Presentation to T lymphocytes

Immunoglobulins (Igs) can activate the complement system, which amplifies the immune response by enhancing chemotaxis, phagocytosis, and release of lymphokines by mononuclear cells that are then presented to T lymphocytes. The processed antigen is recognized by the major histocompatibility complex proteins on the lymphocyte surface, resulting in activation of T and B cells. 

Corticosteroids have antiinflammatory and immunosuppressive properties. They interfere with antigen presentation to T lymphocytes, inhibit prostaglandin and leukotriene synthesis, and inhibit neutrophil and monocyte superoxide radical generation. 

Family history of RA. Genetic studies demonstrate a strong correlation between RA and the presence of major histocompatibility complex class II human leukocyte antigens (HLA), specifically HLA-DR1 and HLA-DR4.4,5 HLA is a molecule associated with the presentation of antigens to T lymphocytes. 

Classically, these receptors have also been divided into three groups. The first of these, the Hj receptors, were described by Schild in 1966. The Hj receptors were discovered in 1972 by Black et al. The Hj receptor subtype was described by Arrang in 1983. The Hj receptor is found in the smooth muscle of the intestines, bronchi, and blood vessels and is blocked by the classical antihistamines. The Hj receptor, present in gastric parietal cells, in guinea pig atria, and in the uterus, does not react to H, blockers but only to specific Hj antagonists. Hj receptors also appear to be involved in the immunoregulatory system and may be present in T lymphocytes, basophil cells, and mast cells. Hj receptors are found predominantly in brain but are also localized in stomach, lung, and cardiac tissue. 

Rituximab is a chimeric monoclonal antibody that targets CD20 lymphocytes (see Chapter 55). This depletion takes place through cell-mediated and complement-dependent cytotoxicity and stimulation of cell apoptosis. Depletion of lymphocytes reduces inflammation by decreasing the presentation of antigens to T lymphocytes and inhibiting the secretion of proinflammatory cytokines. Rituximab rapidly depletes peripheral cells although this depletion neither correlates with efficacy nor with toxicity. 

The major histocompatibility complex (MHC) is part of the system that codes for molecules important in immune recognition, including graft rejection. MHC class I and II molecules present antigen fragments to T-lymphocytes. For example, class I molecules bind viral proteins and present them to the CD8+ T cells. Exogenous antigens such as proteins taken into the cell by endocytosis are processed within the cell and presented to CD4+ cells. 

Benichou G. 1998. The presentation of self and allogeneic MHC peptides to T lymphocytes. Hum Immunol. 59 540-561. 

Figure 32.9. Schematic representation of Type I hypersensitivity. Induction Resident respiratory tract dendritic cells (DC) take and process antigen, mature, migrate to the draining lymph nodes, and present antigen to T lymphocytes. Activated T-lymphocytes, in turn, activate B-cell differentiation into antibody-producing plasma cells. IL-4 promotes Ig isotype class switching from IgM to IgE and promotes mast cell development. IgE is associated with mast cells. Elicitation Allergen crosslinks the mast-cell-bound IgE, thereby causing the release of preformed mediators and cytokines. (See Table 32.7.) Inflammation and bronchoconstriction occur.

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