Immunology: USMLE Step 1 video lessons
Innate and adaptive immunity, hypersensitivity, immunodeficiency and transplantation.
Antigen presentation, T-cell activation and helper subsets, antibody isotypes, tolerance, complement and its deficiencies, hypersensitivity types I to IV, primary immunodeficiencies, transplant rejection and how the different vaccine types work.
5:03MHC I vs MHC II: how antigen presentation works
MHC I vs MHC II comes down to one rule: class I shows what the cell made inside, class II shows what the cell swallowed from outside. Each class has its own machinery and its own T cell.
4:58T-cell activation: the two-signal model
A T cell can recognise its antigen perfectly and still stay asleep. T-cell activation needs a second signal, and the antigen-presenting cell decides whether it is given.
5:13Th1, Th2, Th17 and Treg: helper T-cell subsets
Th1, Th2, Th17 and Treg are chosen by the cytokines around a naive CD4 T cell. Each has an inducer, a master transcription factor, a product and a target.
5:13Antibody isotypes and class switching
Every antibody class has one main job. A B cell can change its class without changing what it recognises, and the helper T cell and the enzyme AID decide how.
5:26Central vs peripheral tolerance: how lymphocytes learn self-tolerance
Receptors are built at random, so some will recognise the body's own molecules. Central tolerance removes them in the thymus and bone marrow; peripheral tolerance catches those that slip through.
5:24Complement system explained: three pathways, one ending
The complement system has three ways in and one way out. Compare how the classical, lectin and alternative pathways start, then follow the shared steps that all three produce.
5:15Complement deficiencies: C1q, C3, C5–C9 and C1 inhibitor
Each missing complement component predicts its own disease. Work out the infection or syndrome from the job that is lost, and the CH50, C3 and C4 pattern follows.
5:20Hypersensitivity types I to IV: the four effectors
Hypersensitivity types I to IV sort allergic and immune damage by what does the harm: IgE, antibody on cells, immune complexes or T cells. Timing is the clue.
5:24B-cell vs T-cell immunodeficiency: predict the infections
Two babies are both immunodeficient, yet their infections differ. Work out which arm of immunity is lost, antibody or cellular, and the pattern of infection follows.
5:19Hyper IgM syndrome: CD40 ligand and class switching
High IgM, yet a deficiency. In its commonest form, the B cell is present but cannot switch class, because the T-cell signal through CD40 ligand fails.
5:20Chronic granulomatous disease: NADPH oxidase and the respiratory burst
The neutrophils are present in normal number, yet they cannot kill. Follow one oxygen molecule through the respiratory burst to see why infections persist in chronic granulomatous disease.
5:01Leukocyte adhesion deficiency: CD18 and neutrophil extravasation
A newborn has a very high white cell count and an infection with no pus. Follow a neutrophil out of the blood to see which step fails in leukocyte adhesion deficiency type 1, and how type 2 differs.
5:51Transplant rejection explained: hyperacute, acute, chronic and GVHD
Is the host attacking the graft, or the graft attacking the host? How to tell the three types of transplant rejection and graft-versus-host disease apart by timing and immune mechanism.
5:41Vaccine types explained: live, inactivated, conjugate and mRNA
Each vaccine platform shows the immune system an antigen in a different way. Match the type to the response it triggers, and see why live vaccines are avoided in immunodeficiency.