scholarly journals Potential Role of Bacterial Infection in Autoimmune Diseases: A New Aspect of Molecular Mimicry

2014 ◽  
Vol 14 (1) ◽  
pp. 7 ◽  
Author(s):  
Jehan Alam ◽  
Yong Chul Kim ◽  
Youngnim Choi
2021 ◽  
Vol 5 (1) ◽  
Author(s):  
Moon Ley Tung ◽  
Bryce Tan ◽  
Robin Cherian ◽  
Bharatendu Chandra

Abstract As the coronavirus disease 2019 (COVID-19) pandemic, which is caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), is spreading rapidly worldwide, it has emerged as a leading cause of mortality, resulting in >1 million deaths over the past 10 months. The pathophysiology of COVID-19 remains unclear, posing a great challenge to the medical management of patients. Recent studies have reported an unusually high prevalence of thromboembolic events in COVID-19 patients, although the mechanism remains elusive. Several studies have reported the presence of aPLs in COVID-19 patients. We have noticed similarities between COVID-19 and APS, which is an autoimmune prothrombotic disease that is often associated with an infective aetiology. Molecular mimicry and endothelial dysfunction could plausibly explain the mechanism of thrombogenesis in acquired APS. In this review, we discuss the clinicopathological similarities between COVID-19 and APS, and the potential role of therapeutic targets based on the anti-phospholipid model for COVID-19 disease.


1996 ◽  
Vol 64 (6) ◽  
pp. 2031-2040 ◽  
Author(s):  
B J Appelmelk ◽  
I Simoons-Smit ◽  
R Negrini ◽  
A P Moran ◽  
G O Aspinall ◽  
...  

2019 ◽  
Vol 48 ◽  
pp. 1-10 ◽  
Author(s):  
Chan-Na Zhao ◽  
Peng Wang ◽  
Yan-Mei Mao ◽  
Yi-Lin Dan ◽  
Qian Wu ◽  
...  

2014 ◽  
Vol 15 (4) ◽  
pp. 223-229
Author(s):  
Bojana Simovic Markovic ◽  
Ljubica Vucicevic ◽  
Sanja Bojic ◽  
Vladislav Volarevic

ABSTRACT Autophagy is a catabolic mechanism in the cell that involves the degradation of unnecessary or dysfunctional cellular components by the lysosomal machinery. Recent studies have indicated that autophagy is a source of autoantigens, thus highlighting its potential role in the pathogenesis of autoimmunity. There are at least three different forms of autophagy: macroautophagy, microautophagy and chaperone-mediated autophagy (CMA). The physiological role of autophagy is to maintain cellular homeostasis by removing long-lived, damaged proteins and dysfunctional organelles and by providing energy. Aberrant autophagy may contribute to chronic inflammatory diseases and autoimmune diseases. An understanding of the complex relationships between autophagy and autophagy-related genes in each autoimmune disease creates the possibility of developing more specific and effective therapeutic strategies. Given the importance of autophagy in immune functions, this review article summarises current knowledge about the role of autophagy in the pathogenesis of autoimmune diseases.


Cells ◽  
2021 ◽  
Vol 10 (4) ◽  
pp. 756
Author(s):  
Aaron Lerner ◽  
Carina Benzvi

Wheat is a most favored staple food worldwide and its major protein is gluten. It is involved in several gluten dependent diseases and lately was suggested to play a role in non-celiac autoimmune diseases. Its involvement in neurodegenerative conditions was recently suggested but no cause-and-effect relationship were established. The present narrative review expands on various aspects of the gluten-gut-brain axes events, mechanisms and pathways that connect wheat and gluten consumption to neurodegenerative disease. Gluten induced dysbiosis, increased intestinal permeabillity, enteric and systemic side effects, cross-reactive antibodies, and the sequence of homologies between brain antigens and gluten are highlighted. This combination may suggest molecular mimicry, alluding to some autoimmune aspects between gluten and neurodegenerative disease. The proverb of Hippocrates coined in 400 BC, “let food be thy medicine,” is critically discussed in the frame of gluten and potential neurodegeneration evolvement.


1981 ◽  
Vol 377 (1 Myasthenia Gr) ◽  
pp. 486-495 ◽  
Author(s):  
Allan L. Goldstein ◽  
Marion M. Zatz ◽  
Teresa L. K. Low ◽  
Robert Jacobs

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