Human abdominal aortic aneurysm (AAA): Evidence for an autoimmune antigen-driven disease

Authors

Song Lu, Mon Health Medical Center, Department of Pathology, Morgantown, WV, USA.
John V. White, Advocate Aurora Health.Follow
Ifeyinwa Nwaneshiudu, Department of Microbiology and Immunology, Temple University School of Medicine, Philadelphia, PA, USA.
Adaobi Nwaneshiudu, Department of Microbiology and Immunology, Temple University School of Medicine, Philadelphia, PA, USA; Cutis Wellness Dermatology and Dermatopathology PLLC, Laredo, TX, USA.
Dimitri S. Monos, Department of Pathology and Laboratory Medicine, University of Pennsylvania, Perelman School of Medicine, The Children's Hospital of Philadelphia, Philadelphia, PA, USA.
Charalambos C. Solomides, Department of Pathology & Laboratory Medicine, Thomas Jefferson University Hospital, Philadelphia, PA, USA.
Emilia L. Oleszak, Department of Biological Sciences and Center for Molecular Medicine, Old Dominion University, Norfolk, VA, USA.
Chris D. Platsoucas, Department of Biological Sciences and Center for Molecular Medicine, Old Dominion University, Norfolk, VA, USA. Electronic address: cplatsoucas@odu.edu.

Recommended Citation

Lu S, White JV, Nwaneshiudu I, et al. Human abdominal aortic aneurysm (AAA): Evidence for an autoimmune antigen-driven disease. Autoimmun Rev. 2022;21(10):103164. doi:10.1016/j.autrev.2022.103164

Affiliations

Advocate Lutheran General Hospital

Abstract

Abdominal aortic aneurism (AAA) is a complex immunological disease with a strong genetic component, and one of the ten leading causes of death of individuals 55-74 years old worldwide. Strong evidence has been accumulated suggesting that AAA is an autoimmune specific antigen-driven disease. Mononuclear cells infiltrating AAA lesions comprised of T and B lymphocytes and other cells expressing early-, intermediate- and late-activation antigens, and the presence of antigen-presenting cells have been documented, demonstrating an ongoing immune response. The three components of the trimolecular complex, T-cell receptor (TCR)/peptide (antigen)/HLA have been identified in AAA, and specifically: (i) clonal expansions of T-cell clones in AAA lesions; (ii) the association of AAA with particular HLA Class I and Class II; and (iii) self or nonself putative AAA-associated antigens. IgG autoantibodies recognizing proteins present in normal aortic tissue have been reported in patients with AAA. Molecular mimicry, defined as the sharing of antigenic epitopes between microorganisms (bacteria, viruses) and self antigens, maybe is responsible for T-cell responses and antibody production in AAA. Also, the frequency and the suppressor activity of CD4 + CD25 + FOXP3+ Tregs and the expression of FOXP3 transcripts and protein have been reported to be significantly impaired in AAA patients vs normal donors.

Document Type

Article

PubMed ID

35926768