Despite considerable progress in the clinical treatment of cardiovascular diseases (CVD), atherosclerosis and its sequelae, myocardial infarction, ischemic heart disease, and stroke continue to represent the leading cause of mortality worldwide. It is now clear that besides traditional cardiovascular risk factors, chronic inflammation in arteries and the heart, accompanies, triggers, and modulates CVD. While novel, unspecific, anti-inflammatory treatments that target down-stream inflammatory signals have started to attract clinical attention, the participation of the cells of the adaptive immune system remains less well-defined. A growing body of evidence suggest that atherosclerosis and ischemic heart disease are driven by an autoimmune response against specific antigens that have the potential to orchestrate cardiovascular inflammation. This autoimmune response encompasses antigen-specific T- and B-lymphocytes, autoantibodies, and various cellular interactions with stromal and innate immune cells. Preclinical models suggest that cardiovascular autoimmunity may be addressable by novel immunomodulation and tolerogenic vaccination against certain autoantigens, which holds great promise of specific, causal, and safe therapeutic strategies in the future. Exact triggers, antigens, and dynamics of this immune response as well as potential targets for future clinical therapies, however, remain only partially understood.
Cardiovascular autoimmunity is a systemic, local event, and highly context-dependent; atherosclerosis affects various organs beyond the heart. Some autoantigens, such as LDLs, are generated in the gut, travel to distant organs through the bloodstream, accumulate in arteries, are transported in the lymphatics, get presented by antigen-presenting cells in lymph nodes, and will be recognized by autoreactive lymphocytes in lymph nodes and tissues. In humans, this response is highly individual, shaped by genetic variation and immunometabolism, develops over decades, and may be amplified by environmental factors. This complexity can only be understood by a holistic and systems immunology approach that defines and integrates autoantigens, immune effectors (antibodies, cytokines), cellular interactions, transcriptional programs, and immune cell heterogeneity with a spatial, functional, and temporal dimension. This Research Topic aims to present and discuss evidence from systems immunology approaches in cardiovascular disease.
In particular, this research should cover:
1) Basic mechanisms of innate and adaptive immune cell generation and function in cardiovascular pathologies.
2) High-dimensionality approach (proteomics, transcriptomics, imaging) to define immune cell heterogeneity in cardiovascular pathologies.
3) Novel tools and concepts to quantify or target CVD-associated immune cell function in mice and humans.
4) Immune cell function at the interface of CVD and metabolism.
5) Comparative analyses of immune cell functionality in CVD in mice and humans.
Despite considerable progress in the clinical treatment of cardiovascular diseases (CVD), atherosclerosis and its sequelae, myocardial infarction, ischemic heart disease, and stroke continue to represent the leading cause of mortality worldwide. It is now clear that besides traditional cardiovascular risk factors, chronic inflammation in arteries and the heart, accompanies, triggers, and modulates CVD. While novel, unspecific, anti-inflammatory treatments that target down-stream inflammatory signals have started to attract clinical attention, the participation of the cells of the adaptive immune system remains less well-defined. A growing body of evidence suggest that atherosclerosis and ischemic heart disease are driven by an autoimmune response against specific antigens that have the potential to orchestrate cardiovascular inflammation. This autoimmune response encompasses antigen-specific T- and B-lymphocytes, autoantibodies, and various cellular interactions with stromal and innate immune cells. Preclinical models suggest that cardiovascular autoimmunity may be addressable by novel immunomodulation and tolerogenic vaccination against certain autoantigens, which holds great promise of specific, causal, and safe therapeutic strategies in the future. Exact triggers, antigens, and dynamics of this immune response as well as potential targets for future clinical therapies, however, remain only partially understood.
Cardiovascular autoimmunity is a systemic, local event, and highly context-dependent; atherosclerosis affects various organs beyond the heart. Some autoantigens, such as LDLs, are generated in the gut, travel to distant organs through the bloodstream, accumulate in arteries, are transported in the lymphatics, get presented by antigen-presenting cells in lymph nodes, and will be recognized by autoreactive lymphocytes in lymph nodes and tissues. In humans, this response is highly individual, shaped by genetic variation and immunometabolism, develops over decades, and may be amplified by environmental factors. This complexity can only be understood by a holistic and systems immunology approach that defines and integrates autoantigens, immune effectors (antibodies, cytokines), cellular interactions, transcriptional programs, and immune cell heterogeneity with a spatial, functional, and temporal dimension. This Research Topic aims to present and discuss evidence from systems immunology approaches in cardiovascular disease.
In particular, this research should cover:
1) Basic mechanisms of innate and adaptive immune cell generation and function in cardiovascular pathologies.
2) High-dimensionality approach (proteomics, transcriptomics, imaging) to define immune cell heterogeneity in cardiovascular pathologies.
3) Novel tools and concepts to quantify or target CVD-associated immune cell function in mice and humans.
4) Immune cell function at the interface of CVD and metabolism.
5) Comparative analyses of immune cell functionality in CVD in mice and humans.
