TY - JOUR
T1 - Role of Adaptive Immunity in the Development and Progression of Heart Failure
T2 - New Evidence
AU - Sánchez-Trujillo, Luis
AU - Vázquez-Garza, Eduardo
AU - Castillo, Elena C.
AU - García-Rivas, Gerardo
AU - Torre-Amione, Guillermo
N1 - Publisher Copyright:
© 2016 IMSS
PY - 2017/1
Y1 - 2017/1
N2 - Heart failure (HF) is considered the endpoint of a variety of cardiac diseases, which are the leading cause of death in adults and considered a growing pandemic worldwide. Independent of the initial form of cardiac injury, there is evidence linking the involvement of the immune system. In HF there is evidence of the participation of TH1, and TH17 cells, which account for sustained pathological chronic inflammation, cell migration, and the induction of specific pathological phenotypes of mononuclear cells. Of equal or even higher relevance are the B lymphocyte activation mechanisms that include production of pro-inflammatory cytokines, chemokines, and cardiac autoantibodies with or without activation of the complement proteins. Both of these unbalanced T- and B-cell pathways of the adaptive immune system are associated with cardiomyocyte death and tissue remodeling by fibrosis leading to a dysfunctional heart. At this time, therapy with neutralizing antibodies and the use of anti-cytokine immunomodulators to counteract the immune system effects have reached a plateau of mixed results in clinical trials. Nevertheless, recent evidence showed promising results in animal models that suggest that modulation of the adaptive immune system cells more than some of their effector molecules could have benefits in HF patients. This review summarizes the role of the adaptive immunity cells in HF, considering the sustained activation of adaptive immune system as a potential contributor to disease progression in humans and experimental models where its regulation provides a new therapeutic target.
AB - Heart failure (HF) is considered the endpoint of a variety of cardiac diseases, which are the leading cause of death in adults and considered a growing pandemic worldwide. Independent of the initial form of cardiac injury, there is evidence linking the involvement of the immune system. In HF there is evidence of the participation of TH1, and TH17 cells, which account for sustained pathological chronic inflammation, cell migration, and the induction of specific pathological phenotypes of mononuclear cells. Of equal or even higher relevance are the B lymphocyte activation mechanisms that include production of pro-inflammatory cytokines, chemokines, and cardiac autoantibodies with or without activation of the complement proteins. Both of these unbalanced T- and B-cell pathways of the adaptive immune system are associated with cardiomyocyte death and tissue remodeling by fibrosis leading to a dysfunctional heart. At this time, therapy with neutralizing antibodies and the use of anti-cytokine immunomodulators to counteract the immune system effects have reached a plateau of mixed results in clinical trials. Nevertheless, recent evidence showed promising results in animal models that suggest that modulation of the adaptive immune system cells more than some of their effector molecules could have benefits in HF patients. This review summarizes the role of the adaptive immunity cells in HF, considering the sustained activation of adaptive immune system as a potential contributor to disease progression in humans and experimental models where its regulation provides a new therapeutic target.
KW - Adaptive immunity
KW - Auto-antibody
KW - B cells
KW - Heart failure
KW - T cells
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U2 - 10.1016/j.arcmed.2016.12.008
DO - 10.1016/j.arcmed.2016.12.008
M3 - Review article
C2 - 28577862
AN - SCOPUS:85020128870
SN - 0188-4409
VL - 48
SP - 1
EP - 11
JO - Archives of Medical Research
JF - Archives of Medical Research
IS - 1
ER -