Polyclonal BCell Activation Can Lead to Autoimmune Disease
Type 2 Diabetes Defeated
A number of viruses and bacteria can induce nonspecific polyclonal B-cell activation. Gram-negative bacteria, cytomegalovirus, and Epstein-Barr virus (EBV) are all known to be such polyclonal activators, inducing the proliferation of numerous clones of B cells that express IgM in the absence of TH cells. If B cells reactive to self-antigens are activated by this mechanism, auto-antibodies can appear. For instance, during infectious mononucleosis, which is caused by EBV, a variety of auto-antibodies are produced, including auto-antibodies reactive to T and B cells, rheumatoid factors, and antinuclear antibodies. Similarly, lymphocytes from patients with SLE produce large quantities of IgM in culture, suggesting that they have been polyclonally activated. Many AIDS patients also show high levels of nonspecific antibody and auto-antibodies to RBCs and platelets. These patients are often coinfected with other viruses such as EBV and cyto-megalovirus, which may induce the polyclonal B-cell activation that results in auto-antibody production.
Insulin gene promoter (PI)
Insulin structural gene
Insulin gene promoter
PI/IFN-y transgene
IFN-y Pancreas
IFN-y Pancreas
Cellular infiltration Transgenic mouse developed IDDM
Cellular infiltration Transgenic mouse developed IDDM
Insulin gene terminator region
Poly A
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Insulin gene terminator region Insulin gene promoter Insulin gene terminator region
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