There are two broad classes of lymphocytes: B cells and T cells. While all lymphocytes start out in the bone marrow, B cells develop in the marrow before entering the bloodstream whereas T cells travel to an organ called the thymus and mature there. B cells and T cells perform different roles. When activated, B cells acquire the ability to make antibodies that attack foreign substances. In contrast, T cells called “killer” T cells sense the presence of infected cells and do away with them directly. Other T cells called “helper” and “suppressor” T cells, assist killer T cells and also help to keep the immune response under control. Once activated (for example, by macrophage-produced cytokines), helper T cells produce immune substances that tell B cells to produce antibodies. T helper cells come in two varieties: TH1 and TH2. Most healthy people have more TH1 cells than TH2 cells, whereas this balance is often reversed in severely injured patients.
- TH1 cells produce the cytokine IFN-γ, which activates macrophages in the classical pathway.
- TH2 cells secrete IL-4, IL-5, and IL-13, which recruit and activate eosinophils and are responsible for the alternative pathway of macrophage activation.
- TH17 cells secrete IL-17 and other cytokines that induce the secretion of chemokines responsible for recruiting neutrophils and monocytes into the reaction.
Lymphocytes and macrophages interact in a bidirectional way, and these interactions play an important role in propagating chronic inflammation. Macrophages display antigens to T cells, express membrane molecules (called costimulators), and produce cytokines (IL-12 and others) that stimulate T cell responses Activated T lymphocytes, in turn, produce cytokines, described earlier, which recruit and activate macrophages and thus promote more antigen presentation and cytokine secretion. The result is a cycle of cellular reactions that fuel and sustain chronic inflammation. In some strong and prolonged inflammatory reactions, the accumulation of lymphocytes, antigen-presenting cells, and plasma cells may assume the morphologic features of lymphoid organs, and akin to lymph nodes, may even contain well-formed germinal centers. This pattern of lymphoid organogenesis is often seen in the synovium of patients with long-standing rheumatoid arthritis and the thyroid of patients with autoimmune thyroiditis.
Eosinophils are characteristically found in inflammatory sites around parasitic infections and as part of immune reactions mediated by IgE, typically associated with allergies. Their recruitment is driven by adhesion molecules similar to those used by neutrophils, and by specific chemokines (e.g., eotaxin) derived from leukocytes and epithelial cells. Eosinophil granules contain major basic protein, a highly charged cationic protein that is toxic to parasites but also causes epithelial cell necrosis. Mast cells are sentinel cells widely distributed in connective tissues throughout the body, and they can participate in both acute and chronic inflammatory responses. In atopic persons (those prone to allergic reactions), mast cells are “armed” with IgE antibody specific for certain environmental antigens. When these antigens are subsequently encountered, the IgE-coated mast cells are triggered to release histamines and AA metabolites that elicit the early vascular changes of acute inflammation. IgE armed mast cells are central players in allergic reactions, including anaphylactic shock . Mast cells can also elaborate cytokines such as TNF and chemokines and may play a beneficial role in combating some infections. An important final point: Although the presence of neutrophils is the hallmark of acute inflammation, many forms of chronic inflammation may continue to show extensive neutrophilic infiltrates, as a result of either persistent microbes or necrotic cells, or mediators elaborated by macrophages. Such inflammatory lesions are sometimes called “acute on chronic”—for example, in inflammation of bones (osteomyelitis).
For more notes on Medical Science click on the link below: