Content uploaded by Julio López Argüelles
Author content
All content in this area was uploaded by Julio López Argüelles on Oct 24, 2019
Content may be subject to copyright.
ACTA SCIENTIFIC MEDICAL SCIENCES (ISSN: 2582-0931)
Volume 3 Issue 11 November 2019
Brief Review of the Etiopathogenics Aspects in Multiple Sclerosis
Julio López Argüelles1*, Dra Leydi M Sosa Aguila2 and Lic Aleima B Rodriguez Carbajal1
1Neurology Department, University Hospital Gustavo Aldereguía Lima. Cienfuegos, Cuba
2Genetic Department, University Hospital Paquito González Cueto. Cienfuegos, Cuba
*Corresponding Author: Julio López Argüelles, Neurology Department, University Hospital Gustavo Aldereguía Lima. Cienfuegos, Cuba.
Review Article
Received: September 30, 2019; Published: October 23, 2019
Abstract
Keywords: Multiple Sclerosis; T Cells; Autoimmune; Pathogenesis
Introduction
have been postulated in order to explain their etio pathogenesis: 1) The existence of a persistent viral infection; 2) The presence of
an autoimmune process with loss of the to-lerance toward antigens of the myelin; and 3) The presence of a phenomenon of molecular
mímic between virales antigens and proteins of the myelin. Exists a generalized consensus of which this secondary mechanism is
event in the pathogenesis of multiple sclerosis is the activation of autoreactive T cells outside the central nervous system, either
-
quins or other T cells.
degenerative disease of the central nervous system. In its etiology
intervene environmental and genetic factors [1]. It is one of the
most frequent neurological disorders in the young adult of non-
traumatic etiology, that affects 2.5 million people in the world. The
40 years, very few cases are developed in the puberty or pasts the
60 years [2-5].
MS affects the female sex in a proportion of 3: 1 in comparison
with the masculine one. Furthermore, the disease is 5 times most
frequent in temperate climates than in the tropical ones. In Europe
are diagnosed approximately 10000 annual cases [6].
Even though the exact cause of the MS is unknown, many sci-
entists think that the destruction of the myelin is due to certain
immunity altered in genetically susceptible individuals, this im-
pathogens, particularly virus and among them Epstein-Barr.
Discussion
Three hypotheses have been postulated in order to explain the
etio¬pathogenesis of MS: 1) The existence of a persistent viral in-
fection; 2) The presence of an autoimmune process with loss of the
tolerance toward antigens of the myelin; and 3) The presence of
a phenomenon of molecular mímic between vi-rales antigens and
proteins of the myelin. Even though numerous indirect evidence
favors the existence of a viral cause as the one responsible for the
onset of the disease, up to the no present virus has been isolated
from tissues of the totality of patients with MS [7-9].
On the other hand, some agents viral postulates inclement as
causes of the disease have been isolated in individuals that did not
suffer MS. If actually occurs a viral infection of the central nervous
system (CNS) during the infancy, then during the puberty or adult
Citation: Julio López Argüelles., et al. “Brief Review of the Etiopathogenics Aspects in Multiple Sclerosis". 2.11 (2019):
110-112.
Brief Review of the Etiopathogenics Aspects in Multiple Sclerosis
111
age some other secondary factor it should trigger the disease or
else to exacerbate it.
Exists a generalized consensus of which this secondary mecha-
nism is probably found to be represented by an autoimmune reac-
tion that attacks somes of the protein components of the myelin [9].
Different observations support this possibility: 1) The anatomico-
pathological characteristics of the demyelinating injuries. In them
presence of lymphocytes and macrophages activated, complement
united to the macrophages, phagocytosis of fragments of myelin,
expression of the complex greater of histocompatibility class II in
-
nally presence of lymphocytes T associated to stress proteins in
the chronic injuries; 2) The similarity of the post-vaccinates inju-
ries observed in MS and the ones that become evident in encepha-
lomyelitis and experimental allergic ence-falitis; 3) The presence
in these patients of anomalies both in lymphocytic T and in the
immunoglobulins; 4) The increase in the activity of the disease in
an immunogenetic «background» in patients that present MS [10].
The evidence previously presented permit pustular the follow-
autogenesis’s T cells against antigens of the myelin, exist normally
in the immune system. Such cells have escaped from thymic mech-
in the pathogenesis of MS is the activation of these autoreactive
cells outside the CNS, either specify, through mechanisms of mo-
-
cally through mechanisms middle by cytokines or other T cells. As
a consequence of the activation, the lymphocytes T acquire the ca-
pacity to be expanded, cause different cytokines, and increase the
expression of adhesion molecules on its surface. This alternative
permits to T lymphocytes to adhere to the endothelial cells that
express the adequate against-receptors, to pass through the peri-
vascular space and to reach thus the CNS [11,12].
united to the greater complex of present histocompatibility in as-
trocytes or cells of the microglia, and are in this way re-activated.
This phenomenon of re-activation implies the production of differ-
free radicals, or nitric oxide [13].
The certain cytokine secretion during the course in MS is found
to be implied both in the induction and in the regulation of the dis-
in MS. Inversely IL-4, IL-10 and TGF-ß are associated with an inhi-
bition of the immune response in the CNS. The secretion of such
cytokines can come from cells CD4+ that have entered the CNS from
-
ies, or else of living cells glial [14].
