It has long been hypothesized that there is a link between autoimmune conditions and the immune response to cancer, and this article covers some of the high points. Autoimmune conditions are a set of complicated failure modes in a very complex system, in which the immune system attacks the patient's own tissues. They are perhaps the least well understood diseases, and this is reflected in the poor state of treatments for autoimmunity: no cures, and the best that can be done for patients is to dampen the overall immune response. Any path forward that grants additional insight into the early development of autoimmunity is welcome.
Generations of in-depth research into human anatomy, histology, and basic physiology have largely explained the physical manifestations of diseases affecting nearly every organ of the body. Yet there remains an entire class of illnesses that present systemically, do not respect the boundaries of organ systems, and wreak havoc on quality of life and longevity. And we still have little idea of what starts the vicious cascade in the first place. This category of maladies is called autoimmune disease, and it is our fundamental lack of knowledge about these disorders that so greatly hinders our ability to prevent, diagnose, and treat them.
There is much we know, or think we know, about the risk factors and manifestations of autoimmune disease, and we even have some diagnostic tests for antibodies that often closely correlate with specific subtypes of disease. However, the fundamental biological mystery remains: What initiates the formation of antibodies that react with the body's own proteins and result in the destructive processes that define autoimmune disease? Have we simply failed to detect an infectious or environmental exposure that initiates the inflammatory cascade? Is there a benefit accrued via autoantibodies that serves an important biological purpose and helps to explain their existence?
While many theories have been and continue to be posited in answer to these etiological questions, a particularly interesting hypothesis first proposed in the 1960s has been reborn and, if it holds true, could have tremendous implications for the fields of rheumatology, oncology, immunology, neurology, endocrinology, and many others: autoimmune disease may represent collateral damage from the body's fight against developing cancers. Scientists have long recognized that patients with certain autoimmune diseases are at increased risk of cancer, but only recently has a possible mechanism been identified. Research involving patients with concurrent cancer and scleroderma revealed somatically mutated genes in the patients' tumors that initiated cellular immunity and cross-reactive humoral immune responses, producing antibodies that reacted to the cancer and are known to play an important role in scleroderma itself. The finding implies that the autoimmune disease may arise as an unintended consequence of the body's own immune response to a developing cancer, which in certain patients will never become clinically evident.