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. Author manuscript; available in PMC: 2013 Dec 1.
Published in final edited form as: Transfusion. 2012 Apr 9;52(12):2706–2716. doi: 10.1111/j.1537-2995.2012.03636.x

Figure 1.

Figure 1

Complement cascade (CC) activation during HSPC mobilization. The CC may become activated through the classical pathway (which is dependent on naturally-occurring antibodies (NA-Ig) and is triggered by complement protein C1q), the lectin pathway, and the alternative pathway (which is triggered by Factors B and D). All three pathways merge at complement protein C3, whose activation leads to the release of C3 anaphylatoxin and complement protein C5. C5 is enzymatically cleaved to release anaphylatoxin C5a. Some alternative mechanisms exist, whereby C5 could be activated by the proteases thrombin and kallikrein. The arginine terminal residue of both C3a and C5a is immediately cleaved to yield desArgC3a and desArgC5a, which have different biological functions. While C3a and desArgC3a cleavage fragments enhance the responsiveness of HSPC to the bone marrow to a stromal-cell derived factor (SDF)-1 gradient, thus promoting their retention in the bone marrow, C5a and desArgC5a facilitate the egress of granulocytes and pave the way for the mobilization of HSPC. The final step of CC activation is the generation of the cytolytic end-product C5b-C9 membrane attack complex (MAC).