Distinctive distribution of lymphocytes in unruptured and previously untreated brain arteriovenous malformation

Yi Guo; Tarik Tihan; Helen Kim; Christopher Hess; Michael T Lawton; William L Young; Yuanli Zhao; Hua Su

doi:10.4103/2347-8659.143674

Distinctive distribution of lymphocytes in unruptured and previously untreated brain arteriovenous malformation

Neuroimmunol Neuroinflamm. 2014;1(3):147-152. doi: 10.4103/2347-8659.143674.

Authors

Yi Guo¹, Tarik Tihan², Helen Kim³, Christopher Hess⁴, Michael T Lawton⁵, William L Young⁶, Yuanli Zhao⁷, Hua Su³

Affiliations

¹ Center for Cerebrovascular Research, Department of Anesthesia and Perioperative Care, University of California, San Francisco, San Francisco, CA 94110, USA ; Department of Neurosurgery, Affiliated Hospital of Hebei University, Baoding 071000 China.
² Department of Pathology, University of California, San Francisco, San Francisco, CA 94110, USA.
³ Center for Cerebrovascular Research, Department of Anesthesia and Perioperative Care, University of California, San Francisco, San Francisco, CA 94110, USA.
⁴ Department of Radiology and Biomedical Imaging, University of California, San Francisco, San Francisco, CA 94110, USA.
⁵ Department of Neurological Surgery, University of California, San Francisco, San Francisco, CA 94110, USA.
⁶ Center for Cerebrovascular Research, Department of Anesthesia and Perioperative Care, University of California, San Francisco, San Francisco, CA 94110, USA ; Department of Neurological Surgery, University of California, San Francisco, San Francisco, CA 94110, USA ; Department of Neurology, University of California, San Francisco, San Francisco, CA 94110, USA.
⁷ Department of Neurosurgery, Beijing Tiantan Hospital, Capital Medical University, Beijing 410011, China.

Abstract

Aim: To test the hypothesis that lymphocyte infiltration in brain arteriovenous malformation (bAVM) is not associated with iron deposition (indicator of microhemorrhage).

Methods: Sections of unruptured, previously untreated bAVM specimens (n=19) were stained immunohistochemically for T-lymphocytes (CD3⁺), B-lymphocytes (CD20⁺), plasma cells (CD138⁺) and macrophages (CD68⁺). Iron deposition was assessed by hematoxylin and eosin and Prussian blue stains. Superficial temporal arteries (STA) were used as control.

Results: Both T lymphocytes and macrophages were present in unruptured, previously untreated bAVM specimens, whereas few B cells and plasma cells were detected. Iron deposition was detected in 8 specimens (42%; 95% confidence interval =20-67%). The samples with iron deposition tended to have more macrophages than those without (666±313 vs 478±174 cells/mm²; P=0.11). T-cells were clustered on the luminal side of the endothelial surface, on the vessel-wall, and in the perivascular regions. There was no correlation between T lymphocyte load and iron deposition (P=0.88). No macrophages and lymphocytes were detected in STA controls.

Conclusions: T-lymphocytes were present in bAVM specimens. Unlike macrophages, the load and location of T-lymphocytes were not associated with iron deposition, suggesting the possibility of an independent cell-mediated immunological mechanism in bAVM pathogenesis.

Keywords: B-lymphocyte; T-lymphocyte; human brain arteriovenous malformation; inflammatory cells; microhemorrhage.

Abstract

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