Role of Nanoparticles in Cancer Immunotherapy
D. Sakthi Kumar, Aswathy Ravindran Girija in Bionanotechnology in Cancer, 2023
Though tumor immunosurveillance hypothesis emphasizes the ability of immune cells to recognize and eliminate cancer cells; however, many patients develop cancer even in the presence of an apparently normal immune system. This indicates that tumor cells are able to escape immune surveillance. To avoid attack from the immune system, tumor cells develop different strategies to escape immune surveillance. Cancer immune evasion is a major limitation for developing an effective therapeutic approach to treat cancer. To have a successful anticancer immune response, the tumor-immunity cycle should be circulated uninterrupted [24]. Blockade at any step in the pathway leads to unresponsiveness. Cancer cells develop different strategies to interrupt the tumor-immunity cycle. In below sections, we review different escape mechanisms employed by cancer cells.
Immunomodulatory Therapies
David E. Thurston, Ilona Pysz in Chemistry and Pharmacology of Anticancer Drugs, 2021
Cancers develop from early premalignant to advanced premalignant lesions, which then progress to become malignant cancers. Immunosurveillance of cancer can have three outcomes: “elimination” in which all cancer cells are completely removed by the immune system, “equilibrium” in which there is a “stalemate” between the immune system and the cancer, or “escape” in which there is unopposed progression of the cancer (Figure 9.3). Having no preexisting immunity allows for unopposed progression of cancer (escape). Some patients will have some antitumor antibodies and relevantly targeted T cells (i.e., preexisting immunity), which may result in either equilibrium or escape depending on the strength of the immunity. However, if this preexisting immunity is boosted using a prophylactic cancer vaccine, the result may be equilibrium or even elimination of the tumor cells, with potentially lifelong protection through immune memory elicited by the vaccine.
Vaccine Trials
Scott Patterson, Byron Jones in Bioequivalence and Statistics in Clinical Pharmacology, 2017
Avoidance of exposure to a disease vector, hand-washing (with soap and in clean water), along with the immune system are the chief means of defense against disease vectors. The immune system recognizes antigens (proteins produced in cells when disease vectors replicate), and upon recognition, responds with specific and nonspecific factors to kill the disease vector. Nonspecific factors are produced all the time by the body — e.g., lymphoid cells, macrophages, complement factors. These float around in the blood, and “eat” or disable any disease vector they recognize. Specific factors are also introduced to the body by prior infection/recovery or by vaccination. These result in antibodies which the body creates automatically in the immune system and/or in cell-mediated immunity when exposed to a disease vector [936].
Uveitis in Patients Treated with CTLA-4 and PD-1 Checkpoint Blockade Inhibition
Published in Ocular Immunology and Inflammation, 2020
Michel M. Sun, Ralph D. Levinson, Artur Filipowicz, Stephen Anesi, Henry J. Kaplan, Wei Wang, Debra A. Goldstein, Sapna Gangaputra, Robert T. Swan, H. Nida Sen, Lynn K. Gordon
This past decade has seen a rapid and dramatic shift in cancer management with the increasingly widespread use of cancer immunotherapy drugs. Immunotherapy is based on the concept of cancer immunosurveillance,1 the idea that a natural function of the immune system includes detection and elimination of transformed host cells, and that by extension, enhancing immune function can amplify antitumor response and aid in the eradication of existing cancers and metastases. This study focuses on the class of immune checkpoint inhibitors, specifically CTLA-4 and PD-1 monoclonal antibody blockade,2 which act by releasing inhibitory “brakes” on immune cells to promote antitumor response.3,4 Use of these immunotherapeutic drugs whose actions work in the spectrum between anti-tumor and anti-self, disrupts the balance of self-tolerance and the well-established roles of the PD-1 and CTLA-4 pathways in autoimmunity.5 The subsequent immune-related adverse events (irAEs) and their management is a critical area of immunotherapeutic research, as autoimmune related toxicity often limits the use of these otherwise effective cancer therapeutics.
In quest of a new therapeutic approach in COVID-19: the endocannabinoid system
Published in Drug Metabolism Reviews, 2021
Ondine Lucaciu, Ovidiu Aghiorghiesei, Nausica Bianca Petrescu, Ioana Codruta Mirica, Horea Rareș Ciprian Benea, Dragoș Apostu
Cannabinoid and immune system. The immune system is defined as a complex network of proteins and cells that protect the body against infections. The cells found within the immune system are macrophages, T cells, B cells, mast cells, basophils, neutrophils, eosinophils, dendritic cells, natural killer cells, natural killer T cells, CD4+ cells, and CD8+ cells (Apostu et al. 2019; Nichols and Kaplan 2020). The main proteins found in the immune systems are signaling proteins (cytokines), complement proteins, and antibodies (Nichols and Kaplan 2020). This system is regulated by other systems as well, such as the endocrine and nervous. The cannabinoid system also plays a part in the immune response (Nichols and Kaplan 2020). Cannabinoid receptors are present throughout the immune system as they are found in B lymphocytes, T4 lymphocytes, T8 lymphocytes, leukocytes, macrophages, microglia, mononuclear cells, mast cells, natural killer cells, spleen, thymus, tonsils, or lymph nodes (Cabral and Griffin-Thomas 2009).
The role of nivolumab combined to immunotherapy and/or chemotherapy in the first-line treatment of advanced Non Small Cell Lung Cancer
Published in Expert Opinion on Biological Therapy, 2021
Danilo Rocco, Luigi Della Gravara, Ciro Battiloro, Cesare Gridelli
One of the latest breakthroughs pertaining the treatment of advanced NSCLC – both in terms of efficacy and tolerability – is represented by PD-1/PD-L1 targeting Immune Checkpoint Inhibitors (ICIs): this class of drugs exert its activity by enhancing the patient’s immune response against cancer cells via a blockade of the aforementioned negative immune checkpoints. Cancer cells can evade immunosurveillance (also) exploiting these negative immune checkpoints. In fact, NSCLC cells can express PD-L1 (Programmed Death Ligand 1) on their surface, which, upon binding its receptor PD-1 (Programmed Death 1) expressed on activated T-cells, suppresses T-cells activation and proliferation. Thus, PD-1/PD-L1 targeting ICIs exert their activity binding either PD-1 or PD-L1, blocking this axis and therefore preventing T-cell suppression and cancer cells immune escape [6]. In the same vein, another targetable negative immune checkpoint is represented by the CTLA4-B7 axis. After antigen-presenting cells bind the MHC I/II-antigens complex to the T-cell receptor on the surface of T-cells, a co-stimulatory second signal is needed in order to activate T-cells: this signal is represented by the binding between B7 on the surface of antigen-presenting cells and CD28 on the surface of T-cells. CTLA-4, expressed on the surface of T-cells, competitively binds B7, preventing T-cells activation and proliferation. Anti-CTLA-4 ICIs block this axis, preventing this inhibition; to this date, ipilimumab is the only FDA (US Food and Drug Administration) and EMA (European Medicines Agency) approved anti-CTLA-4 ICI for the treatment of advanced NSCLC [7].
Related Knowledge Centers
- Adaptive Immune System
- Cancer Immunology
- Humoral Immunity
- Innate Immune System
- Tissue
- Virus
- Pathogen
- Parasitic Worm
- Splinter
- Cell-Mediated Immunity