An immunohistochemical study of Warthin‐Finkeldey cells in measles

Nozawa, Yoshihiro; Ono, Nobutaka; Abe, Masafumi; Sasaki, Hideo; Wakasa, Haruki

doi:10.1111/j.1440-1827.1994.tb01708.x

Cited by 29 publications

(29 citation statements)

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“…Surprisingly, MeV-induced MGC from epithelial cells were found to be viable and dynamic entities capable of transducing intracellular signals throughout their morphological stage changes. Thus, from our in vitro observations, we predict that the physiopathological MGC (WFC) observed in lymph nodes and thymus from MeV-infected children and primates should have a rather long life span in vivo (54,76). However, as described by us and others (13,58,63,82), syncytium apoptosis finally occurs, probably depending on cellular environment deprivation.…”

Section: Discussionmentioning

confidence: 84%

“…WFC are usually observed in germinal centers and interfollicular areas of secondary lymphoid organs and in the thymus. They are heterogeneous and display either B-or T-cell markers (54), although macrophage and DC markers have not yet been investigated. In vitro, MeV infection of human cells, including primary epithelial cells and cDC, induces the formation of MGC, also referred to as syncytia (17,78,82).…”

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confidence: 99%

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Cell-Cell Fusion Induced by Measles Virus Amplifies the Type I Interferon Response

Herschke

Plumet

Duhen

et al. 2007

J Virol

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Section: Discussionmentioning

confidence: 84%

mentioning

confidence: 99%

Cell-Cell Fusion Induced by Measles Virus Amplifies the Type I Interferon Response

Herschke

Plumet

Duhen

et al. 2007

J Virol

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“…In lymph node material of experimentally infected rhesus macaques, giant cells were very infrequent (McChesney et al 1997). In contrast, these Warthin-Finkeldey cells were described in hyperplastic lymphoid tissue in a measles patient at autopsy, although evidence for MV there was provided only by immunohistology, but not by electron microscopy (Nozawa et al 1994). …”

Section: Discussionmentioning

confidence: 93%

“…Giant cell formation and necrosis were reported in lymphoid tissues of MV-infected rhesus macaques, albeit to a moderate extent (McChesney et al 1989;Kobune et al 1996). Giant cell formation in hyperplastic lymphoid tissue was documented in a measles patient at autopsy; however, MV could not be detected in this area (Nozawa et al 1994). Thus, T cell loss in secondary lymphoid tissues may occur, as may induction of apoptosis as seen in cocultures of infected DCs and T cells (Fugier-Vivier et al 1997).…”

Section: Lymphopenia Mechanisms Of Lymphocyte Depletionmentioning

confidence: 96%

Measles Virus-Induced Immunosuppression

Schneider-Schaulies

Current Topics in Microbiology and Immunology

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Immunosuppression is the major cause of infant death associated with acute measles and therefore of substantial clinical importance. Major hallmarks of this generalized modulation of immune functions are (1) lymphopenia, (2) a prolonged cytokine imbalance consistent with suppression of cellular immunity to secondary infections, and (3) silencing of peripheral blood lymphocytes, which cannot expand in response to ex vivo stimulation. Lymphopenia results from depletion, which can occur basically at any stage of lymphocyte development, and evidently, expression of the major MV receptor CD150 plays an important role in targeting these cells. Virus transfer to T cells is thought to be mediated by dendritic cells (DCs), which are considered central to the induction of T cell silencing and functional skewing. As a consequence of MV interaction, viability and functional differentiation of DCs and thereby their expression pattern of co-stimulatory molecules and soluble mediators are modulated. Moreover, MV proteins expressed by these cells actively silence T cells by interfering with signaling pathways essential for T cell activation.

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“…Human thymus hosts T-cell development and is infectible by MV (31,35). However, it has been difficult to examine MV infection of thymocytes in vivo.…”

Section: Discussionmentioning

confidence: 99%

Measles Virus Infects and Suppresses Proliferation of T Lymphocytes from Transgenic Mice Bearing Human Signaling Lymphocytic Activation Molecule

Hahm¹,

Arbour²,

Naniche³

et al. 2003

J Virol

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Humans are the only natural reservoir of measles virus (MV), one of the most contagious viruses known. MV infection and the profound immunosuppression it causes are currently responsible for nearly one million deaths annually. Human signaling lymphocytic activation molecule (hSLAM) was identified as a receptor for wild-type MV as well as for MV strains prepared as vaccines. To better evaluate the role of hSLAM in MV pathogenesis and MV-induced immunosuppression, we created transgenic (tg) mice that expressed the hSLAM molecule under the control of the lck proximal promoter. hSLAM was expressed on CD4؉ and CD8 ؉ T cells in the blood and spleen and also on CD4 Since measles virus (MV) was isolated and attenuated to produce a successful vaccine (7,20), it was shown to cause a progressive central nervous system (CNS) disease (subacute sclerosing panencephalitis) and was found to be capable of suppressing immune responses (28, 53).More recently, two developments have aroused interest in the nature of MV. The first was the discovery of two cell surface receptors for MV, namely, the CD46 molecule, which is a member of the complement regulatory cascade of proteins (6,26,33), and signaling lymphocytic activation molecule (SLAM), a T-cell costimulatory molecule (9, 18, 52). Whereas the CD46 molecule is ubiquitously expressed on all nucleated cells, SLAM is expressed only on immature thymocytes, activated and memory T cells, B cells, and activated monocytes and dendritic cells (4,29,30,40,49). The second development was a better understanding of mechanisms of MV-induced immunosuppression. Although the route of infection by MV is respiratory, and despite its widespread dissemination to the skin, the intestinal tract, and the nervous system, the virus has a strong predilection for lymphoid tissues in the early as well as late stages of the disease. Furthermore, lymphoid tissues and cells provide not only a replication site but also a means of transporting the virus within the body. Since both CD46, constitutively, and SLAM, inducibly, are concomitantly present on cells of the human immune system, the relative individual contribution of either of the two MV receptors in MV-induced immunosuppression has been difficult to sort out. MV has been known to induce mitogen unresponsiveness of T cells by direct infection and contact with infected cells (12,43,56). However, the lack of a suitable small-animal model has impeded progress toward understanding the pathogenic effects of MV, especially its ability to induce immunosuppression, a CNS disease, and virus-immune cell and virus-neuron interactions. Following the identification of MV receptor CD46, investigators in several laboratories have attempted to express human CD46 in transgenic (tg) mice as models that could be infected by MV (16,36,41,57). The human CD46 protein has a 45% homology with mouse CD46 (54). Mice are not infected by MV unless the virus has been adapted to the murine cells by multiple passages (24) or unless human CD46 is expressed in the mouse. In terms of under...

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An immunohistochemical study of Warthin‐Finkeldey cells in measles

Cited by 29 publications

References 11 publications

Cell-Cell Fusion Induced by Measles Virus Amplifies the Type I Interferon Response

Cell-Cell Fusion Induced by Measles Virus Amplifies the Type I Interferon Response

Measles Virus-Induced Immunosuppression

Measles Virus Infects and Suppresses Proliferation of T Lymphocytes from Transgenic Mice Bearing Human Signaling Lymphocytic Activation Molecule

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