About this Research Topic
Immune evasion is a strategy used by pathogenic organisms to evade a host’s immune system in order to optimize their survival probability, and potentially be transmitted to a new host. Over many years the host’s immune system has developed mechanisms to control pathogenic infections (bacterial and parasitic) ranging from the killing of infected cells to blocking the spread of infection through the release of cytokines. Similarly, pathogens have had to develop mechanism to evade the immune system and prevent their clearance.
Controlling pathogenic infections requires both the innate and adaptive immune responses, with the release of soluble mediators (chemokines, cytokines, etc), antibody production and the downregulation of apoptosis. One of the key hallmarks of autoimmune diseases is a dysregulation of cell proliferation. This dysregulation come about from the failure to regulate the cell cycle resulting in a lowered rate of apoptosis and hyperproliferation. Ultimately, this leads to an altered immune response to infections that can lead to the development of autoimmune conditions.
A prime example of this process is an Epstein Barr Virus (EBV) infection. Clinical and epidemiological data has shown a strong association between EBV infections and several autoimmune disorders like Rheumatoid Arthritis, Multiple Sclerosis, and Mysthenia Gravis. These disorders are characterized by the formation of ectopic follicles in atypical areas. Previous research has hypothesised that EBV infections could be responsible for the generation of autoreactive B and T cells to self-antigens. Other hypotheses postulate the EBV infections cause the expansion of autoreactive B cells and the production of superantigenic proteins which specifically inhibit the apoptosis of B cells.
In General, evidence shows that the complexity of immune escape mechanisms could have an important role in the low efficacy of immunotherapies in various diseases. This low efficacy is likely due to changes in expression of immune-modulating molecules during long lasting infections. This research topic aims to define and characterize the mechanisms of immune evasion from pathologies which in turn lead to the development of autoimmune disorders. Establishing these mechanisms will enable clinicians and researchers to develop and improve treatments for these autoimmune disorders.
Within this research topic we welcome the submission of Original research, Review article, Expert opinion, and mini-reviews. We welcome submissions based on these topics (but are not limited to them):
• Genetic and molecular Biology techniques
• Apoptosis
• Immunophenotyping
• Antiviral control by the immune system
• Balance in immune system biology
• Immune diseases and related therapies
Controlling pathogenic infections requires both the innate and adaptive immune responses, with the release of soluble mediators (chemokines, cytokines, etc), antibody production and the downregulation of apoptosis. One of the key hallmarks of autoimmune diseases is a dysregulation of cell proliferation. This dysregulation come about from the failure to regulate the cell cycle resulting in a lowered rate of apoptosis and hyperproliferation. Ultimately, this leads to an altered immune response to infections that can lead to the development of autoimmune conditions.
A prime example of this process is an Epstein Barr Virus (EBV) infection. Clinical and epidemiological data has shown a strong association between EBV infections and several autoimmune disorders like Rheumatoid Arthritis, Multiple Sclerosis, and Mysthenia Gravis. These disorders are characterized by the formation of ectopic follicles in atypical areas. Previous research has hypothesised that EBV infections could be responsible for the generation of autoreactive B and T cells to self-antigens. Other hypotheses postulate the EBV infections cause the expansion of autoreactive B cells and the production of superantigenic proteins which specifically inhibit the apoptosis of B cells.
In General, evidence shows that the complexity of immune escape mechanisms could have an important role in the low efficacy of immunotherapies in various diseases. This low efficacy is likely due to changes in expression of immune-modulating molecules during long lasting infections. This research topic aims to define and characterize the mechanisms of immune evasion from pathologies which in turn lead to the development of autoimmune disorders. Establishing these mechanisms will enable clinicians and researchers to develop and improve treatments for these autoimmune disorders.
Within this research topic we welcome the submission of Original research, Review article, Expert opinion, and mini-reviews. We welcome submissions based on these topics (but are not limited to them):
• Genetic and molecular Biology techniques
• Apoptosis
• Immunophenotyping
• Antiviral control by the immune system
• Balance in immune system biology
• Immune diseases and related therapies
Keywords: autoimmune, immune evasion, autoimmunity, infection, autoimmune disorders, epstein barr virus, rheumatoid arthritis
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