title: Thymic microenvironmental alterations in experimentally induced diabetes.
abstract: Little is known about the immunologic consequences from endocrine changes observed in diabetes. Since a preserved thymic microenvironment is of critical importance for the T cell development and maturation, we have examined the thymus from alloxan-diabetic mice. An intense thymic atrophy accompanied by changes in histological pattern and in thymocyte subpopulations were observed in diabetic mice. Laminin and fibronectin, which are closely associated with thymocytes maturation, were evaluated, but, only laminin presented an altered distribution and density in thymuses from diabetes group. the expression of fibronectin and laminin receptors was found to be decreased in diabetic mice. There was also intense decrease in the expression of two important chemokines for thymus, CCL25 and CXCL12, and in the CCR9 (CCL25 receptor), but the expression of CXCR4 (CXCL12 receptor) did not drop on cells. However, no significant difference was observed in the in vitro thymocytes migratory capacity from diabetic mice. The results show significant alterations in thymus microenvironment in diabetes and offer insights for studies involving endocrine influences on lymphatic organs and T cell maturation.
authors.affiliation: Department of Anatomy, Cell Biology and Physiology, Institute of Biology, State University of Campinas-UNICAMP, Campinas, São Paulo, Brazil.
authors.forename: Patrícia R A
authors.initials: PR
authors.lastname: Nagib
authors.forename: Jacy
authors.initials: J
authors.lastname: Gameiro
authors.forename: Luiz Guilherme
authors.initials: LG
authors.lastname: Stivanin-Silva
authors.forename: Maria Sueli Parreira
authors.initials: MS
authors.lastname: de Arruda
authors.forename: Déa Maria Serra
authors.initials: DM
authors.lastname: Villa-Verde
authors.forename: Wilson
authors.initials: W
authors.lastname: Savino
authors.forename: Liana
authors.initials: L
authors.lastname: Verinaud
mesh_terms: D000496:Alloxan; D000818:Animals; D001284:Atrophy; D001835:Body Weight; D002465:Cell Movement; D002470:Cell Survival; D054377:Chemokine CXCL12 / Q000378:metabolism; D019742:Chemokines, CC / Q000378:metabolism; D003921:Diabetes Mellitus, Experimental / Q000139:chemically induced / Q000378:metabolism* / Q000473:pathology; D003922:Diabetes Mellitus, Type 1 / Q000378:metabolism* / Q000473:pathology; D005353:Fibronectins / Q000378:metabolism; D005434:Flow Cytometry; D039081:Integrin alpha5beta1 / Q000378:metabolism; D007797:Laminin / Q000378:metabolism; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D008856:Microscopy, Fluorescence; D009929:Organ Size; D054388:Receptors, CCR / Q000378:metabolism; D017474:Receptors, Laminin / Q000378:metabolism; D013601:T-Lymphocytes / Q000378:metabolism* / Q000473:pathology; D013950:Thymus Gland / Q000378:metabolism* / Q000473:pathology
chemical_list: C119309:CC chemokine receptor 9; C491541:Ccl25 protein, mouse; D054377:Chemokine CXCL12; D019742:Chemokines, CC; C515256:Cxcl12 protein, mouse; D005353:Fibronectins; D039081:Integrin alpha5beta1; D007797:Laminin; D054388:Receptors, CCR; D017474:Receptors, Laminin; D000496:Alloxan