The BTLA(CD272)-HVEM(CD270) pathway is an important regulatory mechanism for gamma/delta T cell proliferation. A subset of gamma/delta T cells can be induced to have potent anti-Lymphoma activity. The amount of BTLA present on cell surface of these cells inversely correlates with their degree of differentiation. Blockade of this pathway can increases T cell signaling ability, while engagement of T cell BTLA results in arrested T cell proliferation. Manipulation of this pathway may lead to new anti-tumor therapies.
“The co-receptor BTLA negatively regulates human Vγ9Vδ2 T cell proliferation: a potential way of immune escape for lymphoma cells.” Gertner-Dardenne J, Fauriat C, Orlanducci F, Thibult ML, Pastor S, Fitzgibbon J, Bouabdallah R, Xerri L, Olive D Blood. 2013 May 21. [Epub ahead of print] PMID:23692853
“Potent antitumor activity of zoledronic acid-induced Vγ9Vδ2 T cells against primary effusion lymphoma.” Goto H, Matsuda K, Srikoon P, Kariya R, Hattori S, Taura M, Katano H, Okada S. Cancer Lett. 2013 May 1;331(2):174-82. doi: 10.1016/j.canlet.2012.12.021. Epub 2013 Jan 12. PMID:23321500
“Interfering with coinhibitory molecules: BTLA/HVEM as new targets to enhance anti-tumor immunity” Pasero C, Olive D. Immunol Lett. 2013 Mar;151(1-2):71-5. doi: 10.1016/j.imlet.2013.01.008. Epub 2013 Feb 21. PMID:23439006
Relevant Ancell Products:
anti-CD270(HVEM) mAb clone ANC3B7
Blocking anti-CD272(BTLA) mAb clone ANC6E9
Non Blocking anti-CD272(BTLA) mAb clone ANC5A5