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Origin of the chicken splenic reticular cells influences the effect of the infectious bursa disease virus (IBDV) on the extracellular matrix

Effect of infectious bursa disease virus (IBDV strain F52/70) infection was studied by immunohistochemical methods on the splenic extracellular matrix (ECM). The major fibrillar components of the ECM, the type I and III collagens and the main ECM organizing glycoproteins (laminin, tenascin and fibro...

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Bibliographic Details
Published in:Avian pathology 2011-04, Vol.40 (2), p.199-206
Main Authors: Bíró, Éva, Kocsis, Katalin, Nagy, Nándor, Molnár, Dávid, Kabell, Susanne, Palya, Vilmos, Oláh, Imre
Format: Article
Language:English
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Summary:Effect of infectious bursa disease virus (IBDV strain F52/70) infection was studied by immunohistochemical methods on the splenic extracellular matrix (ECM). The major fibrillar components of the ECM, the type I and III collagens and the main ECM organizing glycoproteins (laminin, tenascin and fibronectin) were monitored up to eleven days postinfection (dpi). By 3 dpi the collagens, which form the basic scaffold of the antigen trapping region of the spleen are destroyed, which is followed by deterioration of the glycoproteins. The ECM in the red pulp and the other regions of the white pulp; periarteriolar lymphatic sheath (PALS) and germinal center (GC)) seems to be normal. The reason of the highly different pathological alterations in the ECM between the two regions of the spleen may be explained by the origin of the reticular cells. The reticular cells in the antigen trapping zone and other splenic regions are of hemopoietic and mesenchymal origins, respectively. Possibly, the reticular cells of hemopoietic origin are more susceptible for the IBDV infection, than the mesenchymal ones. Development of the antigen trapping, B dependent zone of the splenic white pulp precedes that of the PALS and GC, suggests, that this region may contribute to B cell maturation. Damage of the ECM in the antigen trapping zones results in impairment of tissue organization, which may contribute to the permanent immunosuppression.
ISSN:0307-9457
1465-3338
DOI:10.1080/03079457.2011.554797