Cookies on this website

We use cookies to ensure that we give you the best experience on our website. If you click 'Accept all cookies' we'll assume that you are happy to receive all cookies and you won't see this message again. If you click 'Reject all non-essential cookies' only necessary cookies providing core functionality such as security, network management, and accessibility will be enabled. Click 'Find out more' for information on how to change your cookie settings.

Wegener's granulomatosis (WG) is an autoimmune disease of as yet unknown etiology. To date it has remained obscure what causes WG or determines disease progression. Case reports suggest that viral infections such as cytomegalovirus (CMV) reactivation may contribute to disease flares. In this study we found a skewing of the phenotype of CMV-specific CD8+tet(ramer)+ T-cells in WG. A marked proportion of these cells displayed a late differentiated "effector memory" T-cell phenotype with decreased expression of CD28 and CD62L, and heterogeneous CD27 expression, features which were also seen in CD8+tet- T-cells in WG, but not in controls. Our results might reflect profound generalized changes in the CD8+ T-cell compartment also affecting virus-specific T-cell responses in WG.

Original publication




Journal article


Cell Immunol

Publication Date





1 - 7


ADP-ribosyl Cyclase, ADP-ribosyl Cyclase 1, Antigens, CD, Antigens, Differentiation, T-Lymphocyte, CD28 Antigens, CD57 Antigens, CD8-Positive T-Lymphocytes, Cell Differentiation, Cytomegalovirus, Cytomegalovirus Infections, Down-Regulation, Female, Granulomatosis with Polyangiitis, HLA-DR Antigens, Humans, Immunosuppressive Agents, L-Selectin, Lectins, C-Type, Male, Membrane Glycoproteins, Phenotype, Tumor Necrosis Factor Receptor Superfamily, Member 7, Up-Regulation