Expression of the ED3 Antigen on Rat Macrophages in Relation to Experimental Autoimmune Diseases

• Published in: Immunobiology (1979) 1992-04, Vol.184 (4), p.311-320
• Main Authors: Damoiseaux, Jan G.M.C., Huitinga, Ingeborg, Döpp, Ed A., Dijkstra, Christine D.
• Format: Article
• Language: English
• Subjects: Animals; Antibodies, Monoclonal - immunology; Antigens, Differentiation - immunology; Autoimmune Diseases - immunology; Biological and medical sciences; Bone Marrow - drug effects; Cells, Cultured; Cytokines - pharmacology; Dexamethasone - pharmacology; Disease Models, Animal; Fundamental and applied biological sciences. Psychology; Fundamental immunology; Hypothalamo-Hypophyseal System - immunology; Immunobiology; Macrophage Activation - immunology; Macrophages - immunology; Monocytes - immunology; Monocytes, macrophages; Myeloid cells: ontogeny, maturation, markers, receptors; Rats; Rats, Inbred Strains; T-Lymphocytes - immunology
• ISSN: 0171-2985; 1878-3279
• DOI: 10.1016/S0171-2985(11)80589-9

Susceptibility to experimental autoimmune diseases (EAD) is rat strain dependent. Susceptible animals are reported to have a defective glucocorticoid response. Although many EAD are regarded as preferentially T cell-mediated, macrophages (Mϕ) play an important role in several different stages of these diseases. In this study we have investigated the possible effect of the disturbed hypothalamic-pituitary (HPA) axis on Mϕ phenotype. Therefore we studied Mϕ differentiation in several different rat strains, especially with regard to the Mϕ specific differentiation antigen as recognized by monoclonal antibody (mAb) ED3. This mAb is, in normal healthy rats, reactive with very restricted Mϕ subpopulations present in the lymphoid organs only. However, in autoimmune diseased tissues many of the infiltrated Mϕ are also ED3-positive. It appeared that Mϕ, in vitro derived from monocytes out of susceptible rat strains, showed a high ED3 expression in contrast to monocyte-derived Mϕ out of resistant rat strains. This difference in ED3 expression appeared to be T cell-mediated. Our results are suggestive for the fact that the impaired HPA-axis in EAD susceptible rat stains affects Mϕ differentiation. The relevance of the observed differences with respect to disease induction, maintenance, or suppression is discussed and obviously needs further investigation.