Immune System Tournament
Two onboarding diagrams orient you in the immune network. Then eight MCAT-DoK quiz rounds: MHC class I vs. class II restriction, the two-signal rule and anergy, the full antigen-presentation sequence, helper T cell subsets and their cytokines, the four hypersensitivity types, the five antibody isotypes, innate vs. adaptive mechanisms, and why HIV's CD4 depletion collapses both arms of immunity.
Where the Adaptive immune system fits in Immune system
The Reactome immune system map splits host defense into two arms: innate immunity, which is fast, germline-encoded, non-specific, and leaves no memory, and adaptive immunity, which takes 1 to 2 weeks on first exposure but is exquisitely antigen-specific and remembers. The highlighted adaptive panel is where lymphocyte selection lives - thymic education of T cells, MHC-restricted antigen presentation, and B cell class switching in germinal centers. Click the highlighted Adaptive immune system panel to enter the tournament.
Click the highlighted Adaptive immune system box to continue.
What this tournament tests
Each task maps to a distinct MCAT cognitive demand. The first two orient you in the broader topology; the next eight test the high-yield mechanism, regulation, sequence and quantitative reasoning that consistently appear on test day.
The Bigger Picture
Anchor the adaptive arm inside the full Reactome immune system map.
Whole-Pathway Overview
Pan and zoom the curated WikiPathways T cell receptor signaling figure before you start answering.
Fill in the Blank
Recall that exogenous peptides are displayed on MHC class II to CD4+ helper T cells.
Disruptor
Predict the fate of a T cell that gets signal 1 without CD28/B7 costimulation.
Sequence Ordering
Trace dendritic cell uptake -> MHC II loading -> lymph node -> signal 1 -> signal 2 -> IL-2 -> clonal expansion -> germinal center.
Match the Pairs
Pair Th1, Th2, Th17, Treg, CD8+ CTL, plasma cell, and follicular dendritic cell with their programs.
Numeric Input
Recall the four Gell and Coombs hypersensitivity types (ACID).
Select All That Apply
Identify TRUE facts about the isotypes: IgM first, IgG placental, IgA mucosal, IgE mast cells.
Odd One Out
Distinguish innate effectors from somatic hypermutation, a purely adaptive process.
HIV Disruptor
Explain why depleting CD4+ helper cells cripples both cell-mediated and humoral immunity.
Public leaderboard
Your score posts to a global, persistent leaderboard scored by points first, time as tiebreaker.
Immunity in 60 seconds
Host defense runs on two arms. Innate immunity acts within minutes to hours using germline-encoded pattern receptors (TLRs), phagocytes, NK cells, and complement - broad, non-specific, no memory. Adaptive immunity is slower on first exposure but is antigen-specific and generates memory, because its receptors are built by V(D)J recombination before any antigen arrives and antigen simply selects the clone that already fits (clonal selection).
Presentation is MHC-restricted. MHC class I is on every nucleated cell and shows ENDOGENOUS cytosolic peptides (viral, tumor) to CD8+ cytotoxic T cells. MHC class II is restricted to professional APCs (dendritic cells, macrophages, B cells) and shows EXOGENOUS peptides to CD4+ helper T cells. Remember the rule of 8: I x 8 = 8 and II x 4 = 8. Activation needs two signals - TCR reading peptide-MHC, plus CD28 engaging B7. Signal 1 alone produces anergy, which is how peripheral tolerance to self is maintained.
Helper output is cytokine-defined: Th1 (IL-12 in, IFN-gamma out; macrophages and intracellular pathogens), Th2 (IL-4 in; IL-4/IL-5/IL-13 out; IgE, eosinophils, helminths), Th17 (IL-17; neutrophils at mucosal barriers), and Treg (FoxP3+, IL-10 and TGF-beta, self-tolerance). B cells that get CD40L plus cytokines enter germinal centers and undergo class switching (new constant region, same specificity) and affinity maturation (somatic hypermutation of the variable region).
The five isotypes divide the labor: IgM first and best at complement fixation, IgG most abundant and the only placenta-crosser, IgA a secretory dimer in mucus and breast milk, IgE on mast cells driving type I hypersensitivity, and IgD on naive B cells. Clinical hooks: primary responses are slow and IgM-heavy while secondary responses are fast and IgG-heavy; active immunity (infection or vaccine) makes memory while passive immunity (maternal IgG, IVIG, antitoxin) is immediate but temporary; HIV destroys CD4+ cells; DiGeorge syndrome aplasia of the thymus destroys T cell development; and hypersensitivity comes in four flavors - ACID.
FAQ
Why does a T cell need two signals instead of one?
Self peptides are displayed on MHC constantly, so antigen recognition alone cannot be the trigger for war. Signal 2 (CD28 binding B7 on the APC) only appears after innate receptors such as TLRs sense a genuine microbial threat and license the dendritic cell. A T cell that gets signal 1 without signal 2 becomes anergic, which is a major peripheral tolerance mechanism. CTLA-4 is the brake that outcompetes CD28 for B7.
What is the difference between class switching and affinity maturation?
Class switching swaps the heavy-chain constant region (IgM to IgG, IgA, or IgE) so the same antigen specificity gains a new effector function; it requires CD40L from a helper T cell plus cytokines and the enzyme AID. Affinity maturation is somatic hypermutation of the variable region followed by selection on follicular dendritic cells, so surviving clones bind the antigen more tightly. Both happen in germinal centers.
Active or passive immunity - how do I tell them apart on the exam?
Active immunity means your own lymphocytes made the response, from natural infection or vaccination. It is slow to develop but produces memory and long-lasting protection. Passive immunity means preformed antibody was transferred in - maternal IgG across the placenta, IgA in breast milk, IVIG, or antitoxin for tetanus, botulism, rabies, or hepatitis B exposure. It works immediately but fades in weeks to months and leaves no memory.
How do the four hypersensitivity types map to diseases?
Type I is IgE and mast cell mediated and immediate: anaphylaxis, atopy, allergic asthma. Type II is antibody against a fixed tissue antigen: autoimmune hemolytic anemia, Goodpasture, myasthenia gravis, rheumatic fever. Type III is immune complex deposition with complement activation: SLE, serum sickness, post-streptococcal glomerulonephritis. Type IV is delayed and T cell mediated with no antibody: PPD test, contact dermatitis, graft rejection.
Do I need an account to play?
No. The tournament is fully public. You get a randomized handle and your score posts to the public leaderboard at the bottom of this page.
Keep going
The fast, non-specific arm that fires first - and licenses adaptive responses by upregulating B7 and MHC II on dendritic cells.
The bridge between antibody and innate lysis - how IgM and IgG recruit C1, opsonize with C3b, and build the membrane attack complex.
Overview diagram: Reactome Pathway R-HSA-168256, licensed CC BY 4.0.