Adoptive Leukocyte Immunotherapy – Innovita Research

Adoptive leukocyte immunotherapy is aimed at stimulating both innate and adaptive antitumor immune responses. It is based on the use of ex vivo activated ( primed) leukocytes isolated from a healthy related donor, as well as on supporting local and systemic antitumor immune responses in the patient’s body. The antitumor activity of adoptive leukocyte immunotherapy is based on the following mechanisms: cytodestructive (N1) activation of granulocytes, classical (M1) activation of macrophages ; activation of NK cells ; immunogenic antigen presentation of endogenous tumor-associated antigens by professional antigen-presenting cells (dendritic cells and macrophages); antitumor activation of T lymphocytes (including ɣδ T cells); costimulatory activity of platelets; recruitment of autologous immune cells in the antitumor process by cytokines and chemokines produced by alloantigen-activated autologous T-lymphocytes.
Adoptive leukocyte immunotherapy can be effectively combined with antitumor vaccination.

Diseases:

  • Melanoma
  • Renal cancer
  • Colorectal cancer
  • Brain tumors
  • Prostate cancer
  • Lung cancer
  • Breast cancer
  • Gastric cancer
  • Thyroid carcinoma
  • Ovarian carcinoma
  • Pancreas cancer

Procedure:

  1. Venous blood (150-350 ml) is taken from a donor closely related to the patient.
  2. The preparation of activated leukocytes is performed according to the original procedure, which is accomplished within 24 hours.
  3. Using minimally invasive technologies, activated leukocytes are injected intravenously, intramuscularly, or directly into the tumor site; the last possibility may require preliminary tumor destruction in some patients. Alternatively, cells can be administered into the nearby tissues after the excision of the primary tumor.
  4. A typical immunotherapeutic regimen is carried out in the course of 7 days in outpatient or inpatient settings.

Related scientific publications:

  • CCL3 Enhances Antitumor Immune Priming in the Lymph Node via IFNγ with Dependency on Natural Killer Cells.
    Allen F, Rauhe P, Askew D, Tong AA, Nthale J, Eid S, Myers JT, Tong C, Huang AY. Front Immunol. 2017 Oct 23;8:1390. doi: 10.3389/fimmu.2017.01390. eCollection 2017.
    https://www.ncbi.nlm.nih.gov/pubmed/29109732
  • Superantigen staphylococcal enterotoxin C1 inhibits the growth of bladder cancer.
    Liu T, Li L, Yin L, Yu H, Jing H, Liu Y, Kong C, Xu M. Biosci Biotechnol Biochem. 2017 Sep;81(9):1741-1746. doi: 10.1080/09168451.2017.1350564. Epub 2017 Jul 17.
    https://www.ncbi.nlm.nih.gov/pubmed/28715277
  • Enhanced Therapeutic Efficacy and Memory of Tumor-Specific CD8 T Cells by Ex Vivo PI3K-δ Inhibition.
    Abu Eid R, Ahmad S, Lin Y, Webb M, Berrong Z, Shrimali R, Kumai T, Ananth S, Rodriguez PC, Celis E, Janik J, Mkrtichyan M, Khleif SN. Cancer Res. 2017 Aug 1;77(15):4135-4145. doi: 10.1158/0008-5472.CAN-16-1925. Epub 2017 Jun 14.
    https://www.ncbi.nlm.nih.gov/pubmed/28615225
  • Breast cancer stem-like cells can promote metastasis by activating platelets and down-regulating antitumor activity of natural killer cells.
    Wang S, Zhang Y, Cong W, Liu J, Zhang Y, Fan H, Xu Y, Lin H. J Tradit Chin Med. 2016 Aug;36(4):530-7.
    https://www.ncbi.nlm.nih.gov/pubmed/28459521
  • Mouse versus Human Neutrophils in Cancer: A Major Knowledge Gap.
    Eruslanov EB, Singhal S, Albelda SM. Trends Cancer. 2017 Feb;3(2):149-160. doi: 10.1016/j.trecan.2016.12.006. Epub 2017 Jan 19.
    https://www.ncbi.nlm.nih.gov/pubmed/28718445