Figure 1. Transmission electron micrograph (osmium collidine uranyl en bloc processing) showing a mast cell (M) and basophil (B) in the ileal submucosa of a patient with Crohn disease. The mast cell is the larger, mononuclear cell; it has more complex plasma-membrane surface and cytoplasmic granules (arrowheads) that are smaller and more numerous than those (arrows) of the basophil. In this section plane, the basophil has two nuclear lobes (n). Several basophil cytoplasmic granules are visible that contain whorls of membrane (curved arrows). Reprinted from Dvorak et al. 1980. Copyright (1980), with permission from Elsevier.

Figure 2. Basophils develop from haematopoietic stem cells in the bone marrow, where they typically complete their differentiation/maturation. They then leave the bone marrow and circulate as mature granulocytes in the peripheral blood. Basophils can be recruited to enter tissues at sites of immunological or inflammatory reactions in response to the local generation of certain lipid mediators, cytokines and/or chemokines (which can be released from mast cells and many other cell types). Increased levels of IgE antibodies, which are found in subjects with allergic diseases or parasite infections, can induce upregulation of surface expression of FcRI on basophils (and mast cells), priming such cells to release increased amounts of mediators after allergen/antigen crosslinking of surface-bound, allergen/antigen-specific IgE. For example, in the ‘sensitization’ phase of an acquired immune response, subjects are ‘sensitized’ by an initial exposure to antigens/allergens derived from parasites (e.g. ticks or worms) or environmental agents (e.g. pollen or insect venom); this results in the production of antigen/allergen-specific IgE antibodies by plasma cells. The host is shown undergoing sensitization against antigens/allergens derived from a parasitic worm and a type of pollen; in such hosts, this process eventually results in the production of IgE antibodies with distinct specificity, for either worm- or pollen-derived antigens/allergens. At some time in the past, this host had been sensitized both to a type of tick and to the venom of a stinging insect (e.g. a wasp). Because basophils and mast cells express many FcRI on their surface, they can simultaneously bind IgE antibodies with specificity for multiple antigens/allergens. In such hosts that have been sensitized to multiple antigens/allergens, basophil degranulation/activation thus can be induced in response to antigens/allergens derived from feeding ticks, worms or environmental agents such as pollen, food or drugs. Systemic degranulation/activation of basophils in the blood (e.g. in response to certain components of medicines, insect venoms, or foods) can contribute to systemic anaphylaxis. Other pathways of basophil activation exist (e.g. by viral products), but are not shown in the diagram (see text). Cytokine release from basophils (e.g. IL-4, IL-13) may have immunoregulatory effects (e.g. by contributing to enhanced IgE production). *Several lines of evidence suggest that basophils are derived from the common myeloid progenitor. †Mast cells, T cells and many other cell types can secrete products that can enhance basophil adhesion, migration and function. ‡The term ‘allergens’ is usually used to refer to antigens that can elicit specific IgE antibody responses in at least some individuals, such as certain components of foods, medicines, pollens, insect venoms, etc.; certain parasites (e.g. ticks, worms) also represent sources of antigens that can induce the development of specific IgE antibody responses. Accordingly, IgE antibodies participate in the pathology of certain allergies as well as in host defence against some parasites. §During an acquired immune response involving T helper type 2 (T_H2) cells, such as those induced by certain parasites or by environmental allergens, production of IL-4 and IL-13 can induce IgE antibody production by plasma cells; T_H2 cells also represent a source of IL-3, which can induce ‘basophilia’ by enhancing basophil production, resulting in increased numbers of basophils in the bone marrow and the blood.