Sandbox:Feham: Difference between revisions

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Types II and III CG — The mixed CGs (types II and III) generally result from chronic inflammatory states, such as connective tissue diseases, like systemic lupus erythematosus or Sjögren's syndrome, or viral infections, such as HCV, although lymphoproliferative disorders have rarely been associated as well. Many of these disease states share B-cell hyperactivation and/or hyperproliferation [13,30], which seem to predispose to the selective expansion of CG-producing B-cell clone(s) [31], but a precise ontology of pathogenic CGs in mixed CG has not been delineated. This paradigm of pathogenesis has been most intensively studied for chronic HCV infection, in which B-cell hyperactivation may result upon direct infection via the cell surface protein CD81 [32], via chronic, antigen-nonspecific stimulation by macromolecular serum complexes containing HCV, including HCV-IgG and HCV-lipoprotein [33,34], or via an HCV antigen-specific mechanism [35], resulting in expansion of specific B-cell clones such as those expressing the WA idiotype [36] or V(H)1-69 [37]. HCV particles are often found in such patients' serum CG complexes, but, at the same time, CG development in hepatitis C infection does not directly require the HCV virion or its components [38]. In this sense, CG development may, in fact, reflect a normal, expected response to regulate immune complexes in states of chronic immune activation.
* Mixed Cryoglobulinemia is a combination of both types II and III.
 
* Mixed CGs is associated with following conditions:
Among patients with HCV infection, the number of circulating T cells with surface markers compatible with a suppressor phenotype may be a feature that differs between patients with cryoglobulinemic vasculitis and those with asymptomatic CG. This was illustrated in a study that compared the percentage of "regulatory" T cells in 69 patients with HCV infection who had symptomatic CG with others with asymptomatic HCV infection [39]. The mean levels of regulatory T cells were significantly lower in those with symptomatic HCV-associated CG than asymptomatic subjects (2.6 versus 7.4 percent, respectively). Whether the diminished proportion of regulatory T cells plays a role in causing vasculitis is uncertain but warrants further exploration.
** '''SLE (systemic lupus erythematous)'''
**  '''Sjögren's syndrome,'''
** '''HCV'''
** '''Lymphoproliferative disorders'''
* Al the above mentioned disorders can cause excessive production of B-cell which can further lead to selective expansion of Cryoglobulinemia producing B-cell clones.
* In HCV infected patients the HCV complexes such as HCV-IgG, HCV-lipoprotein cause B-cell hyper-proliferation through the CD81 leading to expansion of specific B-cell clones such as WA idiotype or V(H)1-69.  
* HCV particles are often found in such patients' serum CG complexes, but, at the same time, CG development in hepatitis C infection does not directly require the HCV virion or its components [38]. In this sense, CG development may, in fact, reflect a normal, expected response to regulate immune complexes in states of chronic immune activation.
* Among patients with HCV infection, the number of circulating T cells with surface markers compatible with a suppressor phenotype may be a feature that differs between patients with cryoglobulinemic vasculitis and those with asymptomatic CG.  
* This was illustrated in a study that compared the percentage of "regulatory" T cells in 69 patients with HCV infection who had symptomatic CG with others with asymptomatic HCV infection [39].  
* The mean levels of regulatory T cells were significantly lower in those with symptomatic HCV-associated CG than asymptomatic subjects (2.6 versus 7.4 percent, respectively).  
* Whether the diminished proportion of regulatory T cells plays a role in causing vasculitis is uncertain but warrants further exploration.

Revision as of 17:22, 23 May 2018

  • Mixed Cryoglobulinemia is a combination of both types II and III.
  • Mixed CGs is associated with following conditions:
    • SLE (systemic lupus erythematous)
    • Sjögren's syndrome,
    • HCV
    • Lymphoproliferative disorders
  • Al the above mentioned disorders can cause excessive production of B-cell which can further lead to selective expansion of Cryoglobulinemia producing B-cell clones.
  • In HCV infected patients the HCV complexes such as HCV-IgG, HCV-lipoprotein cause B-cell hyper-proliferation through the CD81 leading to expansion of specific B-cell clones such as WA idiotype or V(H)1-69.
  • HCV particles are often found in such patients' serum CG complexes, but, at the same time, CG development in hepatitis C infection does not directly require the HCV virion or its components [38]. In this sense, CG development may, in fact, reflect a normal, expected response to regulate immune complexes in states of chronic immune activation.
  • Among patients with HCV infection, the number of circulating T cells with surface markers compatible with a suppressor phenotype may be a feature that differs between patients with cryoglobulinemic vasculitis and those with asymptomatic CG.
  • This was illustrated in a study that compared the percentage of "regulatory" T cells in 69 patients with HCV infection who had symptomatic CG with others with asymptomatic HCV infection [39].
  • The mean levels of regulatory T cells were significantly lower in those with symptomatic HCV-associated CG than asymptomatic subjects (2.6 versus 7.4 percent, respectively).
  • Whether the diminished proportion of regulatory T cells plays a role in causing vasculitis is uncertain but warrants further exploration.
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