| dc.creator |
ÖZBALCI, Demircan |
|
| dc.date |
2021-07-01T00:00:00Z |
|
| dc.date.accessioned |
2021-12-03T11:16:01Z |
|
| dc.date.available |
2021-12-03T11:16:01Z |
|
| dc.identifier |
1dcedeb4-df7b-44ff-b6d2-83579539883c |
|
| dc.identifier |
10.1016/j.mehy.2021.110619 |
|
| dc.identifier |
https://avesis.sdu.edu.tr/publication/details/1dcedeb4-df7b-44ff-b6d2-83579539883c/oai |
|
| dc.identifier.uri |
http://acikerisim.sdu.edu.tr/xmlui/handle/123456789/90301 |
|
| dc.description |
Sars Cov-2, the pathogen which belongs to the beta coronavirus family that is responsible for COVID-19, uses Angiotensin Converting Enzyme 2 (ACE2) as a receptor, which is responsible for controlling the actions of reninangiotensin system (RAS). Sars Cov-2 - ACE2 binding leads to a RAS mediated immune response, which targets especially lungs to form ARDS, which in turn, is the most important cause of mortality in COVID-19. CD8+ T cell response dominates over CD4+ T cell response and natural killer cell dysfunction also leads to CD4+ cell dysfunction in COVID-19; this immune dysregulation leads to inappropriate (ARDS) and inadequate (low or quickly waning antibodies) responses to the disease and unfortunately, prepares the patients for re-infections. The peripheral anergy seen in chronic sarcoidosis has much resemblance to COVID-19; CD8+ T cell accumulation is also responsible for inadequate reaction to tuberculin and antigenic stimulus. This article, based on the similarity of COVID-19 and sarcoidosis, discusses a combination of the therapeutic strategy of the tetanusdiphtheria vaccine and dual RAS inhibition, alongside with hydroxychloroquine and antiviral agents, as a solution to overcome the problems described above. |
|
| dc.language |
eng |
|
| dc.rights |
info:eu-repo/semantics/closedAccess |
|
| dc.title |
A tale of two diseases: Sarcoidosis, COVID-19 and new therapeutic options with dual RAS inhibition and tetanus-diphtheria vaccine |
|
| dc.type |
info:eu-repo/semantics/article |
|