Tumour Immunology + Other Hallmarks of Cancer Flashcards
How are cancer cells sometimes recognised as non-self?
Hallmark of cancer = mutations
- > change in proteins
- > peptides displayed on plasma membrane (act as antigen)
- > which are recognised as non-self
What are the stem cell precursors called in haematopoiesis?
Haematopoietic stem cell
What are the 2 distinct lineages formed in haematopoiesis?
Myeloid
Lymphoid
Where do a lot of immune response occur?
Lymphatic system
What type of immunity involves antibodies? What cells are involved?
Humoral (adaptive) immunity
B-cells
What does adaptive mean?
Immune cells are taught to attack previously encountered antigens on a cell
What does innate mean?
Immune cells recognise new non-self cell surface proteins
What are the 2 types of cellular immunity?
Specific (adaptive)
Nonspecific (innate)
What cells are involved in specific cellular immunity?
T-cells
= Cytotoxic T-cells
= Helper T-cells
= Regulatory T-cells
What do regulatory T-cells do?
In specific cellular response
Inhibit cytotoxic + helper T-cells
What do cytotoxic T-cells do?
Kills target cells
What do help T-cells do?
In specific cellular response
Stimulate cytotoxic T-cells + proliferation of plasma cells (-> increase antibody production)
What is MHC?
Major histocompatibility complex
= cell surface proteins
What type of cells express MHC class I?
Almost all cell types including cancer cells
What type of cell express MHC class II?
Professional immunocytes
= antigen-presenting cells
= e.g. phagocytes
What cell can interact w/ MHC? What part specifically is bound to MHC?
T-cells
T-cell receptors (TCRs)
What is the costimulating molecules for MHC class I?
CD8
What is the costimulating molecules for mHC class II?
CD4
CD8 + CD4 are expressed by which cells?
T-cells
Describe the “war” between cancer + the immune system through cancer progression
Early stages of cancer progression (in situ tumour/premalignant lesion):
= Immune system = highly active
= Typically destroys majority of cancer cells
= Cancer cells recognise as non-self
= Don’t eliminate all cancer cells
Equilibrium:
= Not all cancer cells are targeted
= Dampening of immune system
-> tumour grows
Later stages of cancer progression:
= Mutations allows cancer cells to escape detection by immune system
= Mutations that dampens immune system
-> Tumour grows
What do cancer cells express that binds w/ MHC I?
Tumour-associated antigen (TAAs)
Describe the 2 mechanisms of how cytotoxic T-cells cause apoptosis in cancer cells
1) Cytotoxic T-cells perforate surface of cancer cells (perforin makes channels)
= Releases granzymes to cancer cells
= Granzymes activate caspases inside -> apoptosis
2) Active induction of apoptosis
= Mediated by cytotoxic T-cells
= Release death ligands which bind to death cell receptors on cancer cells
Name the 2 molecules involved in the immune checkpoint
PDL1
CTLA-4
How can cancer cells avoid immune system (immunoevasion)?
Hide from Tc (by repressing expression of MHC/tumour antigens)
Hide stress from NK cells (by repressing expression of stress proteins)
Inactivate immunocytes (Tc + NK) (by secreting immunosuppressive proteins e.g. TGF-beta/IL-10)
Induce Tc apoptosis (by releasing apoptotic/death ligands e.g. FasL)
Develop resistance to FasL mediated apoptosis
Attract other Treg cells that inhibit Tcs
