About this Research Topic
Malignant transformation of human cells is associated with the activation of immunosuppressive biochemical pathways, which allows them to escape immune surveillance. Cytotoxic lymphoid cells, mainly natural killer and T cells, are capable of attacking and eliminating malignant cells. There are several pathways that malignant cells can implement in order to create an immunosuppressive milieu and escape the immune attack, progressing in the disease.
On the other hand, a large number of individuals worldwide are affected by autoimmune disorders such as rheumatoid arthritis, psoriasis, multiple sclerosis, and many others. In autoimmune diseases, autoreactive T cells are considered as key players when acting as both regulatory and effector cells.
Based on the above, immunosuppressive biochemical pathways may become universal targets for immunotherapy in both human malignancies and autoimmune disorders. However, their targeting should lead to the opposite outcomes – downregulation in the case of cancer and activation in the case of autoimmunity.
The goal of this Research Topic is to provide recent advances in our understanding of the molecular and cellular mechanisms of anti-tumor immunity and autoimmune disease and, importantly, biochemical regulation and pharmacological correction of these immune networks.
We call for Original Research, Brief Research Reports, Reviews, Mini-Reviews, and Perspectives manuscripts that address the following topics:
• Recent advances in understanding the molecular mechanisms of anti-tumor immunity
• Novel findings related to tumour immune escape
• Novel approaches in anti-cancer immunotherapy
• Recent advances in understanding the mechanisms underlying autoimmune reactions
• Novel approaches for immunotherapy of autoimmune disease
• Key similarities and differences applicable to immunotherapy of cancer and autoimmune disease
• Pharmacological correction of immunosuppressive pathways
Keywords: cancer progression, cytotoxic lymphocytes (CTLs), autoimmune disease, autoreactive CTLs, immunosuppressive pathways
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