Mechanisms of Induction of Human Gamma Interferon

Dianzani, F.; Monahan, T.M.; Santiano, M; Jordan, Craig A.; Zucca, Mario

doi:10.1016/b978-0-12-406080-7.50048-5

Cited by 4 publications

(4 citation statements)

References 14 publications

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“…IFN alpha production after induction with several agents has been attributed to monocytes, natural killer cells (NK) or B-lymphocytes [11]. Here we confirm that T lymphocytes are poor IFN alpha producers even after induction with HIV and H 9/HIV; furthermore we could rule out the involvement ofmonocytes, because they also are poor responders to these inducers, whereas are fully responsive to NDV, which is known to induce preferentially this cell type [8].…”

Section: Discussionsupporting

confidence: 81%

Acid-labile human interferon alpha production by peripheral blood mononuclear cells stimulated by HIV-infected cells

Capobianchi¹,

Marco²,

Marco³

et al. 1988

Archives of Virology

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We compared the properties of interferon (IFN) induced in peripheral blood mononuclear cells (PBMC) by free infectious HIV to that induced by HIV-infected cells fixed with glutaraldehyde. While the IFN induced by HIV was a conventional IFN alpha, the IFN induced by HIV-infected cells, although sharing with IFN alpha both antigenic properties and molecular weight, was strongly inactivated by treatment at pH lower than 4. The ability to induce acid-labile IFN alpha was exerted both by the chronically-infected cell line H9/HIV and by normal PBMC infected in vitro with HIV, while infection of inducers cells with viruses other than HIV made these cells capable of inducing only acid-stable IFN alpha. The cell involved in the production of this type of IFN seems to be B-lymphocyte. Because the presence of acid-labile IFN alpha in the serum of AIDS patients has been described, we suggest that this unusual IFN derives from interaction between circulating B-lymphocytes and the HIV-infected cells.

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Section: Discussionsupporting

confidence: 81%

Acid-labile human interferon alpha production by peripheral blood mononuclear cells stimulated by HIV-infected cells

Capobianchi¹,

Marco²,

Marco³

et al. 1988

Archives of Virology

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“…It has been reported that the treatment of PBMC with an enzyme capable of deleting mannose residues from their membrane renders these cells unable to produce IFN after induction with virus-infected cells while unaffecting the IFN induction by virions [9]: our present data suggest that the interaction between virus-infected cells and B-lymphocytes is mediated by HLA class II antigens, probably via the carbohydrate containing moiety of these molecules. We have recently shown that another IFN alpha inducer, selectively active on B-lymphocytes, i.e., Mycoplasma pneumoniae, interacts with induced cells at membrane sites involving DR molecules, at variance with a viral inducer, i.e., Newcastle disease virus, which in turn preferentially stimulates macrophages [7].…”

Section: Discussionmentioning

confidence: 67%

Differences in the mechanism of induction of interferon-alpha by Herpes simplex virus and Herpes simplex virus-infected cells

Capobianchi¹,

Malavasi

Marco³

et al. 1988

Archives of Virology

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The cellular source of IFN alpha after induction with Herpes simplex virus type-1 (HSV) and HSV-infected fibroblasts was investigated by using human peripheral blood mononuclear cell (PBMC) populations, purified according to conventional procedures, and which included T- and B-lymphocytes as well as monocytes. It appears that the cells responding to HSV virions are monocytes, whereas the PBMC population induced by HSV-infected cells is represented by B-lymphocytes. Furthermore, by using monoclonal antibody (MoAb) to HLA class I and class II products, it appears that different membrane structures are involved in the induction of IFN by HSV virions, as opposed to HSV-infected cells. In fact, most anti-HLA class II MoAbs inhibit IFN induction by HSV-infected cells, and not IFN induction by HSV virions.

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“…The expression of IFN-e by basal keratinocytes, epidermal dendritic cells, mononuclear cells and by endothelial cells may indicate that the cells have been stimulated to produce IFN. This may be due to a virus infection [7,21]. Whether these cells are virus-infected is at present unknown, but our demonstration of viruslike particles [5] in suction blister fluid from psoriatic lesions is intriguing.…”

Section: Discussionmentioning

confidence: 81%

In situ localization of interferons in psoriatic lesions

et al. 1989

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Summary. An indirect immunofluorescence technique, using murine monoclonal antibodies (MoAbs) against human IFN-~ and human IFN-? was used to study IFNs in cryostat sections from psoriatic skin lesions. The IFNs were more pronounced in sections from highly active psoriasis than in sections from stationary psoriasis. In highly active psoriatic lesions IFN-~ was localized to keratinocytes is stratum basale, to some epidermal dendritic cells, probably Langerhans cells, and to some mononuclear cells in dermis. IFN-~ was usually not detected in sections from stationary psoriasis. IFN-y was localized to stratum corneum, to keratinocytes around microabcesses and to mononnclear cells in the dermal cell infiltrates, predominantly in highly active psoriatic lesions. Both IFN-~ and IFNwere localized to some endothelial cells in the papillary dermis. The MoAbs did not stain sections from unaffected skin from patients with psoriasis or sections from healthy individuals. The findings indicate that the IFN system in the skin may be of significance in the pathophysiology of psoriasis. Key words: Psoriasis -InterferonsPreviously, we demonstrated interferon (IFN) in serum and suction blister fluid from patients with psoriasis using an infectivity inhibition micromethod [4]. Sera from patients with psoriasis had higher levels of IFN than sera from healthy individuals. Higher IFN levels were detected in suction blister fluid from psoriatic skin lesions than in serum and in suction blister fluid from unaffected skin, indicating IFN production in the skin lesions. Characterization experiments indicated the presence of IFN-7 and both acid labile and acid stable IFN-a in blister fluids and sera. Extended studies using an ELISA assay indicate inOffprint requests to ." J. K. Livden, MD (address see above) creased levels of IFN-? in sera from patients with active psoriasis compared with sera from healthy individuals, while sera from patients with stationary psoriasis have decreased levels of IFN-7 (unpublished data). Recently, Kapp et al. [11] found decreased IFN production by peripheral leukocytes from patients with psoriasis.IFN-7 is mainly produced by activated T lymphocytes, whereas IFN-~ is produced by several cell types after various viral and nonviral stimuli. Previously, we demonstrated retrovirus-like particles in suction blister fluids from psoriatic skin lesions [5]. The presence of IFN-a and retrovirus-like particles in blister fluids from psoriatic lesions indicated that virus may be of significance in the pathogenesis of psoriasis [23].Further information on IFN in psoriasis is of particular interest in relation to disease activity and cellular localization. Therefore, we examined sections of psoriatic and normal skin using an immunofluorescence technique with monoclonal antibodies to human IFN-~ and IFN-~.

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Mechanisms of Induction of Human Gamma Interferon

Cited by 4 publications

References 14 publications

Acid-labile human interferon alpha production by peripheral blood mononuclear cells stimulated by HIV-infected cells

Acid-labile human interferon alpha production by peripheral blood mononuclear cells stimulated by HIV-infected cells

Differences in the mechanism of induction of interferon-alpha by Herpes simplex virus and Herpes simplex virus-infected cells

In situ localization of interferons in psoriatic lesions

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