Chlamydia pneumoniae reactive T lymphocytes in the walls of abdominal aortic aneurysms

Abstract

The presence of C. pneumoniae specific T lymphocytes among in vivo activated cells from the AAA tissue specimens suggests that C. pneumoniae participates in the maintenance of the inflammatory response in the tissue and may thus be involved in the progression of the disease.

Aneurysmal Lesions of Patients with Abdominal Aortic Aneurysm Contain Clonally Expanded T Cells

“…4,[12][13][14][15][16][17][18] and nonself origin (19)(20)(21)(22) have been identified. Initiation and propagation of AAA are the two phases of the disease that may be driven by different, although cross-reactive, antigenic determinants.…”

“…v) Putative selfand nonself AAA Ags have been identified, including elastin and elastin fragments (14)(15)(16), collagen types I and III (reviewed in Ref. 4), aortic AAA protein 40 (also known as microbial-associated glycoprotein 36) (12,13,17), oxidized low-density lipoprotein (18), Chlamydia pneumoniae (19,20), Treponema palladium (21), and CMV (22). Molecular mimicry, which is defined as the sharing of antigenic epitopes between microorganisms and host Ags (23), may be responsible for inducing T cell inflammatory responses in AAA.…”

Adaptive cellular immunity in aortic aneurysms: cause, consequence, or context?

“…The triggers of adaptive immunity in AAAs are unknown, but there is often evidence of infection with Chlamydia pneumoniae in individuals with AAAs, and microbial infection might directly stimulate pathological immune responses in AAA tissue (22). Prior microbial infection might also target immune responses to aortic wall proteins through a process of molecular mimicry; alternatively, immune responses against aortic wall structural components may arise secondary to long-standing inflammation and connective tissue destruction, through proteolytic exposure of neoepitopes within matrix proteins.…”

CD16+Monocyte Subsets Are Increased in Large Abdominal Aortic Aneurysms and Are Differentially Related with Circulating and Cell-Associated Biochemical and Inflammatory Biomarkers

“…Current research suggests that atherosclerosis, genetic [1], environmental [2] and immunological [3] factors contribute to the onset and the development of abdominal aortic aneurysms (AAA). Important histological features of the chronic inflammatory response seen in AAA include extreme medial thinning associated to vascular smooth muscle cells (SMC) apoptosis, adventitial inflammatory cell infiltration, elastin fragmentation and degeneration, that are rarely seen in atherosclerotic lesions of other districts, such as carotid and coronary atherosclerosis [4][5][6].…”