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2.
Exp Biol Med (Maywood) ; 230(11): 865-71, 2005 Dec.
Artículo en Inglés | MEDLINE | ID: mdl-16339752

RESUMEN

The Docile strain of lymphocytic choriomeningitis virus (LCMV) induces anemia in a number of inbred strains of mice, including C3HeB/FeJ and CBA/Ht animals. A difference in the kinetics of anemia and in compensatory reticulocytosis suggested that impaired erythropoiesis was the major pathogenic mechanism involved in CBA/Ht mice, but not in C3HeB/FeJ mice. In both mouse strains an antierythrocyte autoantibody production that depended on the presence of functional CD4+ T lymphocytes was observed. Although depletion of T helper lymphocytes prevented anemia in C3HeB/FeJ mice, this treatment largely failed to inhibit the development of the disease in CBA/Ht animals. This observation indicated that the antierythrocyte autoimmune response induced by the infection was at least partly responsible for the anemia of C3HeB/FeJ mice, but not of CBA/Ht mice. Erythrophagocytosis was enhanced in both mouse strains after LCMV infection, but did not appear to be a major cause of anemia. These data clearly indicate that similar disease profiles induced by the same virus in two different host strains can be the result of distinctly different mechanisms.


Asunto(s)
Anemia Hemolítica Autoinmune/inmunología , Infecciones por Arenaviridae/inmunología , Hematopoyesis/inmunología , Virus de la Coriomeningitis Linfocítica , Anemia Hemolítica Autoinmune/etiología , Anemia Hemolítica Autoinmune/patología , Animales , Formación de Anticuerpos/inmunología , Infecciones por Arenaviridae/complicaciones , Infecciones por Arenaviridae/patología , Autoanticuerpos/inmunología , Autofagia/inmunología , Linfocitos T CD4-Positivos/inmunología , Linfocitos T CD4-Positivos/patología , Eritrocitos/inmunología , Depleción Linfocítica , Virus de la Coriomeningitis Linfocítica/inmunología , Ratones , Ratones Endogámicos , Reticulocitosis/inmunología , Especificidad de la Especie
3.
Autoimmun Rev ; 4(4): 247-52, 2005 Apr.
Artículo en Inglés | MEDLINE | ID: mdl-15893720

RESUMEN

Viral infections are involved in the pathogenesis of blood autoimmune diseases such as hemolytic anemia and thrombocytopenia. Although antigenic mimicry has been proposed as a major mechanism by which viruses could trigger the development of such diseases, it is not easy to understand how widely different viruses might induce these blood autoimmune diseases by this sole mechanism. In mice infected with lactate dehydrogenase-elevating virus (LDV), or mouse hepatitis virus, and treated with anti-erythrocyte or anti-platelet monoclonal autoantibodies at a dose insufficient to induce clinical disease by themselves, the infection sharply enhances the pathogenicity of autoantibodies, leading to severe anemia or thrombocytopenia. This effect is observed only with antibodies that induce disease through phagocytosis. Moreover, the phagocytic activity of macrophages from infected mice is increased and the enhancing effect of infection on autoantibody-mediated pathogenicity is strongly suppressed by treatment of mice with clodronate-containing liposomes. Finally, the disease induced by LDV after administration of autoantibodies is largely suppressed in animals deficient for gamma-interferon receptor. Together, these observations suggest that viruses may trigger autoantibody-mediated anemia or thrombocytopenia by activating macrophages through gamma-interferon production, a mechanism that may account for the pathogenic similarities of multiple infectious agents.


Asunto(s)
Anemia Hemolítica Autoinmune/inmunología , Anemia Hemolítica Autoinmune/virología , Autoanticuerpos/toxicidad , Púrpura Trombocitopénica Idiopática/inmunología , Púrpura Trombocitopénica Idiopática/virología , Virosis/complicaciones , Animales , Modelos Animales de Enfermedad , Virus Elevador de Lactato Deshidrogenasa/patogenicidad , Macrófagos/inmunología , Ratones , Fagocitosis/inmunología
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