Immunotherapy treatment activates T cells and B cells that target specific tumor antigens3-5

  • The activated immune system is primed to recognize tumor antigens expressed by each patient’s unique and frequently changing population of cancer cells3
  • Some activated T cells kill tumor cells directly or indirectly3
  • Some activated T cells activate B cells, which become antibody-producing plasma cells3

Learn more by watching
Immunotherapy Is Tumor-Specific (2:10)


Immunotherapy treatment is designed to support the immune system’s ability to adapt its attack over time3,5-8

  • Each patient’s population of tumor cells mutates over time, which may result in resistance to traditional anticancer therapies3
  • When a tumor cell is killed, additional antigens are released, stimulating activation of new populations of T cells and B cells that recognize tumor antigens3,4,6,7
  • This can result in an expanding cascade of immune cells able to recognize cancer cells bearing a variety of tumor antigens as the tumor mutates over time5-8

Learn more by watching
Immunotherapy Is Designed to Support Immune System Adaptability


Immunotherapy treatment stimulates immunologic memory, which
may lead to a prolonged antitumor response3,9-10

  • Some activated immune cells become memory cells, which remain primed to stimulate an immune response when tumor cells bearing target antigens are encountered within the body3,9-10

Learn more by watching
Immunotherapy Empowers a Durable Immune Response

A natural immune response involves 3 different types of cells1:

Antigen Presenting Cells(APCs) identify and uptake foreign antigens to present them to T cells


T cells are activated by APCs to recognize and destroy cells containing foreign antigens


B cells produce antibodies specific to foreign antigens


Adapted from Abbas AK, et al.1


  1. Abbas AK, Lichtman AH. Basic Immunology. 3rd ed. 2011.
  2. Drake CG. Nat Rev Immunol. 2010;10(8):580-593.
  3. Murphy K, Travers P, Walport M, eds. Janeway’s Immunobiology. 7th ed. Garland Science, Taylor & Frances Group, LLC. New York, NY: 2008.
  4. Namm JP, Li Q, Lao X, et al. J Surg Oncol. 2012;105:431-435.
  5. Sharma P, Wagner K, Wolchok JD, Allison JP. Nat Rev Cancer. 2011;11:805-812.
  6. Ribas A, Butterfield LH, Glaspy JA, Economou JS. J Clin Oncol. 2003;21:2415-2432.
  7. Kirkwood JM, Butterfield LH, Tarhini AA, Zarour H, Kalinski P, Ferrone S. CA Cancer J Clin. 2012;62:309-335.
  8. Disis ML, Strickler JH, Wallace D, et al. J Clin Oncol. 2008;26(suppl):(May 20 suppl; abstr 3015).
  9. Klebanoff CA, Gattinoni L, Restifo NP. Immunol Rev. 2006;211:214-224.
  10. Mullins DW, Sheasley SL, Ream RM, Bullock TNJ, Fu Y-X, Engelhard VH. J Exp Med. 2003;198(7):1023-1034.