With continually improving reperfusion strategies and patient care, the overall mortality of acute myocardial infarction (AMI) has been significantly reduced during the past two decades. However, this success is a double-edged sword, as many patients surviving an AMI will progress towards ischemic heart failure (HF) over time. The pathologic causes of ischemic HF are undoubtedly multifactorial. However, the inflammatory response is considered one of the most important causes of pathological remodeling because it spans the whole process of HF development. The macrophage-mediated inflammatory response was once considered a purely harmful factor leading to pathological remodeling and HF. However, growing evidence demonstrates that multiple subgroups of macrophage exist and contribute differently to ischemic HF development. Understanding macrophage populations and how they contribute to post-MI remodeling and consequent ischemic HF is, therefore, critical to understanding and treating the disease. This review focuses on different macrophage populations that regulate post-MI cardiac injury and how immunoregulation therapy may benefit patients with ischemic HF.

With continually improving reperfusion strategies and patient care, the overall mortality of acute myocardial infarction (AMI) has been significantly reduced during the past two decades. However, this success is a double-edged sword, as many patients surviving an AMI will progress towards ischemic heart failure (HF) over time. The pathologic causes of ischemic HF are undoubtedly multifactorial. However, the inflammatory response is considered one of the most important causes of pathological remodeling because it spans the whole process of HF development. The macrophage-mediated inflammatory response was once considered a purely harmful factor leading to pathological remodeling and HF. However, growing evidence demonstrates that multiple subgroups of macrophage exist and contribute differently to ischemic HF development. Understanding macrophage populations and how they contribute to post-MI remodeling and consequent ischemic HF is, therefore, critical to understanding and treating the disease. This review focuses on different macrophage populations that regulate post-MI cardiac injury and how immunoregulation therapy may benefit patients with ischemic HF.

Dendritic cells are professional antigen presenting cells which are being used as adjuvants in tumor vaccination trials. Most clinical protocols currently include 4 to 10 weekly infusions of doses > 10(6) cells, each inoculum coming from a simple culture of blood monocytes. In the present study, several millions of dendritic cells from a single leukapheresis were produced; monocytes were isolated by elutriation and then cultured in Teflon bags in presence of 800 U/ml GM-CSF + 100 micro g/ml IL-13 + 10% fetal calf serum (FCS). The dendritic cells from this single batch were aliquoted in many doses for potential multiple infusions and cryopreserved in 10% DMSO + 2% human albumin in Teflon-kapton Fresenius bags either at -1 degrees C/min using a controlled rate freezer, or putting the bags directly in a -80 degrees C mechanical freezer without controlling the temperature rate. Six experiments were carried out. After one month of cryopreservation, the cells were thawed in a 40 degrees C water bath. Before and after freezing, cells were evaluated for immunophenotype (CD1a, CD14, CD40, CD80, CD83, CD86, CD54, CD58, CD16, CD32, CD64 and HLA-DR) and for their capacity to stimulate allogenic (MLR) or autologous (antigen presentation tests) lymphocytes. The results demonstrated that the mean recovery rates after freezing in liquid nitrogen or at -80 degrees C were (67 +/- 14)% and (71 +/- 13)% respectively, without any significant difference between the two techniques. The immunophenotype was not modified by the freezing-thawing procedure, as well as the lymphocyte stimulating capacities. In conclusion, our study showed that substantial numbers of functional DCs can be derived from peripheral blood monocytes using Teflon bags. DCs can be cryopreserved in a good laboratory practice setting for further clinical trials with an acceptable loss of cells and without modification of their functions.