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Regulation of experimental autoimmune encephalomyelitis by natural killer (NK) cells.

Zhang B, Yamamura T, Kondo T, Fujiwara M, Tabira T - J. Exp. Med. (1997)

Bottom Line: The disease enhancement was associated with augmentation of T cell proliferation and production of Th1 cytokines in response to MOG35-55.We further showed that NK cells inhibit T cell proliferation triggered by antigen or cytokine stimulation.Taken together, we conclude that NK cells are an important regulator for EAE in both induction and effector phases.

View Article: PubMed Central - PubMed

Affiliation: Department of Demyelinating Disease and Aging, National Institute of Neuroscience, Tokyo, Japan.

ABSTRACT
In this report, we establish a regulatory role of natural killer (NK) cells in experimental autoimmune encephalomyelitis (EAE), a prototype T helper cell type 1 (Th1)-mediated disease. Active sensitization of C57BL/6 (B6) mice with the myelin oligodendrocyte glycoprotein (MOG)35-55 peptide induces a mild form of monophasic EAE. When mice were deprived of NK cells by antibody treatment before immunization, they developed a more serious form of EAE associated with relapse. Aggravation of EAE by NK cell deletion was also seen in beta 2-microglobulin-/- (beta 2m-/-) mice, indicating that NK cells can play a regulatory role in a manner independent of CD8+ T cells or NK1.1+ T cells (NK-T cells). The disease enhancement was associated with augmentation of T cell proliferation and production of Th1 cytokines in response to MOG35-55. EAE passively induced by the MOG35-55-specific T cell line was also enhanced by NK cell deletion in B6, beta 2m-/-, and recombination activation gene 2 (RAG-2)-/- mice, indicating that the regulation by NK cells can be independent of T, B, or NK-T cells. We further showed that NK cells inhibit T cell proliferation triggered by antigen or cytokine stimulation. Taken together, we conclude that NK cells are an important regulator for EAE in both induction and effector phases.

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Effect of NK cell deletion on passive EAE in wild-type B6  mice. After activation with MOG35-55 for 3 d, ZB-1 line cells (3 × 106)  were intravenously transferred into wild-type B6 mice pretreated on day  −1 with control mAb (A) or with anti-NK1.1 mAb (B). The mice had  been x irradiated (450 rad) shortly before cell transfer, and received 500  ng of PT immediately after cell transfer.
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Figure 6: Effect of NK cell deletion on passive EAE in wild-type B6 mice. After activation with MOG35-55 for 3 d, ZB-1 line cells (3 × 106) were intravenously transferred into wild-type B6 mice pretreated on day −1 with control mAb (A) or with anti-NK1.1 mAb (B). The mice had been x irradiated (450 rad) shortly before cell transfer, and received 500 ng of PT immediately after cell transfer.

Mentions: To learn whether NK cells have a regulatory effect on the effector phase of EAE as well, we studied the effect of NK cell deletion on EAE passively induced with the ZB-1 line. The line T cells were CD4+ and specifically recognized MOG35-55 in the context of MHC class II (data not shown). Adoptive transfer of 3 × 106 of the line cells did not induce EAE in the B6 mice pretreated with PBS or with control mAb. In contrast, mice pretreated with anti-NK1.1 mAb developed EAE on days 8–10 after cell transfer (Fig. 6 B). The clinical sign of EAE was relatively mild, but persisted for longer than 2 wk. The result proved that NK1.1+ cells inhibit the effector phase of EAE.


Regulation of experimental autoimmune encephalomyelitis by natural killer (NK) cells.

Zhang B, Yamamura T, Kondo T, Fujiwara M, Tabira T - J. Exp. Med. (1997)

Effect of NK cell deletion on passive EAE in wild-type B6  mice. After activation with MOG35-55 for 3 d, ZB-1 line cells (3 × 106)  were intravenously transferred into wild-type B6 mice pretreated on day  −1 with control mAb (A) or with anti-NK1.1 mAb (B). The mice had  been x irradiated (450 rad) shortly before cell transfer, and received 500  ng of PT immediately after cell transfer.
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Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC2199138&req=5

Figure 6: Effect of NK cell deletion on passive EAE in wild-type B6 mice. After activation with MOG35-55 for 3 d, ZB-1 line cells (3 × 106) were intravenously transferred into wild-type B6 mice pretreated on day −1 with control mAb (A) or with anti-NK1.1 mAb (B). The mice had been x irradiated (450 rad) shortly before cell transfer, and received 500 ng of PT immediately after cell transfer.
Mentions: To learn whether NK cells have a regulatory effect on the effector phase of EAE as well, we studied the effect of NK cell deletion on EAE passively induced with the ZB-1 line. The line T cells were CD4+ and specifically recognized MOG35-55 in the context of MHC class II (data not shown). Adoptive transfer of 3 × 106 of the line cells did not induce EAE in the B6 mice pretreated with PBS or with control mAb. In contrast, mice pretreated with anti-NK1.1 mAb developed EAE on days 8–10 after cell transfer (Fig. 6 B). The clinical sign of EAE was relatively mild, but persisted for longer than 2 wk. The result proved that NK1.1+ cells inhibit the effector phase of EAE.

Bottom Line: The disease enhancement was associated with augmentation of T cell proliferation and production of Th1 cytokines in response to MOG35-55.We further showed that NK cells inhibit T cell proliferation triggered by antigen or cytokine stimulation.Taken together, we conclude that NK cells are an important regulator for EAE in both induction and effector phases.

View Article: PubMed Central - PubMed

Affiliation: Department of Demyelinating Disease and Aging, National Institute of Neuroscience, Tokyo, Japan.

ABSTRACT
In this report, we establish a regulatory role of natural killer (NK) cells in experimental autoimmune encephalomyelitis (EAE), a prototype T helper cell type 1 (Th1)-mediated disease. Active sensitization of C57BL/6 (B6) mice with the myelin oligodendrocyte glycoprotein (MOG)35-55 peptide induces a mild form of monophasic EAE. When mice were deprived of NK cells by antibody treatment before immunization, they developed a more serious form of EAE associated with relapse. Aggravation of EAE by NK cell deletion was also seen in beta 2-microglobulin-/- (beta 2m-/-) mice, indicating that NK cells can play a regulatory role in a manner independent of CD8+ T cells or NK1.1+ T cells (NK-T cells). The disease enhancement was associated with augmentation of T cell proliferation and production of Th1 cytokines in response to MOG35-55. EAE passively induced by the MOG35-55-specific T cell line was also enhanced by NK cell deletion in B6, beta 2m-/-, and recombination activation gene 2 (RAG-2)-/- mice, indicating that the regulation by NK cells can be independent of T, B, or NK-T cells. We further showed that NK cells inhibit T cell proliferation triggered by antigen or cytokine stimulation. Taken together, we conclude that NK cells are an important regulator for EAE in both induction and effector phases.

Show MeSH
Related in: MedlinePlus