Not MHC-restricted (using mismatched APCs; not blocked by u-CI I, -II, -Qa, and -TL mAbs) Not MHC-restricted (using 02nrr/--deriv/ed cells)

Schild et al (1994) Cell

76: 29 Havran et al (1991) Science 252: 1430 Lewis and Tigelaar, pers. comm.

Heyborne et al (1994) J Immunol 153: 2918

thereby contributing to autoimmune disease. Both these effects may stem from generic interactions of 78 cells with other lymphoid effector cells. However, most evidence suggests that antigen-specific responses cannot be efficiently induced in a|3 T cell-deficient mice, which are therefore highly immunocompromised toward most pathogens. Several non exclusive reasons for this can be considered. 78 Cells may not recognize a sufficient spectrum of foreign antigens. Thus, when TCR(3_/ mice were repeatedly challenged with coccidia, 78 B cell help was induced, but was not obviously directed at the pathogen. Nonetheless, given the reactivity of many 78 cells to mycobacteria, it is difficult to understand how lim ited antigen specificity alone explains the immunodeficiency of TCRa/3_/" mice toward mycobacteria. Alternatively, there may be inherent differences in the ways that a(3 cells and 78 cells respond to antigen, even though 78 cells reportedly can produce essentially all known effector molecules. Third, 78 cells may be unable to interact efficiently and antigen specifically with professional antigen-presenting cells (APCs), and thereby coordinate a protective immune response. This inefficiency may be due to a failure of 78 cells to recognize foreign antigens presented as peptides on MHC molecules possibly compounded by a failure of 78 cells to express the surface and intracellular molecules that facilitate the efficient interaction of a(3 cells and APCs. The latter differences might underlie differences in the susceptibility of 78 cells and a3 cells to selection during development. They may also explain the lack of evidence for 78 cells converting functionally to memory cells in response to foreign antigen.

A significant role for immunoregulation by 78 cells is indicated by reports that 78 cell-deficient mice show exaggerated lymphoid responses, both to pathogens (TCR8 _/~ mice show heightened immuno-pathology), and to self (TCR8~/_ mice on particular genetic backgrounds show increased autoimmune disease). This may again reflect recognition of activated cffector cells, including otp cells, as indicated in several studies (Table 4).

In summary, there is overwhelming evidence that 78 T cells have a distinct set of antigen specificities, facilitating their response to a variety of conditions. An important result of this in the healthy individual may be immunoregulation. In the immunocompromised, a(3 T cell-deficient individual, such as an AIDS (acquired immune deficiency syndrome) patient, 78 T cells may activate other lymphoid effectors, such as B cells, but the targets of this combined action may more commonly be self than the challenging pathogen. Hence 78 cells both contribute to and regulate immune responses to pathogens and to self.

See also: Antibodies, specificity; Antigen-binding site; Bacteria, immunity to; Mucosa-associated lymphoid tissue (MALT); Mycobacteria, infection and immunity; Stress proteins; T cell receptor, <*P; T cell receptor, evolution of; T cell receptor, recognition by; T lymphocyte differentiation.

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