Limits...
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.

Show MeSH

Related in: MedlinePlus

Effect of NK cell deletion on passive EAE in β2m−/− mice. After activation with MOG35-55 for 3 d, ZB-1 line cells (107) were intravenously  transferred into β2m−/− 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.
© Copyright Policy
Related In: Results  -  Collection


getmorefigures.php?uid=PMC2199138&req=5

Figure 7: Effect of NK cell deletion on passive EAE in β2m−/− mice. After activation with MOG35-55 for 3 d, ZB-1 line cells (107) were intravenously transferred into β2m−/− 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: Using the same line cells, we next induced EAE in β2m−/− mice. To ensure the induction of disease, 107 cells were transferred to the mutant strain. The first sign of EAE was on days 16–17 after transfer in control mice (β2m−/− nonpretreated or pretreated with control mAb). Although the clinical course was variable, none of the mice died of EAE in the observation period 50 d after cell transfer (Fig. 7 A). In contrast, NK cell–deleted β2m−/− mice developed earlier onset of hyperacute EAE and all the mice died within 1 wk after onset (Fig. 7 B) proving that the regulatory role of NK cells in passive EAE can be independent of NK–T cells or CD8+ T cells.


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 β2m−/− mice. After activation with MOG35-55 for 3 d, ZB-1 line cells (107) were intravenously  transferred into β2m−/− 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.
© Copyright Policy
Related In: Results  -  Collection

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

Figure 7: Effect of NK cell deletion on passive EAE in β2m−/− mice. After activation with MOG35-55 for 3 d, ZB-1 line cells (107) were intravenously transferred into β2m−/− 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: Using the same line cells, we next induced EAE in β2m−/− mice. To ensure the induction of disease, 107 cells were transferred to the mutant strain. The first sign of EAE was on days 16–17 after transfer in control mice (β2m−/− nonpretreated or pretreated with control mAb). Although the clinical course was variable, none of the mice died of EAE in the observation period 50 d after cell transfer (Fig. 7 A). In contrast, NK cell–deleted β2m−/− mice developed earlier onset of hyperacute EAE and all the mice died within 1 wk after onset (Fig. 7 B) proving that the regulatory role of NK cells in passive EAE can be independent of NK–T cells or CD8+ T cells.

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