Early infiltration of CD8+ macrophages/microglia to lesions of rat traumatic brain injury.
Local inflammatory responses play an important role in mediating secondary tissue damage in traumatic brain injury. Characterization of leukocytic subpopulations contributing to the early infiltration of the damaged tissue might aid in further understanding of lesion development and contribute to definition of cellular targets for selective immunotherapy. In a rat traumatic brain injury model, significant CD8+ cell accumulation was observed 3 days post-injury. The CD8+ cells were strictly distributed to the pannecrotic areas and around the pannecrotic perimeter. The morphology, time course of accumulation and distribution of CD8+ cells were similar to that of reactive ED1+ and endothelial monocyte-activating polypeptide II+ microglia/macrophages, but different from W3/13+ T cells. Further double-labeling experiments confirmed that the major cellular sources of CD8 were reactive macrophages/microglia. Both the location of these CD8+ macrophages/microglia to the border of the pannecrosis and their co-expression of endothelial monocyte-activating polypeptide II and P2X4 receptor suggest they might have a central role in lesion development and might thus be candidates for development of immunotherapeutic, anti-inflammatory strategies.
Zhang
Z
Z
Institute of Brain Research, University of Tuebingen, Calwer Str. 3, D-72076 Tuebingen, Germany. Electronic address: zhangzhiren@yahoo.com.
Artelt
M
M
Synovo GmbH, Paul-Ehrlich-Str. 15, D-72076 Tuebingen, Germany.
Burnet
M
M
Synovo GmbH, Paul-Ehrlich-Str. 15, D-72076 Tuebingen, Germany.
Trautmann
K
K
Institute of Brain Research, University of Tuebingen, Calwer Str. 3, D-72076 Tuebingen, Germany.
Schluesener
H J
HJ
Institute of Brain Research, University of Tuebingen, Calwer Str. 3, D-72076 Tuebingen, Germany.
D000818:Animals; D001930:Brain Injuries / Q000150:complications / Q000276:immunology* / Q000378:metabolism / Q000473:pathology; D016827:CD8 Antigens / Q000276:immunology* / Q000378:metabolism; D018414:CD8-Positive T-Lymphocytes / Q000502:physiology; D002452:Cell Count / Q000379:methods; D016207:Cytokines / Q000378:metabolism; D053331:Ectodysplasins; D007150:Immunohistochemistry / Q000379:methods; D007249:Inflammation / Q000209:etiology; D008262:Macrophage Activation; D008264:Macrophages / Q000276:immunology / Q000378:metabolism*; D008565:Membrane Proteins / Q000378:metabolism; D017628:Microglia / Q000276:immunology / Q000378:metabolism*; D009363:Neoplasm Proteins / Q000378:metabolism; D016601:RNA-Binding Proteins / Q000378:metabolism; D051381:Rats; D011917:Rats, Inbred Lew; D018048:Receptors, Purinergic P2 / Q000378:metabolism; D058848:Receptors, Purinergic P2X4; D013997:Time Factors; D048069:Tumor Necrosis Factors / Q000378:metabolism
D016827:CD8 Antigens; D016207:Cytokines; D053331:Ectodysplasins; D008565:Membrane Proteins; D009363:Neoplasm Proteins; C548228:P2rx4 protein, rat; D016601:RNA-Binding Proteins; D018048:Receptors, Purinergic P2; D058848:Receptors, Purinergic P2X4; D048069:Tumor Necrosis Factors; C077219:small inducible cytokine subfamily E, member 1