Key result
Transfer of anti-idiotype pulsed B cells induces antiviral antibodies and overt autoimmune myocarditis.
Why the study?
The mechanisms by which anti-idiotype pulsed B cells contribute to the development of autoimmune myocarditis were not fully understood.
Anti-idiotype cell transfer induces autoimmune myocarditis in mice; hypothesis-generating for similar mechanisms in human disease.
Syngeneic mice receiving adoptively transferred enriched B cells or splenocytes pulsed in vitro with polyclonal anti-idiotypic antibodies (anti-Ids) against anti-CVB3 virus antibodies developed coxsackievirus B3 antigen-binding and virus-neutralizing antibodies during a 30-day period, in addition to overt expression of autoimmune myocarditis. Adoptive transfer of anti-Id pulsed T cells resulted in delayed appearance and transient expression of antiviral antibodies, and antiviral antibodies were marginal to absent in syngeneic animals receiving anti-Id pulsed macrophage populations. Proliferation analysis of recipient splenocytes indicated lack of proliferative capacity in response to monoclonal or polyclonal anti-Ids and only marginal proliferative capacity in response to coxsackievirus B3 virus antigen(s). In vitro assessment of delayed hypersensitivity in recipient animals demonstrated some specific immunity to anti-Ids in recipients receiving splenocytes or T cells. Anti-Ids expressing mimicry for heart-associated and/or viral antigen(s) interacting with B cells or other accessory cells suggest an autoantibody or anti-Id triggering of B-cell-mediated mechanisms involved in the development of myocarditis.
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Paque et al. (1992) studied Autoimmune myocarditis. Adoptively transferred enriched B cells or splenocytes pulsed with polyclonal anti-idiotypic antibodies vs. Anti-idiotype pulsed T cells or macrophage populations was evaluated on Development of coxsackievirus B3 antigen-binding and virus-neutralizing antibodies, and overt expression of autoimmune myocarditis. Adoptive transfer of anti-idiotype pulsed B cells or splenocytes in syngeneic mice led to the development of antiviral antibodies and overt autoimmune myocarditis during a 30-day period.
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