PATHOLOGY & ONCOLOGY RESEARCHVol. 2 No. 4, 1996

 Review

Aggrecan: A Target Molecule of Autoimmune Reactions

Edit I BUZÁS1, Katalin MIKECZ2, Tibor T GLANT3

1The Institute of Anatomy, Histology and Embryology, University of Medicine, Debrecen, Hungary
2Department of Biochemistry, Rush Medical University at Rush-Presbyterian-St. Luke's Medical Center, Chicago, USA
3Department of Orthopedic Surgery, Rush Medical University at Rush-Presbyterian-St. Luke's Medical Center, Chicago, USA
4Section of Rheumatology, Department of Internal Medicine, Rush Medical University at Rush-Presbyterian-St. Luke's Medical Center, Chicago, USA

 

Aggrecan in cartilage forms aggregates with hyaluronan and link protein, embedded in a collagen network. It accounts for the compressive stiffness and resilience of the hyaline cartilage. Many forms of inflammatory arthritis were shown to be accompanied with aggrecan degradation and loss from the cartilage. The loss of this major component of cartilage renders the tissue more vulnerable when exposed to abrasive forces. Therefore, aggrecan degradation may significantly contribute to cartilage destruction in arthritis. Furthermore, fragments of degraded aggrecan are released during joint inflammation. Thus, molecules of an avascular, immune-privileged tissue (hyaline cartilage) may become accessible to the cells of the immune system. Similarly, there is a ''leakage'' of aggrecan fragments from cartilage during aging and after joint injury, which may also lead to autosensibilisation. Autoimmune reactivity to aggrecan can be detected in human joint diseases, as well as in animal models of arthritis. The epitopes involved in these processes are currently being identified. Recent data from work with mice suggest a strong immune response focused to the N-terminal G1 domain of aggrecan that leads to arthritis and spondylitis. Pathology & Oncology Research, Vol 2, Nr 4, 219-228, 1996

Key words: proteoglycan; aggrecan; arthritis; spondylitis; autoimmune; cartilage


Received: Aug 23, 1996; accepted: Oct 12, 1996
Correspondence: Edit I BUZÁS, The Institute of Anatomy, Histology and Embryology, University of Medicine, Nagyerdei krt. 98 Debrecen H-4012, Hungary; Tel: 36-52-411600/4119, Fax: 36-52-432290; E-mail: edit@chondron.anat.dote.hu

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