OBJECTIVE: To understand mechanisms regulating the cellular composition of the inflammatory infiltrate in giant cell arteritis (GCA) and to explore whether B lymphocytes, such as neoplastic B cells in chronic lymphocytic leukemia (CLL), can infiltrate the inflamed arterial wall of GCA. METHODS: A Mayo Clinic database search was conducted to identify patients that developed GCA after the onset of CLL between 1950 and 1994. Inflammatory infiltrates were analyzed immunohistochemically for T cells, B cells, and plasma cells. RESULTS: Five patients with CLL were identified who subsequently developed clinical findings suggestive of GCA. Three of the 5 patients had biopsy proven disease, presented with typical clinical and histomorphological features of GCA, and responded promptly to corticosteroid treatment. Leukemic B cells known for their ability to diffusely seed organs were absent in the inflammatory lesions in the temporal artery. Plasma cells that contribute to the vasculitic infiltrate in patients without CLL were markedly reduced in the GCA lesions of patients with CLL. Two other patients had symptoms suggestive of GCA. Their temporal artery specimens were remarkable for small adventitial lymphocytic infiltrates but lacked typical panarteritis. CONCLUSION: The inflammatory infiltrate of GCA is tightly regulated, and cell accumulation in the granulomas is an active, not a passive, mechanism. The inflammatory pathway in GCA is focused on T cells and macrophages and excludes B cells.
OBJECTIVE: To understand mechanisms regulating the cellular composition of the inflammatory infiltrate in giant cell arteritis (GCA) and to explore whether B lymphocytes, such as neoplastic B cells in chronic lymphocytic leukemia (CLL), can infiltrate the inflamed arterial wall of GCA. METHODS: A Mayo Clinic database search was conducted to identify patients that developed GCA after the onset of CLL between 1950 and 1994. Inflammatory infiltrates were analyzed immunohistochemically for T cells, B cells, and plasma cells. RESULTS: Five patients with CLL were identified who subsequently developed clinical findings suggestive of GCA. Three of the 5 patients had biopsy proven disease, presented with typical clinical and histomorphological features of GCA, and responded promptly to corticosteroid treatment. Leukemic B cells known for their ability to diffusely seed organs were absent in the inflammatory lesions in the temporal artery. Plasma cells that contribute to the vasculitic infiltrate in patients without CLL were markedly reduced in the GCA lesions of patients with CLL. Two other patients had symptoms suggestive of GCA. Their temporal artery specimens were remarkable for small adventitial lymphocytic infiltrates but lacked typical panarteritis. CONCLUSION: The inflammatory infiltrate of GCA is tightly regulated, and cell accumulation in the granulomas is an active, not a passive, mechanism. The inflammatory pathway in GCA is focused on T cells and macrophages and excludes B cells.
Authors: M Lopez-Hoyos; M J Bartolome-Pacheco; R Blanco; V Rodriguez-Valverde; V M Martinez-Taboada Journal: Ann Rheum Dis Date: 2004-01 Impact factor: 19.103
Authors: Jacoba C Graver; Annemieke M H Boots; Erlin A Haacke; Arjan Diepstra; Elisabeth Brouwer; Maria Sandovici Journal: Front Immunol Date: 2019-01-29 Impact factor: 7.561