RESEARCH - Infections, B cell receptor activation and autoimmunity: different check-point impairments lead to autoimmunity, clonal B cell expansion and fibrosis in different immunological settings

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Autoimmun Rev. 2007 Dec;7(2):109-13. Epub 2007 Mar 26.

Infections, B cell receptor activation and autoimmunity: Different

check-point impairments lead to autoimmunity, clonal B cell expansion and

fibrosis in different immunological settings.

Ferraccioli G, Tolusso B.

Division of Rheumatology, School of Medicine, Catholic University of the

Sacred Heart-CIC Via Moscati 31, Rome, 00168 Italy.

B cells as autoantibody producing cells are major players in several

autoimmune chronic inflammatory diseases (ACIDs). In some particular

settings (i.e. Sjogren's syndrome, rheumatoid arthritis), the activated B

cells could undergo malignant clonal expansion. Chronic infections by

lymphotropic viruses (hepatitis C virus, Epstein Barr Virus, Herpes 6 and 8

viruses) could amplify the activation process by inducing antiapoptotic

signals that lead to a longer survival of B cell subsets. This might then

lead, through multiple oncogenic events, to benign first and malignant

thereafter clonal B cell expansion. Understanding how the B cell are

activated, how the B cell receptor activation can be maintained under

control, which check-points could be deregulated and lead to a persistent

activation is of crucial importance in benign and malignant diseases. The

evidence suggests that the B cells faulty check-points are different in

chronic lymphocytic leukaemia, in cryoglobulinemia, rheumatoid arthritis,

systemic lupus erythematosus and systemic sclerosis.

PMID: 18035319

http://www.ncbi.nlm.nih.gov/pubmed/18035319?ordinalpos=2 & itool=EntrezSystem2

PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

Not an MD

[Guest guest]

Hi , from what I can gather this post is amazing and potentially very

hopeful. Thanks for sharing it and any other information you may find regarding

this.

Pam

<Matsumura_Clan@...> wrote:

Autoimmun Rev. 2007 Dec;7(2):109-13. Epub 2007 Mar 26.

Infections, B cell receptor activation and autoimmunity: Different

check-point impairments lead to autoimmunity, clonal B cell expansion and

fibrosis in different immunological settings.

Ferraccioli G, Tolusso B.

Division of Rheumatology, School of Medicine, Catholic University of the

Sacred Heart-CIC Via Moscati 31, Rome, 00168 Italy.

B cells as autoantibody producing cells are major players in several

autoimmune chronic inflammatory diseases (ACIDs). In some particular

settings (i.e. Sjogren's syndrome, rheumatoid arthritis), the activated B

cells could undergo malignant clonal expansion. Chronic infections by

lymphotropic viruses (hepatitis C virus, Epstein Barr Virus, Herpes 6 and 8

viruses) could amplify the activation process by inducing antiapoptotic

signals that lead to a longer survival of B cell subsets. This might then

lead, through multiple oncogenic events, to benign first and malignant

thereafter clonal B cell expansion. Understanding how the B cell are

activated, how the B cell receptor activation can be maintained under

control, which check-points could be deregulated and lead to a persistent

activation is of crucial importance in benign and malignant diseases. The

evidence suggests that the B cells faulty check-points are different in

chronic lymphocytic leukaemia, in cryoglobulinemia, rheumatoid arthritis,

systemic lupus erythematosus and systemic sclerosis.

PMID: 18035319

http://www.ncbi.nlm.nih.gov/pubmed/18035319?ordinalpos=2 & itool=EntrezSystem2

PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

Not an MD

Pam Tomlinson

PennCoveAlpacas

Oak Harbor, Wa.

(360-675-8364

" The New Stock Market "

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