ICOS-expressing lymphocytes promote resolution of CD8-mediated lung injury in a mouse model of lung rejection.

ICOS-expressing lymphocytes promote resolution of CD8-mediated lung injury in a mouse model of lung rejection.

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Acute rejection, a common complication of lung transplantation, may promote obliterative bronchiolitis leading footjoy weste herren to graft failure in lung transplant recipients.During acute rejection episodes, CD8(+) T cells can contribute to lung epithelial injury but the mechanisms promoting and controlling CD8-mediated injury in the lung are not well understood.To study the mechanisms regulating CD8(+) T cell-mediated lung rejection, we used a transgenic model in which adoptively transferred ovalbumin (OVA)-specific cytotoxic T lymphocytes (CTL) induce lung injury in mice expressing an ovalbumin transgene in the small airway epithelium of the lungs (CC10-OVA mice).

The lung pathology is similar to findings in humans with acute lung transplant.In the presence of an intact immune response the inflammation resolves by day 30.Using CC10-OVA.

RAG(-/-) mice, we found that CD4(+) T cells and ICOS(+/+) T cells were required for protection against lethal lung injury, while neutrophil depletion was not protective.In addition, CD4(+)Foxp3 (+) ICOS(+) T cells were enriched in the lungs of animals surviving lung injury Canvas Mesh Athletic Running Shoes and ICOS(+/+) Tregs promoted survival in animals that received ICOS(-/-) T cells.Direct comparison of ICOS(-/-) Tregs to ICOS(+/+) Tregs found defects in vitro but no differences in the ability of ICOS(-/-) Tregs to protect from lethal lung injury.

These data suggest that ICOS affects Treg development but is not necessarily required for Treg effector function.