Significance

Even if autoreactivity is a transient physiological state in activated normal peripheral T cells, it could make a substantial contribution to clonal expansion and amplification of immune functions. The functional capabilities of autoreactive T cells have been investigated in a number of laboratories. In general, they have been found to provide the same physiologi cal signals as other CD4 T cells. Both lymphotoxin and interferon y (IFNy) producing autoreactive T,,I and IL-4 secreting autoreactive TH2 have been isolated. Examination of the helper functions of both murine and human autoreactive T cell clones has clearly demonstrated that these T cells can provide helper signals that serve to enhance B cell proliferation and maturation of immunoglobulin secretion. Autoreactive T cells that secrete other lymphokines, including lymphotoxin and IFNy, may play an important role in inflammatory responses. In vivo injection of autoreactive T cell clones in footpads of syngeneic mice induced delayed-type hypersensitivity reactions in the dermis. In addition, autoreactive T cell clones with cytotoxic activity (lymphotoxin secretion) induced skin lesions with infiltration of lymphocytes in the epidermis and epidermal cell damage.

As suggested by these observations, autoreactive T cells could play a role in both normal and pathological immune responses. Their contributions in vivo cannot be fully evaluated until the mechanisms that must limit their expansion have been identified. The available evidence suggests that autoreactive T cells derive from mature antigen-dependent precursors which have undergone a physiological transition that restores their thymic selected ability to respond to self. This could be a normal reversible transition which frequently accompanies specific T cell activation. In this case any mechanism that returns T cells to a resting state would eliminate autoreactive expansion until another cycle of stimulation is induced by a specific foreign antigen. Under conditions of chronic stimulation, when high levels of MHC class II are continuously expressed and/or immune regulation is abnormal, autoreactive T cells could give rise to severe and persistent inflammation.

See also: Thymic epithelium: potential role in regulatory T cell tolerance; Effector lymphocytes; H2 class II; T lymphocyte clonal expansion; T lymphocytes.

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