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Initiation and development of experimental autoimmune neuritis in Lewis rats is independent of the cytotoxic capacity of NKR‐P1A+ cells
Author(s) -
Yu Shuo,
Zhu Yu,
Chen Zhiguo,
Alheim Mats,
Ljungberg Anna,
Zhu Jie
Publication year - 2002
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/jnr.10174
Subject(s) - cytotoxic t cell , medicine , immunology , monoclonal antibody , myelin , antibody , in vitro , biology , endocrinology , central nervous system , biochemistry
Natural killer (NK) cells are implicated in T cell‐mediated autoimmune diseases. Experimental autoimmune neuritis (EAN) is a CD4+ T cell‐mediated animal model of the Guillain‐Barré syndrome in human. The role of NK cells in the initiation and development of EAN remains unclear. In the present study, we demonstrate that anti‐NKR‐P1A monoclonal antibody (mAb) treatment in vivo did not affect the initiation and development of clinical EAN in Lewis rats induced by immunization with peripheral nerve myelin P0 protein peptide 180–199 and Freund's complete adjuvant, as well as the proportion of NKR‐P1A+ cells (including NK cells and NKT cells) in the spleen. Furthermore, inflammatory cell infiltrations and demyelination in the peripheral nervous system (PNS) and in vitro P0 peptide 180–199‐specific splenocyte proliferation were not different in anti‐NKR‐P1A mAb‐treated rats compared to the control antibody‐treated rats. The cytotoxic activity of NKR‐P1A+ cells, determined by NK cell‐sensitive K562 cells as target cells, decreased markedly in anti‐NKR‐P1A mAb‐treated rats, suggesting that decrease of the cytotoxic activities of NKR‐P1A+ cells is not sufficient to alter clinical EAN, although NKR‐P1A+ cells may participate in the pathogenesis of T cell‐mediated autoimmune diseases, such as EAN, by the mechanisms that involve the release of cytokines. © 2002 Wiley‐Liss, Inc.