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.