Sjögren's autoimmunity: how perturbation of recognition in endomembrane traffic may provoke pathological recognition at the cell surface
✍ Scribed by Austin K. Mircheff; J. Peter Gierow; Tao Yang; Jian Zhang; Richard L. Wood; Ana Maria Azzarolo; Dwight W. Warren; Hongtao Zeng; Zhijun Guo; Harvey R. Kaslow; Sarah F. Hamm-Alvarez; Curtis T. Okamoto; Michael Bachmann
- Publisher
- John Wiley and Sons
- Year
- 1998
- Tongue
- English
- Weight
- 207 KB
- Volume
- 11
- Category
- Article
- ISSN
- 0952-3499
No coin nor oath required. For personal study only.
✦ Synopsis
CD4 T cell antigen recognition requires presentation by major histocompatibility complex Class II molecules (MHC II). B cell surface immunoglobulins recognize antigens independently of MHC II, but activation typically requires
CD4 cell cytokines as accessory signals. Plasma membrane-endomembrane traffic in lacrimal gland acinar cells, targets of autoimmune activity in Sjo ¨gren's syndrome, may satisfy both requirements. The Golgi protein galactosyltransferase and the lysosomal proteins cathepsin B and cathepsin D appear at the plasma membranes during sustained secretomotor stimulation. The RNA transcription termination factor La, a frequent target of Sjo ¨gren's autoantibodies, appears in the acinar cell cytoplasm and plasma membranes during viral infection and during in vitro exposure to cytokines. MHC II cycle through endomembrane compartments which contain La, galactosyltransferase, cathepsin B and cathepsin D and which are sites of proteolysis. This traffic may permit trilateral interactions in which B cells recognize autoantigens at the surface membranes, CD4 T cells recognize peptides presented by MHC II, B cells provide accessory signals to CD4 T cells, and CD4 T cells provide cytokines that activate B cells. Acinar cells stimulate lymphocyte proliferation in autologous mixed cell reactions, confirming that they are capable of provoking autoimmune responses.