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(Journal of Leukocyte Biology. 2002;72:1117-1121.)
© 2002 by Society for Leukocyte Biology

Diminution of experimental autoimmune uveoretinitis (EAU) in mice depleted of NK cells

Nobuyoshi Kitaichi^*, Satoshi Kotake, Taiki Morohashi, Kazunori Onoé, Shigeaki Ohno and Andrew W. Taylor^*

^* Schepens Eye Research Institute and the Department of Ophthalmology, Harvard Medical School, Boston, Massachusetts; and
Department of Ophthalmology and Visual Sciences, Hokkaido University Graduate School of Medicine, and
Division of Immunobiology, Institute for Genetic Medicine, Hokkaido University, Sapporo, Japan

Correspondence: Andrew W. Taylor, Ph.D., Schepens Eye Research Institute, 20 Staniford Street, Boston, MA 02114. E-mail: awtaylor{at}vision.eri.harvard.edu

To evaluate the potential role of NK1.1 (CD161c) cells in autoimmune uveoretinitis, we treated experimental autoimmune uveoretinitis (EAU)-susceptible mice with anti-CD161c antibodies (PK136) to deplete natural killer (NK) cells. Injection of anti-CD161c antibodies deleted NK cells from the peripheral blood of EAU-susceptible mice. The T cell proliferative response against the ocular autoantigen K2 was not suppressed in mice treated with anti-CD161c antibody when compared with T cells from control mice. Although mice treated with anti-CD161c developed EAU, the clinical severity on days 17 and 19 after induction of EAU was significantly mild in anti-CD161c-treated mice compared with control mice. In addition, the histopathological severity of EAU was significantly milder in mice treated with anti-CD161c antibodies than controls 21 days after induction of EAU. Our results indicate that the severity of EAU is augmented by NK1.1⁺ NK cells.

Key Words: NK1.1 • anti-CD161c • mouse

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