Assuntos
Linfócitos T CD4-Positivos/imunologia , Linfócitos T CD8-Positivos/imunologia , Vírus da Ectromelia/patogenicidade , Ectromelia Infecciosa/imunologia , Citometria de Fluxo/métodos , Interleucina-17/metabolismo , Animais , Vírus da Ectromelia/imunologia , Ectromelia Infecciosa/virologia , Interleucina-17/genética , Interleucina-17/imunologia , Camundongos , Camundongos Endogâmicos BALB C , Camundongos Endogâmicos C57BL , Linfócitos TRESUMO
AIMS: The objective of this study was to access APC-effector cell cluster formation in genetically susceptible BALB/c (H-2(d) ) mice infected with highly virulent Moscow strain of ectromelia virus (ECTV-MOS) and estimate of lymphocyte activation based upon expression of CD62L and CD44 molecules. METHODS AND RESULTS: APC-effector cell clusters were obtained by enzymatic digestion from draining lymph nodes (DLNs) and spleens of BALB/c mice. We found that APCs infected with ECTV-MOS form unstable clusters with effector cells, and thus may diminish T-cell activation at the early stage of mousepox. Different types of effector cells including T-cell subsets (CD4(+) and CD8(+) ), B cells and polymorphonuclear cells colocalize within individual clusters. Increase in CD19(+) B cells within APC-effector cell clusters during severe clinical mousepox may reflect B-cell activation. CONCLUSIONS: Our studies indicated vigorous changes in APC-effector cell cluster formation in genetically susceptible BALB/c mice during mousepox (up to 2 weeks). ECTV-MOS can modulate APC interactions with effector cells and consequently may impair T-cell activation probably owing to unstable cluster formation and/or subsequent weak stimulation by infected APCs at the early stages of mousepox. SIGNIFICANCE AND IMPACT OF THE STUDY: This is the first report of APC-effector cell cluster formation in BALB/c mice during mousepox. It gives us a new light on the mutual cell-cell interactions and development of the immune response during ECTV-MOS infection.
Assuntos
Células Apresentadoras de Antígenos/imunologia , Vírus da Ectromelia/imunologia , Ectromelia Infecciosa/imunologia , Linfócitos/imunologia , Animais , Células Apresentadoras de Antígenos/citologia , Linfócitos B/imunologia , Linfócitos B/patologia , Modelos Animais de Doenças , Ectromelia Infecciosa/patologia , Regulação da Expressão Gênica/imunologia , Receptores de Hialuronatos/genética , Selectina L/genética , Ativação Linfocitária/imunologia , Linfócitos/patologia , Masculino , Camundongos , Camundongos Endogâmicos BALB C , Subpopulações de Linfócitos T/imunologia , Subpopulações de Linfócitos T/patologiaRESUMO
We describe here a contribution of virus-induced actin tails and filopodia in transmission of Ectromelia virus (ECTV) infection in permissive cells detected by the immunofluorescence and confocal microscopy. Immunoblot analysis revealed profoundly decreased beta-actin levels during ECTV replicative cycle in the infected cells 24 hrs post infection (p.i.). These results provided a basis for the further analysis of ECTV motion in the infected cells as well as for impact of ECTV infection on the cytoskeletal proteins.
