title: Splenic and immune alterations of the Sparc-null mouse accompany a lack of immune response.
abstract: Sparc-null mice have been used as models to assess tumor-host immune cell interactions. However, it is not known if they have a competent immune system. In this study, the immune systems of Sparc wild-type and null mice were compared. Mice were assessed for differences in total body weight, spleen weight and spleen-to-body weight ratios. Spleens were compared with respect to morphology, and Sparc, Ki-67, MOMA-1 and IgM expression. Immune cells in blood, bone marrow and spleen were assessed by blood smears, automated blood panel, and flow cytometry. Additionally, the ability of Sparc-null mice to respond to immune challenge was evaluated using a footpad model. The morphological and immunohistochemical results indicated that Sparc-null spleens had more white pulp, hyperproliferative B cells in the germinal centers, and decreased marginal zones. Sparc-null spleens lacked normal Sparc expression in red and white pulp, marginal zones, endothelial and sinusoidal cells. By flow analysis, B cells were decreased and T cells were increased in the bone marrow. Finally, Sparc-null mice were unable to mount an immune response following footpad lipopolysaccharide challenge. These data confirm that Sparc-null mice have an impaired immune system.
authors.affiliation: Department of Neurosurgery, Barbara Jane Levy Laboratory of Molecular Neuro-Oncology, Hermelin Brain Tumor Center, Henry Ford Hospital, Detroit, MI, USA. nssan@neuro.hfh.edu
authors.forename: S A
authors.initials: SA
authors.lastname: Rempel
authors.forename: R C
authors.initials: RC
authors.lastname: Hawley
authors.forename: J A
authors.initials: JA
authors.lastname: Gutiérrez
authors.forename: E
authors.initials: E
authors.lastname: Mouzon
authors.forename: K R
authors.initials: KR
authors.lastname: Bobbitt
authors.forename: N
authors.initials: N
authors.lastname: Lemke
authors.forename: C R
authors.initials: CR
authors.lastname: Schultz
authors.forename: L R
authors.initials: LR
authors.lastname: Schultz
authors.forename: W
authors.initials: W
authors.lastname: Golembieski
authors.forename: J
authors.initials: J
authors.lastname: Koblinski
authors.forename: S
authors.initials: S
authors.lastname: VanOsdol
authors.forename: C G
authors.initials: CG
authors.lastname: Miller
mesh_terms: D000818:Animals; D001402:B-Lymphocytes / Q000166:cytology / Q000276:immunology / Q000378:metabolism; D001483:Base Sequence; D001835:Body Weight; D017931:DNA Primers / Q000235:genetics; D005434:Flow Cytometry; D015870:Gene Expression; D007108:Immune Tolerance; D008214:Lymphocytes / Q000166:cytology / Q000276:immunology / Q000378:metabolism; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D009929:Organ Size; D015676:Osteonectin / Q000172:deficiency* / Q000235:genetics / Q000276:immunology* / Q000378:metabolism; D013154:Spleen / Q000033:anatomy & histology / Q000276:immunology* / Q000378:metabolism
chemical_list: D017931:DNA Primers; D015676:Osteonectin