Polyclonal BCell Activation Can Lead to Autoimmune Disease

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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 structural gene

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IFN-y gene

Insulin gene terminator region

Insulin gene promoter

Insulin gene terminator region

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IFN-y gene

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FIGURE 20-9

Insulin-dependent diabetes mellitus (IDDM) in transgenic mice. (a) Production of transgenic mice contaIning an IFN-7 transgene linked to the insulin promoter (PI). The transgenics, which expressed the PI/IFN-7 transgene only in the pancreas, developed symptoms characteristic of IDDM. (b) Pancreatic islets of Langerhans from a normal BALB/c mouse (left ) and from PI/IFN-7 transgenics at 3 weeks (right) showing infiltration of inflammatory cells. [Part (b) from N. Sarvetnick, 1988, Cell 52:773.]

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