Immunotherapy relies on harnessing the immune system’s anti-tumor activity to eradicate cancer cells. Several forms of immunotherapy-based treatment for cancer are already in clinical use, and many others are currently under development as a promising therapeutic to treat patients in the future.

We have broadly categorized the types of immunotherapy into two strategies: cell-based therapy, where cells are directly injected back into patients via stem cell or specific immune cell transplantation, and soluble factor-based therapy, in which patients are treated with soluble factors, such as antibodies and/or other proteins, which boost the patient’s immune system and anti-tumor immunity.

Click on each of these immunotherapy categories below to learn more:

In order to effectively clear out tumor cells, the immune system needs to be able to generate an appropriate inflammatory response. However, the fact that most of our immune cells contain a fail-safe mechanism to ensure they are not constantly activated is a double-edged sword. There are a number of markers found on both tumor cells and antigen presenting cells that can downregulate or suppress T cells once the corresponding ligand is bound.


Researchers are now looking into how they can prevent T Cells from binding these tolerance-inducing ligands. This would keep the T Cells active and ready to battle cancer. These markers have come to be known as “immune checkpoint receptors”. Although a number of immune checkpoints are being looked at, the most well-studied combinations include PD-1/PD-L1CTLA-4/CD80 and CD86LAG-3/MHC IITim-3/Galectin 9, and TIGIT/CD155 (PVR). Additionally, the use of recombinant cytokines, such as IFN-α and IL-2, augment anti-tumor inflammatory responses, and have been used in the clinic as a part of immunotherapeutic regimens to treat various malignancies. The direct injection of molecules involved in inflammation, such as TLR9 and anti-OX40 antibodies, has also shown to be effective in providing long-term anti-tumor protection by promoting and maintaining activation of the immune system.



Click on the receptor/ligand or cytokine names below in order to learn more about their cell distribution, function, and therapeutic role in treating cancer. You can also take a look at our thorough Cancer Immunoediting poster, which can be requested for free from our literature page.



Tim-3/Galectin 9

Tim-3 Distribution: Activated T Cells, Th1 Cells, Monocytes, Dendritic Cells.

Galectin 9 Distribution: Lymphocytes, Dendritic Cells, Neutrophils, Eosinophils, Astrocytes, Endothelial Cells, Fibroblasts, thymus Stromal/Epithelial Cells.

Function: Tim-3 (CD366) was initially discovered as a negative regulator of inflammation, as mice lacking Tim-3 developed autoimmune encephalomyelitis (EAE). Upon binding to its ligand Galectin-9, Tim-3 signaling leads to the apoptosis of Tim-3-expressing Th1 cells. Thus, blocking Tim-3/Galectin-9 signaling leads to prolonged Th1-mediated inflammation and anti-tumor responses. Research is underway to develop a clinically relevant blocker for Tim-3, which can then be used in conjunction with other immune checkpoint blockers, such as anti-PD1 and CTLA-4, which may synergistically work to boost the immune system.

Therapeutics: In a study of solid tumors, lowered Galectin-9 expression was correlated with reduced disease progression. In a B16F10 melanoma mouse model, combined blockade of TIM-3 and PD-1 or TIM-3 and CTLA-4, was more effective in prolonging survival when compared to blocking to an individual marker alone. In addition, the combination of anti-CTLA-4, anti-TIM-3 and anti-LAG-3 antibody treatments has produced further suppression of B16F10 tumor growth.

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PD-1 Distribution: Activated T Cells, Tregs, B Cells, NK Cells, Myeloid Cells.

PD-L1 Distribution: Broadly expressed on hematopoietic and non-hematopoietic cells, including T Cells, B Cells, NK Cells, Monocytes, Macrophages, Granulocytes, and Dendritic Cells.

Function: Activation of PD-1/CD279 signaling via binding to its ligands (PD-L1, PD-L2) leads to downstream signaling that results in cell death. Blockage of PD-1 expressed on activated T Cells and its ligands PD-L1 and PD-L2 expressed on tumor cells dampens this cell death process, thus allowing survival of activated T Cells that can infiltrate and kill tumor cells.

