title: The splenic marginal zone is absent in alymphoplastic aly mutant mice.
abstract: aly is a unique spontaneous autosomal recessive mutation in mice that causes a deficiency in the systemic lymph nodes (LN) and Peyer's patches (PP). aly also induces abnormal histological findings in the spleen and a deficiency in humoral and cell-mediated immune functions, although lymphocytes of the aly/aly mouse show virtually normal immune responses in vitro. We studied the structure of the spleen of aly mice in detail by immunohistochemistry and electron microscopy. We found that the spleen of the aly/aly mouse was deficient in the expression of specific antigens for marginal metallophils (MM), marginal zone macrophages (MZM) and fibroblastic reticular cells (FRC), which are components of the marginal zone (MZ) of the spleen. Morphological analysis indicated that the aly/aly spleen is deficient in the structure of MZ, which may, in part, account for the severe immunodeficiency in the aly/aly mouse. We then performed reciprocal bone marrow transplantation experiments (BMT) between normal and aly mice and found a clear correlation between the formation of LN and the development of the splenic MZ in these mice; i.e. successful development of LN was invariably associated with the appearance of the MZ structure, whereas the failure of LN development was always associated with the absence of the development of MZ. These BMT results suggest that a common factor may regulate the generation of both LN and MZ of the spleen.
authors.affiliation: The First Department of Internal Medicine, Tokyo Medical and Dental University, Japan.
authors.forename: R
authors.initials: R
authors.lastname: Koike
authors.forename: T
authors.initials: T
authors.lastname: Nishimura
authors.forename: R
authors.initials: R
authors.lastname: Yasumizu
authors.forename: H
authors.initials: H
authors.lastname: Tanaka
authors.forename: Y
authors.initials: Y
authors.lastname: Hataba
authors.forename: Y
authors.initials: Y
authors.lastname: Hataba
authors.forename: T
authors.initials: T
authors.lastname: Watanabe
authors.forename: S
authors.initials: S
authors.lastname: Miyawaki
authors.forename: M
authors.initials: M
authors.lastname: Miyasaka
mesh_terms: D000818:Animals; D016026:Bone Marrow Transplantation / Q000473:pathology; D015815:Cell Adhesion Molecules; D005260:Female; D007136:Immunoglobulins / Q000032:analysis; D007153:Immunologic Deficiency Syndromes / Q000235:genetics* / Q000276:immunology / Q000473:pathology*; D008264:Macrophages / Q000276:immunology / Q000473:pathology; D008297:Male; D051379:Mice; D008809:Mice, Inbred C3H; D008817:Mice, Mutant Strains; D009088:Mucoproteins / Q000032:analysis; D013154:Spleen / Q000002:abnormalities* / Q000276:immunology
chemical_list: D015815:Cell Adhesion Molecules; D007136:Immunoglobulins; C489082:Madcam1 protein, mouse; D009088:Mucoproteins