Complement activation by immune complexes induces inflammation, but during this process the nature of the complexes is altered. Once immune complexes have attained sufficient lattice to activate complement, further increase of the lattice and immune precipitation are limited by the incorporation of complement components. The presence of complement components in immune complexes facilitates their disposal from circulation by complement receptors on red cells in humans. Without complement activation the disposal of immune complexes of sufficient lattice is mediated by Fc receptors. The development of immune deposits in tissues can arise by several mechanisms. Circulating immune complexes may be deposited in a number of vascular beds. Immune deposits in tissues may also arise by local formation. This process may involve structural antigens in tissues, cell surface antigens that are shed after interaction with specific antibodies or antigens that have become planted in tissues and then combine with antibodies. Charge-charge interactions enhance deposition of immune complexes in several organs, involving fixed negative charges in tissues and positive charges on antigens or antibodies in immune complexes. Successful detection of immune deposits in dermal vessels requires the examination of fresh lesions. Local vascular changes contribute significantly to deposition of immune complexes in dermal vessels. Charge-charge interactions enhance this deposition and contribute to the development of deposits at the dermal-epidermal junction in experimental animals.