Humoral Immunity - Pathogenesis and Clinical Findings
Antigens (Ag) are produced from pathogens (bacteria, viruses, fungi, parasites) or the patient (via trauma, tumor, metabolism), & circulate in plasma, lymph, or other tissue
• T cell-dependent Ag: Ag-presenting cells (such as dendritic cells or macrophages) present Ag to CD4+ helper T cells and activate them. Activated helper-T cells then stimulate B cells
• T cell-independent Ag: Ags such as peptides, carbohydrates and lipids may be directly recognized by B cells, triggering their activation
• Complement: Circulating serum complement proteins detect and bind Ag. Ags tagged with C3 complement fragment bind B cell co-receptor complex and enhance B cell activation.
• Differentiation (into memory B cells or plasma cells)
• Plasma cells produce antibodies, which contribute to immunity in 3 ways:
- Opsonization: Abs coat pathogens, helping recognition by phagocytes
- Neutralization: Abs bind to pathogen surface molecules that are needed to invade host cells, thereby neutralizing them
- Activate Complement: Abs activate complement proteins via the classical pathway (see Complement Activation slide)
• Memory B cells are long-lived detectors -> Memory B cells sequester in storage sites (e.g. lymph nodes, spleen) or circulate in the blood -> Memory B cells proliferate and differentiate into plasma cells in response to re-exposure to antigen -> Incr Rate and amplitude of secondary immune response on repeat exposure
#Humoral #Immunity #pathophysiology #immunology
