Dysregulated cytokine expression by CD4+ T cells from post-septic mice modulates both Th1 and Th2-mediated granulomatous lung inflammation.

The inability of post-septic CD4+ T cells to commit to either the T H 1 or T H 2 lineage may be significant for survivors of severe sepsis, especially in regards to secondary infections of the lung which require a directed cytokine response for clearance of the invading microorganism.

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