Many of the earlier descriptive reports about immunopathology anteceded the advent of recombinant DNA technology. As in most other areas of immunology, these methods now allow for a different approach to earlier questions in this field.

One change is that with the availability of recombinant cytokines, the role of these molecules has been recognized increasingly as mediators of immunopathologic events. For example, circulating recombinant tumor necrosis factor can cause widespread tissue damage; and local injection of recombinant interferon γ modifies the immunopathology of cutaneous leishmaniasis. Another is that the role of T cell immunopathology – cytotoxic events as a cause of damage rather than elimination of infected cells – has been increasingly recognized. Likewise, failure to induce a response (i.e. failure at the level of presentation) has been identified as a more significant form of immunopathology than was previously appreciated, based upon the experience with the acquired immune deficiency syndrome (AIDS).

Most recently, there has also been increasing awareness that the immunopathologic processes implicated in a particular disease may not involve a particular gene that encodes for a particular product, such as immunoglobulin. Rather, there may be dysregulation at the molecular level, via a controlling enhancer or suppressor sequence. It is from such concepts that the molecular immunopathology of the future is likely to develop.