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lymphoid organs is inhibited, and injection of NAD(P) into mice markedly decreases T<br />

cell homing. Note: 41 is not ADP-ribosylated, and B cells don’t express ART2, hence<br />

their homing is not affected.<br />

Ectopeptidases regulate chemokines<br />

CD26 is an ectoenzyme that cleaves N-terminal dipeptides containing either proline or<br />

alanine residues from polypeptides. CD26 is expressed de novo on activated T and B<br />

cells, NK cells, and endothelial cells. Numerous bioactive peptides are cleaved by CD26,<br />

including chemokines. Cleavage of chemokines by CD26 reduces their ability to bind and<br />

activate chemokine receptors, whereas their ability to serve as chemoattracts can be<br />

enhanced (eg CCL5). Rodents that are deficient in CD26 have increased infiltration of<br />

leukocytes into the lung and joints in models of asthma and arthritis, suggesting that<br />

CD26 plays a role in inhibiting inflammation.<br />

Sheddases<br />

CD156b is a sheddase that cleaves L-selectin from the surface of thymocytes. Other<br />

sheddases are also involved. L-selectin is shed from lymphocytes to prevent re-entry of<br />

activated T cells to secondary lymphoid organs.<br />

Ectoenzymes in the control of leukocyte traffic<br />

The nucleotidases CD39 and CD73 regulate the balance of ATP and adenosine, and the<br />

activation of leukocyte integrins and vascular cell adhesion molecules. CD26<br />

proteolytically modifies the activities of chemokines, whereas sheddases cleave leukocyte<br />

cell adhesion molecules such as L-selectin. ADP ribosyltransferases such as ART2<br />

modify and inactivate adhesion molecules.

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