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Antigen presenting and effector cell cluster formation in BALB/c mice during mousepox: model studies *
Author(s) -
Szulc L.,
Boratynska A.,
Martyniszyn L.,
Niemialtowski M.G.
Publication year - 2010
Publication title -
journal of applied microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.889
H-Index - 156
eISSN - 1365-2672
pISSN - 1364-5072
DOI - 10.1111/j.1365-2672.2010.04813.x
Subject(s) - effector , antigen , virology , biology , microbiology and biotechnology , immunology
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.