Therapeutics: Blocking the interaction between PD-1 and PD-L1 showed increased anti-tumor T cell responses in pancreatic carcinomas, B16 melanoma, and CT26 colon carcinoma. Combining CTLA-4 antibody (Ipilimumab) and anti-PD1 antibody (Nivolumab) treatments has resulted in greater anti-tumor responses, with 80% of patients showing tumor regression.

Anti-PD-1 antagonistic antibodies

  • Nivolumab (Opdivo®, Bristol-Myers Squibb)
  • Pembrolizumab (Keytruda®, Merck)
  • Pidilizumab (Cure Tech)


Anti-PD-L1 antagonistic antibodies

  • Atezolizumab (Tecentriq®, Roche)
  • Avelumab (Bavencio®, Pfizer)
  • Durvalumab (Imfinzi®, AstraZeneca)


PD-1 Gene Therapy: CRISPR gene-editing tested in a person for the first time

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CTLA-4/CD80 and CD86

CTLA-4 Distribution: Activated T and B Cells, Tregs.

CD80 and CD86 Distribution: Activated B Cells and T Cells, Macrophages, and Dendritic Cells.

Function: CD80 and CD86 (also known as B7-1 and B7-2, respectively) are upregulated on Antigen Presenting Cells (APCs) upon activation of the Toll-Like Receptor (TLR) pathways, and contribute to the activation of T cells by binding to the co-stimulatory molecule CD28. CTLA-4 (or CD152) is upregulated on T Cells upon activation, and binds to CD80 and CD86 with stronger affinity compared CD28. This allows preferential complex formation between CD80, CD86 with CTLA-4 instead of CD28. The engagement of the CTLA-4/CD80, CD86 complex results the attenuation of T cell activation, leading to an immunomodulatory effect. Blockage of CTLA-4 signaling thus allows for prolonged T Cell activation, and anti-tumor T Cells to infiltrate cancer cells.

Therapeutics: CTLA-4 became the first immune checkpoint to be tested for potential cancer treatments. In vivo treatment with anti-CTLA-4 antibodies depleted Tregs, increased CD8+ T Cells, and restored T effector function. Treatment with Ipilimumab (an anti-CTLA-4 antibody) increased metastatic melanoma patient survival. While there were a number of toxic side effects to method, the FDA has approved it for treatment of melanoma. A new treatment, Pembrolizumab, is being considered as an alternative as it has shown improvements over Ipilimumab in terms of survival and side effects.

Anti-CTLA-4 antagonistic antibodies

  • Ipilimumab (Yervoy®, Bristol-Myers Squibb)


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LAG3 Distribution: Activated/tolerized T Cells, Tregs, NK Cells, Plasmacytoid Dendritic Cells.

MHC II Distribution: B Cells, Dendritic Cells, Monocytes, Macrophages, activated T Cell subsets.

Function: LAG-3 (CD223) is expressed primarily on activated CD4+ T Cells, and its primary binding target is MHC Class II molecules expressed on APCs. While the detailed mechanism is not well understood, LAG-3 activation leads to an immunomodulatory effect, believed to be via the secretion of the anti-inflammatory cytokine IL-10. Due to its immunosuppressive function, researchers are in the process of developing antagonistic antibodies against LAG-3, which will attenuate immunomodulatory signals and prolong anti-tumor inflammatory responses.

Therapeutics: While not as well characterized as other immune checkpoints, pre-clinical studies have shown that treatment with anti-LAG-3 and anti-PD-1 antibodies displayed synergistic anti-tumor effects.

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TIGIT Distribution: Activated T Cells, NK Cells, Tregs, Tfh Cells.

PVR Distribution: APCs, T Cells, some tumor cells.

Function: TIGIT (Vstm3) is a receptor of the Ig superfamily that is primarily expressed on activated T Cells. Several different ligands have been noted to bind with TIGIT, such as CD226 (DNAM-1), CD112, and CD155 (PVR), but CD155 is noted to bind with highest affinity. As TIGIT activation leads to an immunomodulatory effect on activated T Cells and TIGIT-deficient mice develop autoimmune diseases, it is believed to be a negative regulator of immune responses. However, evidence suggests that the downstream function of TIGIT activation is ligand dependent - while CD112 binding is anti-inflammatory, binding of CD226 to TIGIT has also noted to be a positive co-stimulatory signal that can also augment the immune response.

