Chapter18CellularImmunity

• Is due to T cells
• Eliminates intercellular pathogens
• Transplanted tissues
• Cancer
• Kills infected host cells
• Helps macrophages kill phagocytosed pathogens
• Difficult to passively transfer

• CD8 are killer T cells (Tc)
• CD4 are Helper T cells (Th)

Present extracellular antigen on MHC II

Types - Dendritic cells, Macrophages, B cells, CD4 T cells bind and then "help"

All cells present intracellular antigen on MHC I and CH8 T cells bind, then "kill"

• MCH proteins = tissue typing antigens
• Class 1 MHC is on all nucleated cells - presents antigen on Tc (CD8)

Class 2 MHC is on professional Antigen Presenting Cells - presents antigen to Th1 and Th2 (CD4)

• MHC1 - loads in the golgi
• Loads with "self" molecules
• Binds with CD8 cells

• They load out side the golgi in a vesical.
• Loads with "non-self" molecules
• Binds with CD4 cells

• Develop in the Thymus - TCR are generated randomly in those T cells
• TCR must bind MHC 1 or MHC 2 for the T cell to survive - Cells that do not bind are signaled to undergo apoptosis
• Because Tcells are selected for their ability to bind self MHC, foreign MHC (transplants) trigger T cell rejection
• Immature T cells binding too tightly to self peptide on self MHC are also killed.

• Tc (cytotoxic (killer) T cells = CD8 recognize and kill virus-infected host cells
• Th1 cells = CD4 signal infected macrophages to kill pathogens in their pagosomes
• Th2 cells = CD4 signal B cells to divide and make antibodies

• Tc go to the infection site and find and kill virus-infected cells
• They kill by releasing perforin makes pores in target cell) and granzymes (cause apoptosis)
• Tc also kill tumor cells

• Skin testing for TH1 function or delayed type hypersensitivity
• as small amount of antigen is injected under the skin and a reaction os recorded
• if you have a positive reaction it means your body has been infected by TB and now have antibodies for it.

Antigen signal and Th2 signal

Stimulate with harmless but similar antigen to generate memory cells and antibody

• Whole cell
• Live attenuated (weakened) virus
• Killed virus
• Subunit / Toxoid
• Recombinant

All will generate active immunity

• Killed cell or inactivated virus is heated
• Dead, but still has antigenicity
• is injected and iummunity starts but pathogen can not multiply

• Can replicate in host
• Induces Tc Cells and antibodies
• Unsafe for immunosuppressed people
• Example: MMR

• Cannot replicate in host
• Safe, induces neutralizing antibodies
• Example: Rabies, Influenza
• "killed" vaccine

• Parts of pathogen - careful as to what subunits used
• Safe, generate antibodies
• Example: Pertussis (acellular) Pneumococcal pneumonia (capsule)

• Inactivated toxin molecules
• Safe, generate neutralizing antibodies
• Example: diphtheria, tetanus

• The use of a plasmid attached to a vector
• Example: Hepatits B virus

• Still under development
• injecting a plasmid directly into and changing our own DNA to be resistant
• Currently used for horses

• Allergies are IgE (antibody) immune response to harmless antigens
• The immune response causes the disease - Hypersensitivity
• Other hypersenstivities are caused by IgG or by Th1 or Tc activities
• Autoimmune reactions occur against self antigens

• Immediate hypersensitivity
• Reaction in 30min
• Inflammation
• Symptoms depend on where allergen enters and how severe the immune response is

• Pollens
• Pet dander
• Dust mite feces
• Food antigens

• IgG/IgM antibodies bind RBC antigens
• Complement is activated, lyses RBC
• ADCC: macrophages or NK cells bind antibody-coated RBC and kill them

• Rh - mother having a Rh + fetus the body will attack the fetus
• Medication allergies
• Mismatched blood (transfusion reaction)
• Rheumatic fever- occurs after infection (Strep Throat)
• Autoimmune hemolytic anemia - Body attacks own RBCs