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ISSN: 2638-5945

Open Access Journal of Oncology and Medicine

Editorial(ISSN: 2638-5945)

Cancer and Advantages of Immunosuppression Volume 1 - Issue 2

Mirta D Ambra*
  • Academy of Medicine and Science, South America

Received: March 05, 2018;   Published: March 09, 2018

*Corresponding author: Mirta D Ambra, Academy of Medicine and Science, Headquarters The Netherlands, Argentina, South America

DOI: 10.32474/OAJOM.2018.01.000108

 

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Abbrevations: NK: Natural Killer; GVHD: Graft-vs-Host Disease; CRS: Cytokine Release Syndrome

Editorial

As oncologists learn to target the immune response to “self and non-self,” a delicate therapy balance will eventually be achieved with predictable outcomes, benefits, and toxicity in the fightThe study of how the immune system recognizes friend and foe, or as the immunologist Sir Macfarlane Burnet phrased it, “distinguishes between self and non-self,” has driven important discoveries that are transforming our ability to treat cancer.

Over the last few clinicians have unraveled the interactions (both innate and adaptive immunity) that lead to the eradication of viruses, bacteria, parasites, and now, cancer. Notable cellular players include T cells, B cells, natural killer (NK) cells, neutrophils, eosinophils, basophils, dendritic cells, and macrophages, along with a host of secreted mediators - antibodies, complement, cytokines, and chemokines - each of which fulfills particular immunologic functions. Processes, autoimmune disease can be a consequence. These diseases also occur if shared. When the immune system fails to regulate these antigens are recognized by the immune system in cells; one example is Lambert-Eaton syndrome. Monoclonal antibodies that target tumour reactive T cells (eg, nivolumab and pembrolizumab) can also cause autoimmune disease; other examples include graft-vs-host disease (GVHD) in allogeneic bone marrow transplant recipients and cytokine release syndrome (CRS), which is associated with adoptive T cell therap.

ute Myeloid Leukemia (AML). Blood 128: 763.
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