor frequency of T cells, specifically of the CD4 subgroup, in patients with MS when compared to healthy controls, which identify MBP, proteolipid protein (PLP), MOG, or other such antigens from myelin. Regrettably, because similar positive results are obtained from normal.

Related Posts