Cryptococcus neoformans virulence in immunocompromised hosts is primarily due to its polysaccharide capsule. The capsule's main mechanism of immune evasion involves:
- A Inhibiting phagocytosis by preventing C3b and IgG opsonin binding to the cryptococcal cell wall
- B Shedding large amounts of glucuronoxylomannan (GXM) that act as a decoy to consume antibody, impair phagocyte migration, reduce antigen presentation by interfering with MHC II, and shift immunity towards Th2 via IL-4/IL-13 skewing ✓
- C Activating regulatory T cells (Tregs) directly through TLR2 binding to capsular mannoproteins
- D Producing melanin that quenches reactive oxygen species generated by phagocyte NADPH oxidase
Explanation
The polysaccharide capsule of C. neoformans, composed predominantly of glucuronoxylomannan (GXM), exerts multiple immunosuppressive effects: it sheds massive quantities into surrounding tissues that consume specific antibodies (antibody decoy effect), inhibits phagocyte migration and opsonophagocytosis, impairs antigen presentation by reducing MHC class II expression on dendritic cells, and promotes Th2 cytokine polarization (IL-4, IL-13) over protective Th1 responses (IFN-γ, IL-12) needed for fungal clearance. Melanin is a separate virulence factor that scavenges ROS; it is produced by the laccase enzyme using catecholamine substrates. Direct Treg activation via TLR2 is not the primary capsular immune evasion mechanism.
Reference: Ananthanarayan & Paniker's Textbook of Microbiology, 11th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.