264 Robert A. Aronowitz This concern about the vaccine has its origin in the belief that some late-stage complications of LD were caused by immune mechanisms rather than by direct effects of the infection. In particular, LD experts have speculated that some LD-associated arthritis, particularly cases that are not responsive to antibiotics, is due to the body’s immune attack on joints triggered by spirochete infection. Evidence for an autoimmune explanation of “treatment-resistant” LD-associated arthritis has included clinical similarities with rheumatoid arthritis, long understood as an autoimmune process, and the failure to find spirochetes in the affected joints. It is a small step from belief in an autoimmune mechanism for LD- related arthritis to concerns that the LD vaccine could induce autoimmu- nity. What if the antigens used in the vaccine were the same spirochete bits that caused autoimmunity following natural infection? Moreover, the heterodox community frequently cited autoimmunity as the me- diating mechanism for the chronic fatigue, pain, and other signs and symptoms that were prominent—and most contested and feared—in the alternative LD construction. If the vaccine itself caused a syndrome that was the same or similar to chronic Lyme disease, then these “side effects” constituted evidence in support of the alternative disease definition. And if the vaccine did not cause these symptoms, then the heterodox posi- tion, to which putative autoimmune mechanisms were central, could be undermined. These uncertain and contested beliefs about autoimmunity were the fertile soil from which opposition to the vaccine arose. Central to the case against the vaccine was the considerable scientific speculation in the years just before the vaccine’s introduction that OspA itself was the culprit antigen that triggered treatment-resistant LD-arthritis via molecular mimicry. Allen Steere, who is credited with discovering LD in the 1970s, did much of this research. He had suggested a possible connection between individuals who express HLA DR4 antigen (HLA antigens play crucial roles in distinguishing self from nonself and are frequently evoked to explain who develops autoimmunity), exposure to OspA, and subsequent treatment-resistant arthritis. There was some evidence that the OspA protein was similar to a human protein named LFA-1, which may play a role in autoimmune arthritis (Kalish, Leong, and Steere 1993). To some observers, Steere’s role in advancing and legitimating these concerns was paradoxical. After all, he helped develop the vaccine and