Adicional cells CD4+ can contribute to the activation of B Cells
and consequently to the production of antibodies against different
components of the myelin. Different studies have demonstrated
that the macrophages not only produce DE myelinization through
mechanisms of phagocytosis of the myelin but also through the
cytokines, toxic metabolites of the oxygen and eicosanoids. These
factors can in turn stimulate other cells and to contribute to local
tissue damage affecting both the myelin and the oligodendrocytes
and increasing the permeability of the hematoencephalic barrier,
-
Which are the mechanisms by which the immunological factors,
and consequently the clinical manifestations, can be limited in EM?
Exists sustanciales evidence that suggests that during the recu-
that the local apoptosis of the T cells is an important factor in the
-
logical effect of the phenomenon of demyelination is the limitation
in the management of the electric impulse saltatorial from a node
of Ranvier, to the next node. Such limitation in the transmission of
the nerve impulse can be manifested either as a decrement in the
action to frequencies discharges or else by a blockade total of the
management [11].
Other alterations in the management of the Tambien nerve im-
-
ample the generation of ectopic potentials for action, or else the
-
Citation: Julio López Argüelles., et al. “Brief Review of the Etiopathogenics Aspects in Multiple Sclerosis". 2.11 (2019):
110-112.
112
Brief Review of the Etiopathogenics Aspects in Multiple Sclerosis
-
impulse. This series of defects in the transmission of the nerve im-
pulse mediate the majority of the clinical anomalies observed in
demyelinating diseases [13,15].
In spite of the foregoing other authors in addition describe the
possibility of the action of a related secondary factor with an anti-
aging gene that is associated with autoimmune disease and multi-
ple sclerosis and the diets (high calorie, xenobiotics) that suppress
the gene with relevance to autoimmunity [16,18].
Conclusions: The current studies emphasize the presence of
an autoimmune phenomenon in the etiopathogeneses of multiple
sclerosis, resulting in the symptomatic variability, the type of dis-
ease and the evolution of the disease.
Bibliography
None to declare.
1. Bartulos IM., et al. “Epidemiological study of multiple sclero-
sis in La Rioja”. Neurologia 30.9 (2014): 552-560.
2. Tullman MJ. “Overview of the epidemiology, diagnosis, and
disease progression associated with multiple sclerosis”. The
19.2 (2013): s15-s20.
3. Alajbegovic A., et al. “Epidemiology of multiple sclerosis in
Bosnia and Herzegovina”.
8.1 (2011): 56-60.
4. Handel AE., et al. “The epidemiology of multiple sclerosis in
Scotland: inferences from hospital admissions”. PLoS One 6.1
(2011): e14606.
5. Manack A., et al. “Epidemiology and healthcare utilization of
neurogenic bladder patients in a US claims database”. Neurou
rology and Urodynamics 30.3 (2011): 395-401.
6. Boiko AN., et al. “Clinical epidemiology of multiple sclerosis
in Moscow. Discriptive epidemiology in population of one re-
gion of Moscow”. (2013):
8-14.
7. Lisak RP. “Human retrovirus pHEV-W envelope protein and
the pathogenesis of multiple sclerosis”. Proceedings of the
National Academy of Sciences of the United States of America
116.30 (2019):14791-14793.
8. Nourbakhsh B and Mowry EM. “Multiple Sclerosis Risk Factors
and Pathogenesis”. 25.3 (2019):
596-610.
9. Martin R and McFarland HF. “Immunology of Multiple Sclero-
sis and experimental allergic encephalomyelitis”. In: Raine CS,
McFarland HF, editors. Multiple Sclerosis: clinical and patho-
genic basis. London: Chapman and Hall (1997): 221-242.
10. Zarobkiewicz MK., et al. “Gammadelta T lymphocytes in the
pathogenesis of multiple sclerosis and experimental autoim-
mune encephalomyelitis”. Journal of Neuroimmunology 330
(2019): 67-73.
11. Tarlinton RE., et al. “The Interaction between Viral and Envi-
ronmental Risk Factors in the Pathogenesis of Multiple Scle-
rosis”. 20.2 (2019):
303.
12. Dziedzic A and Bijak M. “Interactions between platelets and
leukocytes in pathogenesis of multiple sclerosis”. Advances in
28.2 (2019): 277-285.
13. Oksenberg JR. “Pathogenesis of Multiple Sclerosis: Relation-
ship to therapeutic strategies”. In: Goodkin DE, Rudick RA,
editors. Multiple Sclerosis. Advances in clinical trial design,
treatment and future perspectives. 2nd ed. London: Springer-
Verlag (1997): 17-46.
14. Teniente-Serra A., et al. “Immunomonitoring Lymphocyte Sub-
populations in Multiple Sclerosis Patients”. (2017).
15. Lucchinetti CF and Rodriguez M. “The controversy surround-
ing the pathogenesis of the multiple sclerosis lesion”.
Clinic Proceedings 72.7 (1997): 665-678.
16. Increased Risk for Obesity and Diabetes with Neurodegenera-
tion in Developing Countries. Top 10 Contribution on Genetics.
Chapter 1, EBook (2018).
17. Nimmagadda VK., et al. “SIRT1 and NAD+ precursors: Thera-
peutic targets in multiple sclerosis a review”. Journal of Neuro
immunology 304 (2017): 29-34.
18. Foolad F., et al. “Sirtuins in Multiple Sclerosis: The crossroad of
neurodegeneration, autoimmunity and metabolism”.
Sclerosis and Related Disorders 34 (2019): 47-58.
Volume 3 Issue 11 November 2019
© All rights are reserved by Julio López Argüelles., et al.
Citation: Julio López Argüelles., et al. “Brief Review of the Etiopathogenics Aspects in Multiple Sclerosis". 2.11 (2019):
110-112.
