Immunology Made Easy

Neutrophils act as the first line of defense in innate immunity, using granules, degranulation, and phagocytosis to kill bacteria and fungi and form extracellular traps.

Macrophages perform phagocytosis of infected cells and microorganisms, aided by opsonization and antibody-mediated signals that promote uptake. Cytokine production by macrophages helps destroy infected cells and inhibit malaria parasite growth.

Explore how innate immunity detects microbes via PRRs, activates NF-κB to stimulate macrophages, and drives acute inflammation with endothelial changes and neutrophil recruitment.

Explain acute inflammation as an innate response: vasodilation raises blood flow and redness; neutrophils and macrophages migrate to infection sites via leukocyte migration, guided by interleukins and TNF.

Adaptive immunity, driven by lymphocytes, produces immunoglobulins (antibodies) that neutralize antigens and uses T cells to help or kill infected cells, yielding highly specific, long-lasting protection.

Antigen presenting cells activate T cells to drive adaptive immunity, stimulating B cells to produce antibodies and form memory B and T cells, plus helper and cytotoxic T cells.

B lymphocytes arise from hematopoietic stem cells in bone marrow, differentiate into B1 and B2 lineages, mature there, and become memory B cells or plasma cells in lymph nodes.

Explain the four hypersensitivity types i, ii, iii, and iv, covering antigens, mediators, and key examples like serum sickness and vasculitis.

Type 4 hypersensitivity is a delayed, T cell–mediated immune response that damages tissue. It involves memory responses, contact dermatitis from poison ivy, and tuberculosis with granuloma formation and lung distortion.