exotoxins A protein toxin produced and secreted by a bacterium.
experimental autoimmune encephalomyelitis (EAE) An inﬂammatory disease of the central nervous system that develops after mice are immunized with neural antigens in a strong adjuvant.
extrachromosomal DNA   DNA not contained within chromosomes, such as the circular DNA produced by V(D)J recombination occurring between RSSs in the same chromosomal orientation and is eventually lost from the cell.
extravasation The movement of cells or ﬂuid from within blood vessels into the surrounding tissues.
extrinsic pathway of apoptosis A pathway triggered by extracellular ligands binding to specific cell-surface receptors (death receptors) that signal the cell to undergo programmed cell death (apoptosis).
Fab fragment Antibody fragment composed of a single antigen-binding arm of an antibody without the Fc region, produced by cleavage of IgG by the enzyme papain. It contains the complete light chain plus the amino-terminal variable region and first constant region of the heavy chain, held together by an interchain disulfide bond.
F(abʹ)2 fragment Antibody fragment composed of two linked antigen-binding arms (Fab fragments) without the Fc regions, produced by cleavage of IgG with the enzyme pepsin.
factor B   Protein in the alternative pathway of complement activation, in which it is cleaved to Ba and an active protease, Bb, the latter binding to C3b to form the alternative pathway C3 convertase, C3bBb.
factor D A serine protease in the alternative pathway of complement activation, which cleaves factor B into Ba and Bb.
factor H   Complement-regulatory protein in plasma that binds C3b and competes with factor B to displace Bb from the convertase.
factor H binding protein (fHbp) A protein produced by the pathogen Neisseria meningitidis that recruits factor H to its membrane, thereby inactivating C3b deposited on its surface, and evading destruction by complement.
factor I   Complement-regulatory protease in plasma that cleaves C3b to the inactive derivative iC3b, thus preventing the formation of a C3 convertase.
factor I deficiency A genetically determined lack of the complement-regulatory protein factor I. This results in uncontrolled complement activation, so that complement proteins rapidly become depleted. Those with the deficiency suffer repeated bacterial infections, especially with ubiquitous pyogenic bacteria.
factor P Plasma protein released by activated neutrophils that stabilizes the C3 convertase C3bBb of the alternative pathway.
familial cold autoinflammatory syndrome (FCAS) An episodic autoinﬂammatory disease caused by mutations in the gene NLRP3, encoding NLRP3, a member of the NOD-like receptor family and a component of the inﬂammasome. The symptoms are induced by exposure to cold.
familial hemophagocytic lymphohistiocytosis (FHL) A family of progressive and potentially lethal inﬂammatory diseases caused by an inherited deficiency of one of several proteins involved in the formation or release of cytolytic granules. Large numbers of polyclonal CD8-positive T cells accumulate in lymphoid and other organs, and this is associated with activated macrophages that phagocytose blood cells, including erythrocytes and leukocytes.
familial Mediterranean fever (FMF) A severe autoinﬂammatory disease, inherited as an autosomal recessive disorder. It is caused by mutation in the gene (MEFV) that encodes the protein pyrin, which is expressed in granulocytes and monocytes. In patients with this disorder, defective pyrin is thought to spontaneously activate inﬂammasomes.