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1.
J Interferon Cytokine Res ; 38(2): 45-68, 2018 02.
Article in English | MEDLINE | ID: mdl-29443657

ABSTRACT

The development of the T- and natural killer (NK) cell growth factor IL-2 has been a sentinel force ushering in the era of immunotherapy in cancer. With the advent of clinical grade recombinant IL-2 in the mid-1980s, oncologists could for the first time directly manipulate lymphocyte populations with systemic therapy. By itself, recombinant IL-2 can induce clinical responses in up to 15% of patients with metastatic cancer or renal cell carcinoma. When administered with adoptively transferred tumor-reactive lymphocytes, IL-2 promotes T cell engraftment and response rates of up to 50% in metastatic melanoma patients. Importantly, these IL-2-driven responses can yield complete and durable responses in a subset of patients. However, the use of IL-2 is limited by toxicity and concern of the expansion of T regulatory cells. To overcome these limitations and improve response rates, other T cell growth factors, including IL-15 and modified forms of IL-2, are in clinical development. Administering T cell growth factors in combination with other agents, such as immune checkpoint pathway inhibitors, may also improve efficacy. In this study, we review the development of T- and NK cell growth factors and highlight current combinatorial approaches based on these reagents.


Subject(s)
Immunotherapy , Interleukin-2/immunology , Neoplasms/immunology , Neoplasms/therapy , Animals , Humans
4.
Sci Transl Med ; 7(311): 311ra170, 2015 Oct 28.
Article in English | MEDLINE | ID: mdl-26511507

ABSTRACT

Interleukin-2 (IL-2) is a lymphocyte growth factor that is an important component of many immune-based cancer therapies. The efficacy of IL-2 is thought to be limited by the expansion of T regulatory cells, which express the high-affinity IL-2 receptor subunit IL-2Rα. IL-15 is under investigation as an alternative to IL-2. Although both cytokines signal through IL-2Rßγ, IL-15 does not bind IL-2Rα and therefore induces less T regulatory cell expansion. However, we found that transferred effector CD8(+) T cells induced curative responses in lymphoreplete mice only with IL-2-based therapy. Although conventional in vitro assays showed similar effector T cell responsiveness to IL-2 and IL-15, upon removal of free cytokine, IL-2 mediated sustained signaling dependent on IL-2Rα. Mechanistically, IL-2Rα sustained signaling by promoting a cell surface IL-2 reservoir and recycling of IL-2 back to the cell surface. Our results demonstrate that IL-2Rα endows T cells with the ability to compete temporally for limited IL-2 via mechanisms beyond ligand affinity. These results suggest that strategies to enhance IL-2Rα expression on tumor-reactive lymphocytes may facilitate the development of more effective IL-2-based therapies.


Subject(s)
Immunotherapy/methods , Interleukin-2 Receptor alpha Subunit/metabolism , Interleukin-2/immunology , Animals , CD8-Positive T-Lymphocytes/immunology , Cell Line, Tumor , Cells, Cultured , Interleukin-15/therapeutic use , Interleukin-2/therapeutic use , Interleukin-2 Receptor alpha Subunit/genetics , Melanoma, Experimental/immunology , Melanoma, Experimental/therapy , Mice , Mice, Inbred C57BL , Mice, Transgenic , Microscopy, Confocal , Signal Transduction/physiology , T-Lymphocytes, Regulatory/immunology
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