Immunohistochemical analysis of lymphoid and macrophage cell subsets and their immunologic activation markers in temporal arteritis. Influence of corticosteroid treatment.
To determine the phenotype of infiltrating mononuclear cells in patients with temporal arteritis (TA), we performed immunohistochemical studies on temporal artery biopsy specimens from 24 patients with biopsy-proven TA. Interdigitating reticulum cells (IRC) were observed in 41% of the patients; disease duration was significantly shorter in these patients than in patients lacking IRC (mean 1.5 months versus 3.8 months). Infiltrating cells consisted predominantly of HLA-DR-expressing macrophages and T lymphocytes, especially of the CD4 subset. There were few B cells and no K cells. No relationship between cellular distribution and disease duration or treatment was found. Interleukin-2 receptor expression was observed in 87.5% of biopsy specimens obtained prior to or within the first 4 days of treatment with prednisone, but in only 14% of specimens obtained later. The presence of IRC in patients with TA suggests an autoimmune reaction directed against an antigenic substance that resides in the arterial wall and is presented and processed in situ. DR-expressing macrophages activated by CD4+ T lymphocytes may contribute to arterial damage in TA. Corticosteroids do not modify cellular distribution but induce important functional changes, as demonstrated by the disappearance of interleukin-2 receptor expression in patients treated for more than 4 days.
Cid
M C
MC
Department of Internal Medicine, Hospital Clínico y Provincial, Barcelona, Spain.
Campo
E
E
Ercilla
G
G
Palacin
A
A
Vilaseca
J
J
Villalta
J
J
Ingelmo
M
M
D000911:Antibodies, Monoclonal; D000943:Antigens, Differentiation / Q000032:analysis; D003713:Dendritic Cells / Q000473:pathology; D013700:Giant Cell Arteritis / Q000188:drug therapy / Q000276:immunology / Q000378:metabolism / Q000473:pathology*; D006684:HLA-DR Antigens / Q000032:analysis; D006801:Humans; D007150:Immunohistochemistry; D007694:Killer Cells, Natural / Q000473:pathology; D008214:Lymphocytes / Q000145:classification / Q000276:immunology / Q000473:pathology*; D008264:Macrophages / Q000276:immunology / Q000473:pathology*; D009113:Muramidase / Q000032:analysis; D011241:Prednisone / Q000627:therapeutic use*; D015375:Receptors, Interleukin-2 / Q000032:analysis; D009418:S100 Proteins / Q000032:analysis; D013699:Temporal Arteries / Q000473:pathology*
D000911:Antibodies, Monoclonal; D000943:Antigens, Differentiation; D006684:HLA-DR Antigens; D015375:Receptors, Interleukin-2; D009418:S100 Proteins; D009113:Muramidase; D011241:Prednisone