Modulation of Immune-Inflammatory Responses in Abdominal Aortic Aneurysm: Emerging Molecular Targets.

Publisher: Hindawi Publishing Corporation Country of Publication: Egypt NLM ID: 101627166 Publication Model: eCollection Cited Medium: Internet ISSN: 2314-7156 (Electronic) Linking ISSN: 23147156 NLM ISO Abbreviation: J Immunol Res Subsets: MEDLINE

Original Publication: Cairo, Egypt : Hindawi Publishing Corporation, [2014]-

Immunity* ; Immunomodulation*; Aortic Aneurysm, Abdominal/*etiology ; Aortic Aneurysm, Abdominal/*metabolism ; Inflammation/*complications ; Inflammation/*immunology; Animals ; Aortic Aneurysm, Abdominal/pathology ; Aortic Aneurysm, Abdominal/therapy ; Cytokines/metabolism ; Humans ; Immunity, Innate ; Immunoglobulins/immunology ; Inflammation/metabolism ; Inflammation Mediators/metabolism ; Molecular Targeted Therapy ; Toll-Like Receptors/metabolism

Abdominal aortic aneurysm (AAA), a deadly vascular disease in human, is a chronic degenerative process of the abdominal aorta. In this process, inflammatory responses and immune system work efficiently by inflammatory cell attraction, proinflammatory factor secretion and subsequently MMP upregulation. Previous studies have demonstrated various inflammatory cell types in AAA of human and animals. The majority of cells, such as macrophages, CD4+ T cells, and B cells, play an important role in the diseased aortic wall through phenotypic modulation. Furthermore, immunoglobulins also greatly affect the functions and differentiation of immune cells in AAA. Recent evidence suggests that innate immune system, especially Toll-like receptors, chemokine receptors, and complements are involved in the progression of AAAs. We discussed the innate immune system, inflammatory cells, immunoglobulins, immune-mediated mechanisms, and key cytokines in the pathogenesis of AAA and particularly emphasis on a further trend and application of these interventions. This current understanding may offer new insights into the role of inflammation and immune response in AAA.

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0 (Cytokines)
0 (Immunoglobulins)
0 (Inflammation Mediators)
0 (Toll-Like Receptors)

Date Created: 20180704 Date Completed: 20181018 Latest Revision: 20181114

20240105

PMC6008668

10.1155/2018/7213760

29967801