Abdominal aortic aneurysm (AAA) is an immune-mediated disease with a genetic component. The multifactorial pathophysiology is not clear and there is still no pharmacotherapy to slow the growth of aneurysms. The signal integration of cell-surface KIRs (killer cell immunoglobulin-like receptors) with HLA (ligands, human leukocyte class I antigen molecules) modulates the activity of natural killer immune cells. The genetic diversity of the KIR/HLA system is associated with the risk of immune disorders. This study was a multivariate analysis of the association between genetic variants of KIRs, HLA ligands, clinical data and AAA formation. Genotyping was performed by single polymerase chain reaction with sequence-specific primers using commercial assays. Patients with HLA-A-Bw4 have a larger aneurysm by an average of 4 mm (p = 0.008). We observed a relationship between aneurysm diameter and BMI in patients with AAA and co-existing CAD; its shape was determined by the presence of HLA-A-Bw4. There was also a nearly 10% difference in KIR3DL1 allele frequency between the study and control groups. High expression of the cell surface receptor KIR3DL1 may protect, to some extent, against AAA. The presence of HLA-A-Bw4 may affect the rate of aneurysm growth and represents a potential regional pathogenetic risk of autoimmune injury to the aneurysmal aorta.

Transdifferentiation, also known as direct reprogramming, is the transformation of one terminally differentiated cell type into another mature cell type, while bypassing the stage of pluripotency. In leukemia, this phenomenon has a dual significance: on the one hand, it is an adaptive mechanism driving tumor survival and resistance to treatment, and on the other, it offers a potential opportunity for innovative therapies. Of particular interest is the directional transdifferentiation (mostly partial) toward dendritic cell-like phenotypes, which increases the immunogenicity of cancer cells. Mastering this process could define a new generation of immunotherapies that leverage the inherent plasticity of leukemic cells to achieve therapeutic benefits. In this brief review, we attempt to gather information concerning the molecular mechanism of this process and point to the role of dendritic cells as a crucial element of anticancer, particularly anti-leukemia innate and acquired, immunity. Thus, in vitro and in vivo techniques of inducing transformation of the leukemia cells into cancer antigen-presenting cells and the application of these technologies in current and future therapies are discussed.