Tuberculosis
This feature of Mycobacterium tuberculosis allows it to resist gram staining.
What is mycolic acid?
This antibody is produced first in a primary response.
What is IgM?
These are the most abundant granulocytes that phagocytose bacteria.
What are neutrophils (PMNs)?
This is the molecule a T cell must recognize on an APC during Signal 1.
What is MHC?
This event occurs during Signal 1 when BCRs bind and cluster.
What is BCR cross-linking?
This TB stage is walled off inside granulomas and shows no symptoms.
What is latent TB infection (LTBI)?
This antibody is the most abundant in secretions like saliva and tears.
What is IgA?
This PRR detects dsRNA in the cytoplasm.
What is RLR?
This molecule on the T cell delivers Signal 2 when it binds B7.
What is CD28?
These are three molecules upregulated during partial activation.
What are MHC II, B7, and CD40?
This is why TB becomes drug-resistant quickly.
What is its slow generation time increasing mutation accumulation?
This function involves antibodies coating a pathogen to enhance phagocytosis.
What is opsonization?
These two complement fragments drive inflammation.
What are C3a and C5a?
This happens to a naïve T cell if it receives Signal 1 without co-stimulation.
What is anergy (or deletion)?
This required interaction between B cells and T cells completes full activation.
What is CD40–CD40L binding?
This test measures IFN-γ release to detect TB infection.
What is an IGRA?
This antibody crosses the placenta in pregnant women, enabling the baby to have a "bulletproof vest" from pathogens for several months.
What is IgG?
This is the process by which macrophages fuse lysosomes with the phagosome.
What is phagolysosome formation?
These two cytotoxic molecules released by Tc cells induce apoptosis in target cells.
What are perforin and granzymes?
This process improves antibody–antigen binding strength during clonal expansion.
What is affinity maturation?
The probability of resistance to both INH (10⁻⁶) and RIF (10⁻⁷) is this.
What is 10⁻¹³?
This structural feature gives IgM its strong complement-activating ability.
What is the pentamer/J-chain?
This structural feature prevents C3b binding and inhibits phagocytosis—hint: Streptococcus pneumoneae has this as a virulence factor.
What is a capsule?
This explains why NK cells kill virus-infected cells that downregulate MHC I, while CD8 T cells cannot.
What is “missing self” recognition by NK cells?
Failure of this specific step results in a patient producing only IgM.
What is class switching?