Therapeutics: Preclinical studies suggest that TIGIT blockade synergizes with both Tim-3 and PD-1 inhibition in tumor clearance, opening potential avenues for modulating TIGIT-signaling in immunotherapy.

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OX40 (CD134)/OX40L

OX40 Distribution: Activated T Cells.

OX40L Distribution: APCs, T Cells, some tumor cells.

Function: OX40 (CD134, TNFRSF4) is a member of the TNF receptor family that is expressed on activated T lymphocytes including Th1, Th2, Th17, and Treg cells. The interaction of OX40 with OX40L results in B Cell proliferation and antibody secretion, regulation of primary T Cell expansion, and T Cell survival by promoting the secretion of IL-2.

Therapeutics: Preclinical studies have suggested that OX40, OX40L agonists can boost immune responses that can augment anti-tumor T Cell activity, and are currently under investigation as a promising target for immunotherapy. Agonistic Anti-OX40 antibodies have been particularly effective when injected, along with a combination of TLR9 and its activating CpG DNA, to act as a “cancer vaccine” that has shown sustained, long-term protection against cancer in preclinical models.

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Interferon-α (IFN-α)

IFN-α expression: ubiquitously expressed in virally infected cells, highly secreted by Plasmacytoid Dendritic Cells.

IFNAR (IFNAR1, IFNAR2) distribution: ubiquitously expressed on all cell types.

Function: IFN-α is a Type I Interferon (along with IFN-β) that is produced by virally infected cells. They promote anti-viral responses in neighboring cells by inducing the upregulation of IFN-stimulated genes. Plasmacytoid Dendritic Cells are the main source of IFN-α in response to invading pathogens. In innate immunity, type I IFNs play a crucial role in Dendritic Cell maturation, B and NK Cell activation, priming of primary antibody responses, and memory CD8+ T Cell proliferation. IFN-α enhances TLR responsiveness in Macrophages by up-regulating the expression of TLR3, TLR4, and TLR7, and thus IFN-α regulates the TLR-dependent gene expression of IFN-α, IFN-β, IL-28, and IL-29. There are several subtypes of IFN-α including IFN-α2, α4, α10, α14, and α21.

Therapeutics: IFN-α has classically been used in the treatment of chronic hepatitis C (CHC) but it has also been used to treat several types of lymphoid malignancies, including hairy cell leukemia, chronic myeloid leukemia, and follicular lymphoma. Specifically, one pegylated form of IFN-α2 (also known as the anti-viral drug Interferon Alfa-2b) has been shown to be most effective therapeutically in treating cancers, while the other pegylated form (Interferon Alfa-2a) is primarily used in the clinic to treat CHC. The exact mechanism of action by which IFN-α promotes antitumor activity is not well understood, but it is primarily thought to be via the activation of NK Cells.

Recombinant Interferon Alfa-2a

  • Pegasys® (Genentech)


Recombinant Interferon Alfa-2b

  • PegIntron® (Intron®-A, Sylatron™, Merck)


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Interleukin 2 (IL-2)

IL-2 expression: Secreted by activated CD4+ T Cells, some Dendritic Cells, Thymocytes

IL-2R distribution: Activated T and B Cells, Regulatory T Cells, Thymocyte subsets

Function: IL-2 is primarily secreted by activated CD4+ T Cells, and binds to its target cells via the receptor complex consisting of IL-2Rα (CD25), IL-2Rβ (CD122) and CD132. Activation of the IL-2-dependent pathway promotes T Cell proliferation and survival.

Therapeutics: Recombinant IL-2 has been used clinically to treat metastatic melanoma and renal cell carcinoma by the activation of T Cells with anti-tumor activity.

Recombinant IL-2

  • Aldesleukin (Proleukin®, Prometheus)


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