       Document 0366
 DOCN  M9620366
 TI    Loss of follicular dendritic cells in murine-acquired immunodeficiency
       syndrome.
 DT    9602
 AU    Masuda A; Burton GF; Szakal AK; Tew JG; Department of Microbiology and
       Immunology, Virginia Commonwealth; University, Richmond, USA.
 SO    Lab Invest. 1995 Oct;73(4):511-20. Unique Identifier : AIDSLINE
       MED/96027912
 AB    BACKGROUND: The disease caused by HIV-1 leads to the destruction of
       follicular dendritic cells (FDC) and the follicular architecture in
       secondary lymphoid tissues. The murine acquired immunodeficiency
       syndrome (MAIDS, caused by LP-BM5) serves as an animal model for study
       of mechanisms involved in development of retrovirus-induced
       immunodeficiencies. The present study was undertaken to determine
       whether LP-BM5 infection leads to the destruction of murine FDC and the
       normal follicular architecture in secondary lymphoid tissues.
       EXPERIMENTAL DESIGN: Mice were infected with LP-BM5, and the follicular
       architecture and FDC networks were assessed. The pathologic changes
       observed were correlated with FDC function. RESULTS: Three weeks after
       infection, FDC networks were present, and they often appeared
       hyperplastic. However, by 1 month after infection, distorted lymphoid
       follicles were apparent, and the intensity of FDC labeling began to
       decline. FDC disappeared first in the spleen, and in hyperimmunized
       mice, FDC in draining lymph nodes disappeared before FDC in nondraining
       lymph nodes. By 4 months, the normal follicular localization of B cells
       was missing, and FDC were not detectable in most tissues. As the FDC and
       the normal lymphoid architecture degenerated, extrafollicular foci of
       immunoblasts and plasma cells appeared in areas typically reserved for T
       cells, and the Thy 1.2+ T cells were dispersed. Of interest, the total
       number of Ig-producing cells increased as the disease progressed; in
       contrast, the number of anti-human serum albumin-producing cells in mice
       immunized with human serum albumin before infection decreased.
       CONCLUSIONS: These data indicate that, like HIV-1 infection, LP-BM5
       infection leads to the loss of FDC and the normal follicular
       architecture. However, morphologic changes were not observed until after
       FDC had lost their normal ability to trap and retain Ag. These data
       indicate that retroviral infections may cause FDC dysfunctions long
       before FDC are destroyed.
 DE    Animal  Autoradiography  B-Lymphocytes/CYTOLOGY/PATHOLOGY  Dendritic
       Cells/*PATHOLOGY  Disease Models, Animal  Immunohistochemistry  Lymph
       Nodes/CYTOLOGY/PATHOLOGY  Lymphoid Tissue/CYTOLOGY/*PATHOLOGY  Mice
       Mice, Inbred C57BL  Murine Acquired Immunodeficiency Syndrome/*PATHOLOGY
       Plasma Cells/CYTOLOGY/PATHOLOGY  Silver/METABOLISM
       Spleen/CYTOLOGY/PATHOLOGY  Support, U.S. Gov't, P.H.S.
       T-Lymphocytes/CYTOLOGY/PATHOLOGY  JOURNAL ARTICLE

       SOURCE: National Library of Medicine.  NOTICE: This material may be
       protected by Copyright Law (Title 17, U.S.Code).

