Immune responses are often a double-edged sword. Their essential role in protecting against infections is critical for survival, as shown by the fatal consequences of untreated immunodeficiency diseases (to be discussed in Chapter 18). To ensure effective protection, a broad range of innate and adaptive immune mechanisms has evolved, typically enabling responses tailored to the specific pathogen entering the body. However, immune responses are inherently destructive, and when excessive, persistent, or misdirected, they can harm the body. This chapter has focused on such conditions, including the four classes of hypersensitivity reactions and chronic inflammation.

Type I hypersensitivity reactions, commonly known as allergies, are mediated by IgE antibodies bound to FcεRI receptors on mast cells, basophils, and eosinophils, which become cross-linked by recognized antigens. This triggers degranulation, releasing mediators responsible for allergy symptoms. These symptoms may manifest locally, such as in the respiratory tract for airborne allergens or in the gastrointestinal tract for food allergens, but they can also be systemic if the allergen enters the bloodstream, as with insect stings, drugs like penicillin, and certain foods. Although IgE and granulocyte degranulation likely evolved to combat parasitic worms and animal or insect venoms, some allergic reactions, such as hay fever, are mostly inconveniences, while others, like anaphylaxis and asthma, are maladaptive and potentially life-threatening.

Type II and Type III hypersensitivity reactions involve normal IgM and IgG antibody-antigen interactions that become harmful when excessive or misdirected. Type II reactions arise from extensive cell destruction, as seen in transfusion reactions involving incompatible blood types.