Hypersensitivity pneumonitis is classified as

Ref Robbins 9/e p117 Once complexes are deposited in the tissue, the third phase, the inflammatory reaction, ensues. During this phase (approximately 10 days after antigen administration), clini- cal features such as fever, uicaria, ahralgias, lymph node enlargement, and proteinuria appear. Wherever immune complexes deposit, characteristic tissue damage occurs. The immune complexes activate the complement system, leading to the release of biologically active frag- ments such as the anaphylatoxins (C3a and C5a), which increase vascular permeability and are chemotactic for neutrophils and monocytes (Chapter 2). The complexes also bind to Fcg receptors on neutrophils and monocytes, activating these cells. Attempted phagocytosis of immune complexes by the leukocytes results in the secretion of a variety of additional pro-inflammatory substances, includ- ing prostaglandins, vasodilator peptides, and chemotactic substances, as well as lysosomal enzymes capable of digest- ing basement membrane, collagen, elastin, and cailage, and reactive-oxygen species that damage tissues. Immune complexes can also cause platelet aggregation and activate Hageman factor; both of these reactions augment the inflammatory process and initiate formation of micro- thrombi, which contribute to the tissue injury by producing local ischemia (Fig. 4-11). The resultant pathologic lesion is termed vasculitis if it occurs in blood vessels, glomerulo- nephritis if it occurs in renal glomeruli, ahritis if it occurs in the joints, and so on. Predictably, the antibody classes that induce such lesions are complement-fixing antibodies (i.e., IgG and IgM) and antibodies that bind to phagocyte Fc receptors (IgG). During the active phase of the disease, consumption of complement may result in decreased serum complement levels. The role of complement- and Fc receptor-dependent inflammation in the pathogenesis of the tissue injury is suppoed by the observation that experimental depletion of serum complement levels or knockout of Fc receptors in mice greatly reduces the severity of lesions, as does deple- tion of neutrophils.