Some infections don’t develop within our cells – many are extracellular.
Once these pathogens have gotten past the first line of defense, our skin, resident mast cells and macrophages jump into action. Histamine is released and blood flow to the site of infection is increased. PAMPs are recognized, driving the phagocytosis of the invading pathogen and production of alarm cytokines that help recruit more immune cells to the site of infection.
Neutrophils and immature macrophages arrive, allowing for the phagocytosis of more and more pathogen.
Typically, this is sufficient to resolve infection. In some cases, the load of pathogen is too overwhelming of the innate immune response, and the pathogen goes on to multiple and spread beyond the site of infection.
Dendritic cells at the site of infection take in the pathogen, carrying information to the lymph node where they proceed to activate CD4 T cells.
After interacting with pathogen-derived antigens and receiving signals from activated CD4 T cells, B cells are also activated.
They proceed to produce different types of antibodies (through class-switching), and further differentiate into plasma cells (antibody-making factories) or memory B cells (important for future responses)
Antibodies circulate throughout the body. They can bind to the pathogen and neutralize it, and make phagocytosis more effective by opsonizing the pathogen.
This article’s content was created based upon the background accrued over the course of the author’s Honours BSc Degree in Microbiology & Immunology, which included Immunology, Virology, and Bacterial Pathogenesis course-work and exposure to topics from Janeway’s Immunobiology.
