gamma delta cells are attractive candidates for mediators of autoimmun
e disease. They can expand in germ-free mice, probably through recogni
tion of autoantigens, and gamma delta-cell-deficient mice, unlike mice
deficient in alpha beta T cells or B cells, show no severe defects in
the immune response to foreign antigen challenge. A capacity of gamma
delta cells to effect or regulate tissue damage is also plausible, gi
ven their ready localization to tissues, and their myriad of effector
functions. Added to this, attempts to reconstruct the physiological co
urse of autoimmune diseases with only autoreactive alpha beta T cells
seem invariably to fall short for lack of other unidentified players.
gamma delta cells and their putative ligands have been linked to autoi
mmune conditions, and recent experiments confirm that gamma delta cell
s play a significant role in autoimmune disease in vivo.