Addressin
Addressin is a type of cell adhesion molecule (CAM) that plays a crucial role in the immune system. It is involved in the process of leukocyte extravasation, which is the movement of leukocytes out of the circulatory system and towards the site of tissue damage or infection.
Structure and Function[edit | edit source]
Addressins are a group of CAMs that are expressed on the endothelial cells lining the blood vessels. They are characterized by their ability to bind to specific integrin molecules on the surface of leukocytes. This binding interaction is a key step in the process of leukocyte extravasation.
The binding of addressins to integrins allows leukocytes to adhere to the endothelial cells. This adhesion is the first step in the process of extravasation. Following adhesion, the leukocytes can then migrate through the endothelial layer and into the tissue.
Role in Immune Response[edit | edit source]
Addressins play a critical role in the immune response. By facilitating the movement of leukocytes out of the blood and into tissues, they help to ensure that these immune cells can reach the site of infection or tissue damage.
In addition to their role in leukocyte extravasation, addressins also play a role in the homing of lymphocytes to specific tissues. Certain types of addressins are expressed only in specific tissues, and these addressins can bind to specific integrins on the surface of lymphocytes. This interaction allows the lymphocytes to be directed to the appropriate tissue.
Clinical Significance[edit | edit source]
Given their role in the immune response, addressins are of significant clinical interest. Abnormalities in addressin expression or function can contribute to a variety of diseases, including autoimmune diseases, inflammatory diseases, and cancer.
For example, in autoimmune diseases, the inappropriate extravasation of leukocytes can lead to tissue damage. Similarly, in cancer, tumor cells can exploit the addressin-integrin interaction to spread to other parts of the body.
See Also[edit | edit source]
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