Immunological studies in giant cell arteritis

Abstract

The results of investigations on the humoral immunological mechanisms are conflicting in giant cell arteritis (GCA) and have not been able to explain the pathological findings in the inflamed arterial wall. Altogether, immunological studies suggest that a cell-mediated immune reaction, possibly against an autologous antigen, occurs locally in the arteritic lesions of GCA. The excellent effect of treatment with glucocorticosteroids on the inflammation in GCA can also be explained by this model. The glucocorticosteroids inhibit the synthesis of interleukin-1 (IL-1) by the macrophages and suppress the IL-2 production from the T cells (Palacios, 1982). The observed HLA-DR expression in the arterial wall can be accounted for by the sum of macrophages and activated T cells, the macrophages being the most probable antigen-presenting cells. The interdigitating reticulum cells observed in some of the GCA patients may also be involved in antigen presentation. What the antigen(s) may be is, however, still unknown, as are the factors initiating the inflammatory process. It has recently been possible to extract T lymphocytes from the inflamed tissue and to culture these cells in vitro. After culture, it is possible to study the gene for the T-cell receptor, and probably even the antigenic specificity of the T cells. I hope that this approach may lead to a better understanding of the pathogenic mechanisms in GCA.