Which of the following type of hypersensitivity reactions occur in farmer's lung diseas
Ref Robbins 8/e p207; 9/e p210 Inflammatory Reactions Elicited by CD4+ T Cells The sequence of events in T cell-mediated inflammatory reactions begins with the first exposure to antigen and is essentially the same as the reactions of cell-mediated immunity (Fig. 4-4). Naive CD4+ T lymphocytes recognize peptide antigens of self or microbial proteins in association with class II MHC molecules on the surface of DCs (or macrophages) that have processed the antigens. If the DCs produce IL-12, the naive T cells differentiate into effector cells of the TH1 type. The cytokine IFN-g, made by NK cells and by the TH1 cells themselves, fuher promotes TH1 dif- ferentiation, providing a powerful positive feedback loop. If the APCs produce IL-1, IL-6, or IL-23 instead of IL-12, the CD4+ cells develop into TH17 effectors. On subsequent exposure to the antigen, the previously generated effector cells are recruited to the site of antigen exposure and are activated by the antigen presented by local APCs. The TH1 cells secrete IFN-g, which is the most potent macrophage- activating cytokine known. Activated macrophages have increased phagocytic and microbicidal activity. Activated macrophages also express more class II MHC molecules and costimulators, leading to augmented antigen presenta- tion capacity, and the cells secrete more IL-12, thus stimu- lating more TH1 responses. Upon activation by antigen, TH17 effector cells secrete IL-17 and several other cytokines, which promote the recruitment of neutrophils (and mono- cytes) and thus induce inflammation. Because the cyto- kines produced by the T cells enhance leukocyte recruitment and activation, these inflammatory reactions become chronic unless the offending agent is eliminated or the cycle is interrupted therapeutically. In fact, inflammation occurs as an early response to microbes and dead cells (Chapter 2), but it is greatly increased and prolonged when T cells are involved. Delayed-type hypersensitivity (DTH), described next, is an illustrative model of T cell-mediated inflammation and tissue injury. The same reactions are the underlying basis for several diseases. Contact dermatitis is an example of tissue injury resulting from T cell-mediated inflammation. It is evoked by contact with pentadecylcatechol (also known as urushiol, the active component of poison ivy and poison oak, which probably becomes antigenic by binding to a host protein). On reexposure of a previously exposed person to the plants, sensitized TH1 CD4+ cells accumulate in the dermis and migrate toward the antigen within the epidermis. Here they release cytokines that damage kera- tinocytes, causing separation of these cells and formation of an intraepidermal vesicle, and inflammation manifested as a vesicular dermatitis. It has long been thought that several systemic diseases, such as type 1 diabetes and mul- tiple sclerosis, are caused by TH1 and TH17 reactions against self antigens, and Crohn disease may be caused by uncon- trolled reactions involving the same T cells but directed against intestinal bacteria. T cell-mediated inflammation also plays a role in the rejection of transplants, described later in the chapter.
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General anatomy