The invasion of pathogens, such as viruses and bacteria, triggers host immune response. The humoral immune response is an important anti-infection weapon of adaptive immunity. However, the humoral immune response shows two sides of the same coin: on one hand, pathogen-specific antibodies could eliminate pathogens and prevent disease progression whereas on the other hand, aberrant humoral immune responses are deleterious, leading to increased pathogen replication, severer tissue damage, and exacerbated disease outcome.
As a therapeutic strategy, antibodies, neutralizing antibodies in particular, are used to block pathogen invasion into target cells. For example, convalescent plasma is used to treat COVID-19 in clinic, and certain artificial monoclonal antibodies have been authorized for emergency use for the COVID-19 treatment. However, with the evolution of pathogens, the efficacy of the antibodies may be reduced. Therefore, it is imperative to develop new antibodies or devise improved strategies to fight against new variants.
The coin of humoral immune response has its reverse side. For example, HIV infection results in abnormal activation and exhaustion of B cells as well as deficiencies in the development of memory B cells. In some situations, antibodies can be deleterious and promote the pathogenesis caused by the pathogens, e.g., auto-antibodies against type I interferons are considered a risk factor of COVID-19. In addition, one concern of antibody-based therapy against infectious diseases is a phenomenon called antibody-dependent enhancement (ADE) where preexisting antibodies can enhance viral infection and/or result in severe symptoms. Thus, it is essential to develop novel strategies to generate therapeutical antibodies without ADE.
In this Research Topic, we aim to explore the two sides of humoral immune response, the antibody-based therapy and the deleterious and aberrant humoral immune response. We welcome the submission of Original Research Articles, Reviews, Case Reports, Clinical Trials, Methods, and Perspectives that address, but are not limited to, the following subtopics:
• Antibodies as therapeutics and preventions for viral infections
• Designing new strategies for effective neutralizing antibodies against virus variants
• Potential ADE risk in antibody-based therapy and developing antibodies without ADE
• The pathogenesis of ADE in viral infectious diseases
• Memory B cell dysregulation induced by viral infection
• Key molecules in regulating B cell activation and plasma cell differentiation
The invasion of pathogens, such as viruses and bacteria, triggers host immune response. The humoral immune response is an important anti-infection weapon of adaptive immunity. However, the humoral immune response shows two sides of the same coin: on one hand, pathogen-specific antibodies could eliminate pathogens and prevent disease progression whereas on the other hand, aberrant humoral immune responses are deleterious, leading to increased pathogen replication, severer tissue damage, and exacerbated disease outcome.
As a therapeutic strategy, antibodies, neutralizing antibodies in particular, are used to block pathogen invasion into target cells. For example, convalescent plasma is used to treat COVID-19 in clinic, and certain artificial monoclonal antibodies have been authorized for emergency use for the COVID-19 treatment. However, with the evolution of pathogens, the efficacy of the antibodies may be reduced. Therefore, it is imperative to develop new antibodies or devise improved strategies to fight against new variants.
The coin of humoral immune response has its reverse side. For example, HIV infection results in abnormal activation and exhaustion of B cells as well as deficiencies in the development of memory B cells. In some situations, antibodies can be deleterious and promote the pathogenesis caused by the pathogens, e.g., auto-antibodies against type I interferons are considered a risk factor of COVID-19. In addition, one concern of antibody-based therapy against infectious diseases is a phenomenon called antibody-dependent enhancement (ADE) where preexisting antibodies can enhance viral infection and/or result in severe symptoms. Thus, it is essential to develop novel strategies to generate therapeutical antibodies without ADE.
In this Research Topic, we aim to explore the two sides of humoral immune response, the antibody-based therapy and the deleterious and aberrant humoral immune response. We welcome the submission of Original Research Articles, Reviews, Case Reports, Clinical Trials, Methods, and Perspectives that address, but are not limited to, the following subtopics:
• Antibodies as therapeutics and preventions for viral infections
• Designing new strategies for effective neutralizing antibodies against virus variants
• Potential ADE risk in antibody-based therapy and developing antibodies without ADE
• The pathogenesis of ADE in viral infectious diseases
• Memory B cell dysregulation induced by viral infection
• Key molecules in regulating B cell activation and plasma cell differentiation
