Immune related adverse events (irAEs)

Specific treatment for patients with cancer relies on the generation of lymphocytes that recognize tumor antigens and eliminate them in vivo.

Immunotherapy modifies the immune system by augmenting or suppressing immune responses to obtain a desired effect.

Immunomodulators have found applications in dermatology, rheumatology, immunology, and oncology.

IRAEs oh strongly associated with beneficial responses, likely reflecting systemic immune competence. 


Vaccination programs have been successful in increasing the number of tumor antigen reactive lymphocytes in the circulation of patients, but only sporadic responses have been reported.

Two distinct types of cancer immunotherapy exist: passive immunotherapy using the components of the immune system to direct targeted cytotoxic activity against cancer cells, without necessarily initiating immune response, and active immunotherapy which actively triggers an endogenous immune response.

Passive immunotherapy includes the use of monoclonal antibodies produced by B cells in response to specific antigen.

Adaptive immune responsesare mediated by cellular and humeral components with cytotoxic T lymphocytes (CD4 and CD8 positive T cells) having a key role.

The immune system should recognize alterations in the genetic code within tumor cells as being foreign, and should eradicate abnormal cells through immune surveillance.


Immunotherapy drugs can enhance the immunologic response to MET-expressing tumor cells, or actively by stimulating immune cells and altering differentiation/growth of tumor cells.


The administration of monoclonal antibodies (mAbs) is a form of passive 

Immunotherapy.


Monoclonal antibodies  facilitate destruction of tumor cells by complement-dependent cytotoxicity (CDC) and cell-mediated cytotoxicity (ADCC). 


In complement-dependent cytotoxicity , the monoclonal antibody binds to specific antigen, leading to activation of the complement cascade, which in turn leads to formation of pores in tumor cells. 


In cell-mediated cytotoxicity (ADCC) the Fab domain of a mAb binds to a tumor antigen, and Fc domain binds to Fc receptors present on effector cells, which are phagocytes and NK cells, thus forming a bridge between an effector and a target cells. 


Chronic exposure to tobacco carcinogens and accumulation of mutations overtime can lead to T-cell exhaustion and trigger T Cells to turn it off and this may be manifested through the upregulation of the programmed death ligand (PD-L1) on tumor cells, which can inhibit T cell function by binding to programmed death 1 (PD-1) on T cells.






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