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Vol. 13. Issue 51.
Pages 72 (April 2011)
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Vol. 13. Issue 51.
Pages 72 (April 2011)
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About Primary Biliary Cirrhosis
Acerca de la cirrosis biliar primaria
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José de Jesús Román-Sandovala, Misael Uribea, Nahum Méndez-Sáncheza
a Liver Research Unit. Medica Sur Clinic and Foundation. Mexico City. Mexico
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In the present review Montano-Loza and Mason published in this issue, analyzed the main clinical, histological, biochemical characteristics of primary biliary cirrhosis (PBC). In addition, those researchers point out the genetic and environmental factors associated with the development of PBC in order to explain if there is or not any association of microbial etiology in PBC.

In fact, some studies have suggested a microbial etiology for PBC, based on the premise of molecular similarity between the human 2-OADC-E2 and the corresponding bacterial proteins.1 In addition, a viral association in PBC has also been suggested based on viral particles identified in the bile duct epithelial cells (BECs) from patients with PBC by electron microscopy, a retroviral sequence cloned from BECs and a proviral genome of a beta retrovirus cloned from the lymph node from patients with PBC.2,3

However, since PBC is considered an autoimmune disease, it is important to mention that a hypothesis on the role of microbial etiology (parasite, bacteria, yeast or virus) suggest that an infectious agent displays epitopes immunologically resembling host determinants. Also, due to the minor antigenic differences between the two, the pathogen's epitope is able to induce an immune response that breaks tolerance to the host epitope. The cross-reactive T or B cell is then able to induce a pathogenic autoimmune response that leads to disease.4

On the other hand, innate immunity is suspected to play a key role in various forms of autoimmunity, but the precise mechanisms involved in activating and propagating autoreactive T and B cells have remained obscure. One frequent cause of innate immune activation is represented by overt or unrecognized bacterial or viral infections, but revealing microbial involvement and understanding the cellular and molecular mechanisms leading to autoimmunity generally remain a challenge.5

In summary, Montano-Loza and Mason have nicely reviewed the main factors involved in the etiopathogenesis of PBC and we concluded that although the etiology of PBC remains unknown, the infectious agents need to be carefully reevaluated in order to prove their role in the etiopathogenesis of PBC.


Correspondence: Nahum Méndez-Sánchez, MD, PhD.

Puente de Piedra 150, Col. Toriello Guerra, Tlalpan 14050, Mexico City, Mexico.

Phone: (+525) 55424 7200 Ext. 4215; Fax: (+525) 55 666- 4031.

E-mail:nmendez@medicasur.org.mx

Bibliography
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Leung PSC, Coppel RL, Gershwin ME..
Etiology of primary biliary cirrhosis: The search for the culprit..
, 25 (Semin Liver Dis 2005), pp. 327-336
[2]
Mason A, Nair S..
Primary biliary cirrhosis: new thoughts on pathophysiology and treatment..
, 4 (Curr Gastroenterol Rep 2002), pp. 45-51
[3]
Xu L, Shen Z, Guo L, et al..
Does a betaretrovirus infectiontrigger primary biliary cirrhosis? Proc Natl Acad Sci USA 2003..
, 100 pp. 8454-8459
[4]
Davies JM..
Molecular mimicry: can epitope mimicry induce autoimmune disease? Immunol Cell Biol 1997..
, 75 pp. 113-26
[5]
Mattner J, Savage PB, Leung P, et al..
Liver autoimmunity triggered by microbial activation of natural killer T cells..
, 15 (Cell Host Microbe 2008), pp. 3
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