Infection of autoreactive B lymphocytes with EBV, causing chronic autoimmune diseases

I hypothesize that human chronic autoimmune diseases are based on infection of autoreactive B lymphocytes by Epstein–Barr virus (EBV), in the following proposed scenario. During primary infection, autoreactive B cells are infected by EBV, proliferate and become latently infected memory B cells, whic...

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Bibliographic Details
Published in:Trends in immunology 2003-11, Vol.24 (11), p.584-588
Main Author: Pender, Michael P.
Format: Article
Language:English
Subjects:
Autoimmune diseases
Autoimmune Diseases - etiology
Autoimmune Diseases - immunology
Autoimmune Diseases - virology
Autoimmunity
B-Lymphocytes - immunology
Cytotoxicity
Disease
Epstein-Barr virus
Epstein-Barr Virus Infections - etiology
Epstein-Barr Virus Infections - immunology
Genes, MHC Class II
Herpes viruses
Herpesvirus 4, Human - pathogenicity
Humans
Hypotheses
Immune system
Lupus Erythematosus, Systemic - etiology
Lupus Erythematosus, Systemic - immunology
Lupus Erythematosus, Systemic - virology
Lymphocytes
Medical research
Models, Immunological
Multiple sclerosis
Multiple Sclerosis - etiology
Multiple Sclerosis - immunology
Multiple Sclerosis - virology
Rheumatoid arthritis
Studies
T-Lymphocytes - immunology
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Summary:I hypothesize that human chronic autoimmune diseases are based on infection of autoreactive B lymphocytes by Epstein–Barr virus (EBV), in the following proposed scenario. During primary infection, autoreactive B cells are infected by EBV, proliferate and become latently infected memory B cells, which are resistant to the apoptosis that occurs during normal B-cell homeostasis because they express virus-encoded anti-apoptotic molecules. Genetic susceptibility to the effects of B-cell infection by EBV leads to an increased number of latently infected autoreactive memory B cells, which lodge in organs where their target antigen is expressed, and act there as antigen-presenting cells. When CD4 + T cells that recognize antigens within the target organ are activated in lymphoid organs by cross-reactivity with infectious agents, they migrate to the target organ but fail to undergo activation-induced apoptosis because they receive a co-stimulatory survival signal from the infected B cells. The autoreactive T cells proliferate and produce cytokines, which recruit other inflammatory cells, with resultant target organ damage and chronic autoimmune disease.
ISSN:1471-4906
1471-4981
DOI:10.1016/j.it.2003.09.005