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Although the media (inner layer, asterisk) is relatively unaffected, a dense lymphoplasmacytic infiltrate is present on the adventitial aspect (outer layer) of the aorta, and a vein obliterated by inflammation is indicative of obliterative phlebitis (arrow). Storiform fibrosis (Panel B, hematoxylin and eosin) is characteristic of IgG4-related disease, such as IgG4-related dacryoadenitis. IgG4 with two different antigen-combining sites behaves as a monovalent antibody. In vitro analyses suggest that Fc interactions between IgG4 molecules are an intermediate stage preceding Fab-arm exchange (Panel C). These interactions may prevent inflammatory responses by shielding Fc portions from other immune-related molecules.
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A number of autoimmune diseases that affect diverse organ systems have recently been noted to be related to IgG4 autoantibodies. Because of the instability of the disulfide bonds between heavy chains of IgG4, some IgG4 antibodies form intrachain disulfide bonds in the hinge region and consist of heavy chains linked by noncovalent interaction (Panel B). IgG4 is transformed to an asymmetric, bispecific antibody by exchanging half-molecules with other IgG4 molecules (Panel D). A tissue specimen from a patient with IgG4-related aortitis shows virtually the entire wall of the aorta (Panel A, hematoxylin and eosin). IgG4 molecules are released from plasma cells as symmetric homobivalent antibodies (Panel A). Media in This Article Figure 1 Biologic Characteristics of IgG4. The authors review the spectrum of IgG4-related disease and the current status of diagnostic and management approaches.
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