Studies of the function of natural killer-interferon system in patients with Sjögren syndrome.

Minato, Nagahiro; Takeda, Atsushi; Kano, Shogo; Takaku, Fumimaro

doi:10.1172/jci110484

Cited by 41 publications

(11 citation statements)

References 27 publications

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“…The TPA-Con A CM was harvested after a 72-h incubation, and immediately added to the EC cultures for the lymphocyte-EC adhesion assay and endothelial DR expression assay. The interferon (IFN) activity in the TPA-Con A CM was determined by microcytopathic effect inhibition assay using encephalomyocarditis virus and FL cells (human amnion-derived cell line) as described elsewhere (21 Giemsa-stained.…”

Section: Methodsmentioning

confidence: 99%

Mechanisms of lymphocyte adhesion to human vascular endothelial cells in culture. T lymphocyte adhesion to endothelial cells through endothelial HLA-DR antigens induced by gamma interferon.

Masuyama¹,

Minato²,

Kano³

1986

J. Clin. Invest.

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167

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The effects of interferons (IFNs) on lymphocyte adhesion to cultured human vascular endothelial cells (EC) were investigated using an in, vitro assay. Endothelial cells obtained from umbilical vein were first cultured at a low density 'with a conditioned medium (CM) from 12-0-tetra decanoylphorbol 13-acetate-concanavalin A (TPA-Con A) stimulated human peripheral blood lymphocytes (PBL), or with recombinant (r) gamma interferon (IFN-7y) or r alpha interferon (IFN-x), and then were incubated with freshly isolated PBL. Natural IFN-'Y in the TPA-Con A CM and rIFN-7 (12.5-500 U/ml) induced major histocompatibility complex-class II antigens (HLA-DR, HLA-DP, and HLA-DQ) and significant lymphocyte adhesion to the EC, whereas rIFN-a did not, The lymphocyte adhesion to the EC and the expression of DR antigens on the EC were well correlated in terms of both kinetics and the dose-response pattern of rIFNy. When EC expressing I region associated (Ia) antigen were preincubated with monoclonal anti-DR antibody before the addition of lyunjhocytes, the lymphocyte adhesionwas significantly inhibited in both allogeneic and syngeneic combinations, whereas anti-HLA-DP, anti-HLA-DQ, and anti-HLA-ABC antibodies sdid not inhibit the binding at all. Cell fractionation experiments indicated that the majority of lymphocytes adhering to la-expressed EC were Leu-3' T cells, whose binding was again almost completely inhibited by anti-DR antibody. .Moreover, anti-Leu3a, but not anti-Leu-2a, antibody effectively inhibited the. T cell adhesion to the EC. These results strongly suggest that the interaction of the Leu-3(T4) receptor ofT cells with IFN-y-induced DR antigens on EC plays a central role in the selective adhesion of Leu-3' T cell to EC.

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Section: Methodsmentioning

confidence: 99%

Mechanisms of lymphocyte adhesion to human vascular endothelial cells in culture. T lymphocyte adhesion to endothelial cells through endothelial HLA-DR antigens induced by gamma interferon.

Masuyama¹,

Minato²,

Kano³

1986

J. Clin. Invest.

Self Cite

167

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“…HeLa-Ms cell monolayers was done as previously reported (Minato et al, 1982). Briefly, 1 ml of mononuclear cells at a concentration of 5 x lo6 cells/ml in RPMI 1640 medium containing 10% FCS were cultured for 18 h with 1 x lo5 HeLa-Ms cell monolayers in 24-well Linbro multiculture dishes (Flow Laboratories Inc., Rockville, Maryland, U.S.A.).…”

Section: Treatment Of Mononuclear Cells With Hela-ms Cells Treatmentmentioning

confidence: 99%

Natural killer‐interferon system in patients with preleukaemic states

et al. 1984

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The natural killer (NK)-interferon (IFN) system was investigated in patients with preleukaemic states. Endogenous NK cell activity was markedly reduced in all 12 patients studied. No significant correlation was observed between the activity of NK cells and the percentage of blast cells in the peripheral blood or bone marrow. The frequency of large granular lymphocytes (LGL) in lymphocytes of the peripheral blood was not reduced in most patients. The percentage of target binding cells in patients was essentially the same as that in normal controls, and the activity of NK cells from normal donors was not affected by the coexistence of mononuclear cells obtained from the peripheral blood of patients. Furthermore, the alpha-IFN production in response to HeLa cells persistently infected with measles virus was reduced in all patients studied, except for one case with acquired idiopathic sideroblastic anaemia. The augmented activity of NK cells induced by alpha-IFN was variable, but remained at lower levels than the endogenous activity of NK cells in normal controls. These findings suggest that not only the intrinsic defect and reduced number of NK cells but also the dysfunction of the NK-IFN system may be responsible for the reduced activity of NK cells in patients with preleukaemic states.

