info:eu-repo/semantics/article
Immature mouse granulocytic myeloid cells are characterized by production of ficolin-B
Registro en:
Weber Steffens, Dorothea; Hunold, Katja; Kürschner, Johanna; Giraldez Martinez, Sonia ; Elumalai, Preetham; et al.; Immature mouse granulocytic myeloid cells are characterized by production of ficolin-B; Elsevier; Molecular Immunology; 56; 4; 12-2013; 488-496
0161-5890
CONICET Digital
CONICET
Autor
Weber Steffens, Dorothea
Hunold, Katja
Kürschner, Johanna
Giraldez Martinez, Sonia
Elumalai, Preetham
Schmidt, Dominic
Trevani, Analía Silvina
Runza, Valeria L.
Männel, Daniela N.
Resumen
Ficolins activate the lectin pathway of the complement system upon binding to carbohydrate patterns on pathogens. To characterize the producer cells of ficolin-B the expression of mouse ficolin-B, the orthologue of human M-ficolin, was studied in macrophages and dendritic cells during differentiation from bone marrow cells, in primary granulocytes, and during differentiation of granulocytes derived from ER-Hoxb8 cells. Expression of ficolin-B mRNA declined in all myeloid cell types to low levels during terminal differentiation. However, in contrast to macrophages and dendritic cells, ficolin-B expression was enhanced upon activation in granulocytes. High expression of ficolin-B was observed in primary immature neutrophilic CD11b+ Ly-6Cint Ly-6Ghigh granulocytes when isolated from the bone marrow, in particular during sepsis. Ficolin-B was demonstrated in lysates of primary granulocytes, ER-Hoxb8-derived granulocytes, bone marrow-derived macrophages, and dendritic cells. Native ficolin-B from cell lysates and supernatants of granulocytes activated the lectin pathway as measured by binding to MASP-2 and inducing C4 deposition. Specific staining demonstrated intra-cellular or cell associated ficolin-B protein in activated immature granulocytes deposited in a granular fashion. This study shows that ficolin-B is stored in and set free from immature granulocytic myeloid cells indicating a role in the early infection-induced cellular response of these inflammatory cells. Fil: Weber Steffens, Dorothea. Universitat Regensburg; Alemania Fil: Hunold, Katja. Universitat Regensburg; Alemania Fil: Kürschner, Johanna. Universitat Regensburg; Alemania Fil: Giraldez Martinez, Sonia. Universitat Regensburg; Alemania Fil: Elumalai, Preetham. Universitat Regensburg; Alemania Fil: Schmidt, Dominic. Universitat Regensburg; Alemania Fil: Trevani, Analía Silvina. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; Argentina Fil: Runza, Valeria L.. Universitat Regensburg; Alemania Fil: Männel, Daniela N.. Universitat Regensburg; Alemania