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Anti‐idiotype interactions are not required for the protective effect of intravenous immunoglobulin in a murine model of passively transferred immune thrombocytopenia
Author(s) -
Lazarus A. H.,
Song S.,
Freedman J.,
Crow A. R.
Publication year - 2000
Publication title -
transfusion medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.471
H-Index - 59
eISSN - 1365-3148
pISSN - 0958-7578
DOI - 10.1046/j.1365-3148.2000.00261-23.x
Subject(s) - antibody , immunology , idiotype , medicine , autoantibody , immune system , thrombocytopenic purpura , immune thrombocytopenia , autoimmunity , autoimmune disease , monoclonal antibody
The use of intravenous immunoglobulin (IVIg) as a treatment for autoimmune disease was first realized in the reversal of thrombocytopenia in Immune Thrombocytopenic Purpura (ITP) and, based upon this finding, it is currently used to treat an increasing number of autoimmune states and to prevent graft rejection. Previous reports, as well as much recent literature, have implied that the reactivity of variable region‐reactive (anti‐idiotypic) antibodies predominantly accounts for the beneficial effects of IVIg. Anti‐idiotypic antibodies reactive with endogenous Ig, autoantibodies, and those anti‐idiotype antibodies that modulate immune function have been implicated. Herein, we demonstrate that IVIg ameliorates thrombocytopenia in a passively transferred model of ITP (P‐ITP) and that anti‐idiotype antibodies present in IVIg ameliorates thrombocytopenia in a passively transferred model of ITP (P‐ITP) and that anti‐idiotype antibodies present in IVIg are not required for its protective effect. Both IVIg and an anti‐idiotype‐depleted IVIg protected equally against thrombocytopenia. As well, immunocompromised (SCID) mice, which lack endogenous IgM/G/A/D necessary for any idiotype‐anti–idiotype interactions, were protected by IVIg against thrombocytopenia to the same degree as normal mice.