such as "Introduction", "Conclusion"..etc
Auto-antibodies specific to different "self" molecules have been found in the sera of tumor
bearers, which could be taken as an evidence for frequent joint activity of anti-tumor immunity and autoimmunity.
This emphasizes the idea that tumor patients can mount tumor immunity which could be, in part,
auto-immunity. In contrast to patients with auto-immune diseases, in the majority, if not all, tumor patients
the immune system is unable to combat tumor growth.
Tumors seem to find ways to generate tolerance in the immune system by activating the control
mechanisms of auto-immune reaction responsible for the tolerance against "self" molecules. These
mechanisms include a down-regulation of MHC class I molecules and cellular constituents involved in the
antigen processing and presentation pathways (20). Tumors can also induce several different biochemical
defects in physiology of T lymphocytes. In addition, the immune response against tumors is hindered by
the functional hierarchy in the immunogenicity of T and B cell determinants, abnormalities occurring in the
communication between the cells of innate and adoptive immunity, as well as the inadequate cytokine
Notwithstanding these and other escape mechanisms, in few cancer patients a spontaneous
regression of malignant tumors was observed (23,24). Data about potential coupling of auto-antibodies and
prolonged/sustained survival or even spontaneous tumor regression corroborate the previous observation.
Breast cancer patients with a natural humoral response to MUC-1 and/or hsp90 exhibited a better outcome
(25,26). Similar to immunological events in some auto-immune diseases, tumor in regression exhibited
mainly a Th1 type response, as well as non-pathogenic auto-antibodies, but thus the form of auto-immunity
did not always develop into the auto-immune disease. There is data that about the potential coupling of
tumor immunity with auto-immunity has been suggested by the clinical observation that the patients with
metastatic melanoma who develop vitiligo have a better prognosis (27). In addition, there are observations
that support a possible protective role for the auto-immune diseases in cancer patients. In this respect, the
mortality rate of cancer patients with multiple sclerosis was found to be significantly lower than that of
cancer patients in general (23). This could be associated with the activation of control anti-auto-immune
mechanisms which may also inhibit auto-immunity and anti-tumor activity of the immune system.
In conclusion, the potential coupling of tumor immunity with auto-immunity has been suggested by the
clinical observation that patients with metastatic tumor who develop auto-immune phenomena have a better
prognosis and are more likely to respond to therapy (27,28). The differences in mechanisms underlying
tumor immunity and auto-immunity could be a consequence of fundamental differences in effector
mechanisms used to kill tumor cells versus normal cells. At the same time, the mechanisms controlling
"self"-destructive immune reaction might be one of the important factors of anti-tumor immunity failure.
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