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“…The origin and character of the factor(s) assumed to be present in sera of patients with HPV-induced anogenital lesions and responsible for specific inhibition of Sk-v cell lysis are as yet unknown. The "target-specificity" of the factor(s) excludes any relationship with a variety of non-specific factors inhibiting NCMC such as prostaglandins (Bankhurst, 1982), NK-specific antibodies (Goto et al, 1980), immune complexes (Silverman and Cathcart, 1980) or deficiency in production of NK-cell-augmenting factors (Minato et al, 1982). Serum factors inhibitory for NK-cell activity, apparently unrelated to immune complexes or anti-lymphocyte antibodies, have previously been detected in autoimmune disorders (Miyasaka et al, 1983) and in cancer patients (Holmes et al, 1986).…”

Section: Discussionmentioning

confidence: 99%

Abrogated NK‐cell lysis of human papillomavirus (HPV)‐16‐bearing keratinocytes in patients with pre‐cancerous and cancerous HPV‐induced anogenital lesions

Malejczyk¹,

Majewski²,

Jabłońska³

et al. 1989

Intl Journal of Cancer

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Natural-cell-mediated cytotoxicity against K-562 erythroleukemic cells and human papillomavirus (HPV)-16 harboring Sk-v keratinocytes was tested in 38 age- and sex-matched healthy volunteers and in patients with HPV-induced benign and malignant anogenital lesions: 9 persons with HPV-16-induced bowenoid papulosis (BP), 8 with anogenital carcinomas (5 with HPV-16- or 33-associated squamous-cell carcinomas of Bowen's type and 3 with HPV-6-associated Buschke-Loewenstein verrucous carcinomas) and 12 with HPV-6-induced condylomata acuminata. Both K-562 and Sk-v cells were killed by a non-adherent CD16+ subset of PBMC as revealed by cell fractionation on the basis of their adherence to plastic and by treatment with Leu-IIb monoclonal antibody (MAb) and complement. "Cold" target competitive assays demonstrated that both cell types inhibited lysis of labelled Sk-v cells. In patients with BP and anogenital carcinomas induced by HPV-16 or 33, there was a significant (at least at p less than 0.01) decrease of Sk-v cell lysis as compared with the healthy control group. Anti-K-562 activity was not affected. In patients with anogenital carcinomas the degree of Sk-v lysis was decreased in proportion to the duration of lesions (correlation coefficient-r = -0.79). Neither anti-K-562 nor anti-Sk-v cytotoxicities were significantly affected in patients with condylomata and with HPV-6 associated verrucous carcinomas. Short-term (3 hr) pre-incubation of normal PBMC with sera from patients with BP and HPV-16-associated anogenital carcinomas resulted in significant inhibition of their ability to lyse Sk-v cells. Lysis of K-562 cells remained unaffected. In patients with carcinomas, the suppressive effect of sera was associated with a lowering of the ability of their PBMC to lyse Sk-v cells (r = -0.79). In patients with longer tumor persistence, the suppressive effect of serum was proportionally higher (r = 0.86).

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Studies of the function of natural killer-interferon system in patients with Sjögren syndrome.

Cited by 41 publications

References 27 publications

Mechanisms of lymphocyte adhesion to human vascular endothelial cells in culture. T lymphocyte adhesion to endothelial cells through endothelial HLA-DR antigens induced by gamma interferon.

Mechanisms of lymphocyte adhesion to human vascular endothelial cells in culture. T lymphocyte adhesion to endothelial cells through endothelial HLA-DR antigens induced by gamma interferon.

Natural killer‐interferon system in patients with preleukaemic states

Abrogated NK‐cell lysis of human papillomavirus (HPV)‐16‐bearing keratinocytes in patients with pre‐cancerous and cancerous HPV‐induced anogenital lesions

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