Suppression of development of experimental autoimmune XXXX with isogeneic monoclonal anti-idiotopic antibody.

@entity9176 @entity1737 @entity425 @entity35 @entity934
We have made use of isogeneic anti-idiotopic (anti-Id) monoclonal antibodies (mAb to modify experimental autoimmune @entity1737 (EAMG) in Lewis @entity35 . High-avidity anti-Id mAb HC-4A (Kd = 0.1 nM) and HC-29 (Kd = 0.1 nM) were produced against an anti- @entity934 receptor (anti- @entity9176 ) Lewis- @entity35 mAb 132A (Kd = 0.34 nM) that is capable of inducing passive-transfer EAMG. mAb HC-4A and HC-29 define separate framework Id cross-reactive with anti- @entity9176 mAb recognizing different @entity9176 epitopes. Animals were preinjected i.p. with either anti-Id mAb or with control mAb and then were actively immunized 2 wk later with purified @entity9176 . All animals had elevated total serum anti- @entity9176 antibody titers, despite the absence of @entity425 or decremental electromyographic findings. Animals preinjected with control mAb developed serum anti- @entity9176 titers of 1.34 +/- 0.29 microM (mean +/- SEM) and reduced muscle @entity9176 content to 30 percent of normal. Animals injected with 0.5 mg/kg of either anti-Id had significantly lower serum anti- @entity9176 titers, 0.55 +/- 0.1, p less than 0.05, and normal muscle @entity9176 content. Both the 132A Id and the anti-Id complementary to 132A were detected in the serum of all of the animals preinjected with this dose of either anti-Id HC-29 or HC-4A, whereas both were detected in a much smaller percentage of the animals receiving control mAb. These results show that pretreatment with anti-Id not only perturbs this Id-anti-Id network, but also suppresses the overall polyclonal anti- @entity9176 response with resultant protection of actively immunized animals from EAMG.
