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original-paper | 20-December-2021

Histopathological Analysis of Acinetobacter baumannii Lung Infection in a Mouse Model

be clarified (Eveillard et al. 2010). Animal models for bacterial infection are often considered valuable tools for developing new drugs and vaccines (Byrne et al. 2020). Some mouse models of A. baumannii infection have been established, and immune responses and treatments against the pathogen have been analyzed (Crandon et al. 2009; Qiu et al. 2009a; 2009b; Jacobs et al. 2010). In particular, neutrophils and alveolar macrophages (AMs) play important roles in host resistance to respiratory

SHIGERU TANSHO-NAGAKAWA, YOSHINORI SATO, TSUNEYUKI UBAGAI, TAKANE KIKUCHI-UEDA, GO KAMOSHIDA, SATOSHI NISHIDA, YASUO ONO

Polish Journal of Microbiology, Volume 70 , ISSUE 4, 469–477

Review | 15-May-2020

Review: immune thrombocytopenic purpura: an update for immunohematologists

Immune thrombocytopenic purpura (ITP) is an acquired disease in which autoantibodies to platelets cause their sequestration and destruction by mononuclear macrophages, principally in the spleen. If increased production of platelets by megakaryocytes does not compensate for platelet destruction, the number of circulating platelets decreases (thrombocytopenia), resulting in a characteristic bleeding tendency (purpura). While most children with the disease experience a relatively short and benign

S. Gerald Sandler

Immunohematology, Volume 20 , ISSUE 2, 112–117

Article | 14-October-2020

Serologic aspects of treating immune thrombocytopenic purpura using intravenous Rh immune globulin

In patients with immune thrombocytopenic purpura (ITP), IgG autoantibody-coated platelets are phagocytized by mononuclear macrophages, primarily in the spleen. Intravenous Rh immune globulin (IV RhIG) has been used since 1983 to treat D+, nonsplenectomized patients with ITP. The beneficial therapeutic effect of IV RhIG is attributed to competitive inhibition of phagocytosis of IgG-coated platelets by IgG anti-D-coated D+ red blood cells (reticuloendothelial or Fc receptor blockade). Following

Can M. Savasman, S. Gerald Sandler

Immunohematology, Volume 17 , ISSUE 4, 106–110

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