Inhibition of Antibody-Dependent Cellular Cytotoxicity and Natural Cytotoxicity by Retinoic Acid

Eremin, O.; Ashby, J.; Rhodes, J.

doi:10.1159/000233581

Cited by 15 publications

(9 citation statements)

References 15 publications

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“…These results are in agreement with the report of McKerrow et al of depressed NK cell activity in acne patients treated with 1.0 mg/kg per day isotretinoin 17 . Two other groups have previously shown that treatment of lymphocytes with retinoic acid in vitro strongly inhibits NK activity, acting antagonistically to the immunostimulatory effects of IFN 18 , 19 . In contrast, Pigatto et al showed that patients with acne or psoriasis treated with etretinate 1.0 mg/kg per day had enhanced NK activity, while an isotretinoin‐treated group did not show any significant changes, both in vivo and in vitro 20 .…”

Section: Discussionsupporting

confidence: 93%

Effect of isotretinoin therapy on natural killer cell activity in patients with xeroderma pigmentosum

Anolik

Giovanna

Gaspari

1998

British Journal of Dermatology

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Xeroderma pigmentosum (XP) is a rare autosomal recessive disorder characterized by sun sensitivity, defective DNA repair, markedly increased susceptibility to skin cancer, and a variety of immunological defects, including defective natural killer (NK) cell activity. Retinoid therapy has been demonstrated to protect effectively against the development of skin cancers in patients with XP, although its mechanism of action is unknown. We describe a series of eight XP patients, six of whom were given oral isotretinoin. The NK cell activity was not affected by low-dose isotretinoin, i.e. 0.5 mg/kg per day. However, higher doses of isotretinoin, e.g. 1.0 mg/kg per day, produced a significant decrease in NK cell function, at the same time as producing a reduction in the frequency of development of skin cancers. Retinoid therapy may have a skin cancer preventing effect by enhancing other immune effector mechanisms or via epithelial cell differentiation.

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Section: Discussionsupporting

confidence: 93%

Effect of isotretinoin therapy on natural killer cell activity in patients with xeroderma pigmentosum

Anolik

Giovanna

Gaspari

1998

British Journal of Dermatology

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“…This finding is in agreement with those of Eremin et al (1984) who reported an inhibition of T lymphocyte rosettes with retinoic acid treatment. However, it is unclear whether the decrease of lymphocytes forming E-rosettes after incubation in vitro with retinoids and carotenes is actually due to decreased Figure 4 Effect of retinoids and carotenes on natural killer (NK) cell activity.…”

Section: Discussionsupporting

confidence: 93%

“…In fact, it has been reported that NK activity, phagocytic and tumouricidal activities of macrophages are enhanced by incubation with retinoids in vitro(Goldfarb & Herberman,1981;Tachibana et al,1984). On the other hand,Eremin et al (1984) found that retinoic acid inhibited antibody-dependent cellular cytotoxicity and natural cytotoxicity of human blood lymphocytes. With the exception of the higher concentration (10~ M) of retinol and retinal, our studies showed no augmentation or reduction of NK activity after incubation in vitro with any concentrations of retinoids or carotenes.…”

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confidence: 99%

Effects of Retinoids on Human Lymphocyte Functions in vitro

1985

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1 E-Rosette formation in vitro, lymphocyte mitogenesis and natural killer (NK) activity of human blood lymphocytes were strongly inhibited by high concentration (10 -4 M) of retinol or retinal. Other retinoids at 10-4 M (retinoic acid and 13-cis-retinoic acid) and lower concentrations (10-7 or 10-9 M) of retinol, retinal and carotenes also inhibited E-rosette formation. 2 Lymphocyte transformation responses induced by concanavalin A (Con A) or pokeweed mitogen (PWM) were also inhibited while NK activity was not affected. 3 There was a remarkable depression of the total number of viable lymphocytes after incubation with retinol or retinal 10-4 M. However, other retinoids, 10-7 and 10-9 M of retinol and retinal and carotenes did not show marked decrease of lymphocyte number or viability even after prolonged incubation (48 h). 4 The mechanism of inhibition by retinol or retinal (10-4 M) is due in part to the decrease of viable lymphocytes. It is unclear how other retinoids, carotenes and lower concentrations (10-7 or 10-9 M) of retinol or retinal inhibit E-rosette formation or lymphocyte transformation.

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“…Previous in vitro studies of the effects of retinoids on NK cell activity and IFN production suggest that retinoids inhibit these functions (42)(43)(44)(45)(46). Although some of our XP patients (patients 1, 2, 3, 5, and 7) were being treated with isotretinoin at the time we assayed their NK cell activity, it is unlikely that our ex vivo study of lymphocytes from XP patients simply reflect the effects ofretinoids on NK cell function.…”

Section: Discussionmentioning

confidence: 92%

Impaired interferon production and natural killer cell activation in patients with the skin cancer-prone disorder, xeroderma pigmentosum.

Gaspari

Fleisher²,

Kraemer³

1993

J. Clin. Invest.

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Xeroderma pigmentosum (XP) is a rare autosomal recessive disorder with sun sensitivity, markedly increased skin cancer susceptibility, and defective DNA repair without consistently identified symptoms of immune deficiency. We examined natural killer (NK) cell activity and interferon production in peripheral blood lymphocytes (PBL) of eight XP patients who had multiple primary skin cancers. The XP patients had normal numbers ofT cells and NK cells, as well as normal lymphokineactivated killer cell activity and normal tumor necrosis factor-a production. Unstimulated NK cell function was 40% of normal controls in five XP patients, but was normal in three other XP patients. However, PBL from all the XP patients tested showed no enhancement of NK activity by the interferon inducer, polyinosinic acid:polycytidilic acid (polyIC) but enhancement by interferon-a was normal, suggesting an impairment in interferon production. Parallel studies in non-XP skin cancer patients revealed that both unstimulated and polyIC-enhanced NK activity were normal. Further investigation using PBL from XP patients revealed that the production of interferon-vy after stimulation with interferon inducers (polyIC, interleukin 2, or K562 tumor cells) was 13-43% of normals. These data indicate that XP lymphocytes have a defect in production of interferons and suggest that defective interferon production, as well as DNA repair defects, may play an important role in the susceptibility of XP patients to skin cancer. (J. Clin. Invest. 1993.

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Inhibition of Antibody-Dependent Cellular Cytotoxicity and Natural Cytotoxicity by Retinoic Acid

Cited by 15 publications

References 15 publications

Effect of isotretinoin therapy on natural killer cell activity in patients with xeroderma pigmentosum

Effect of isotretinoin therapy on natural killer cell activity in patients with xeroderma pigmentosum

Effects of Retinoids on Human Lymphocyte Functions in vitro

Impaired interferon production and natural killer cell activation in patients with the skin cancer-prone disorder, xeroderma pigmentosum.

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