Fig. 2

Acute lymphoblastic leukemia’s potential treatments targeting chemokines and their receptors. Chemokine antagonists and immunotoxins combined with chemotherapy may significantly optimize prognosis of ALL patients. CXCR4 antagonists have been proved to inhibit CXCL12-mediated chemotaxis and reverse drug resistance. AMD3100, TC14012 and BL-8040 can block the chemotactic function of the CXCL12/CXCR4 axis, interfere with the bone marrow microenvironment on which leukemia cells depend to survive, and mobilize these leukemia cells into the peripheral circulation, thereby increasing the sensitivity of leukemia cells to chemotherapeutic drugs. CCL25-PE38 fusion protein could effectively induce the apoptosis of CCR9 positive T-ALL cells. Immunotoxin PE38 is internalized via the endolysosomal system, first transported to the Golgi and further to the ER where it is activated. Activated PE38 ribosylates ADP and inactivate EF2, thus halting protein synthesis and eventually leads to apoptosis. Monoclonal antibodies 91R and 92R could inhibit the growth of T-ALL cells transplanted into immunodeficient mice. Competitive antagonist of CCR5 maraviroc inhibits CCR5-activated signaling proteins JAK and STAT3, which may lead to apoptosis, and inhibition of survival, proliferation and migration