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home:diseases:hlh [07.26.2010] – inge | home:diseases:hlh [07.26.2010] – inge | ||
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* The immune system is activated. High levels of serum TNF-α, interleukins, | * The immune system is activated. High levels of serum TNF-α, interleukins, | ||
* HLH has been associated with Epstein-Barr virus infection, (({{pubmed> | * HLH has been associated with Epstein-Barr virus infection, (({{pubmed> | ||
- | * Treatment of infections can reduce hemophagocytosis (({{pubmed> | + | * Treatment of infections can reduce hemophagocytosis (({{pubmed> |
==== Possible mechanism for hemophagocytosis ==== | ==== Possible mechanism for hemophagocytosis ==== | ||
- | The actual hemophagocytosis may be viewed as a result of overstimulated macrophages. While blood cells may harbour infectious agents and therefore the infected individual could benefit from the macrophages attacking the blood cells, there is also the possibility that hemophagocytosis benefits the infectious agent. Bacteria in hemophagocytic macrophages could access nutrients from the ingested cells, or hemophagocytic macrophages could reduce bacteria-killing activity by killing the very cells that could attack them. Yet, other macrophages could still be sufficiently activated to generate additional hemophagocytic macrophages (nix , detweiler) | + | The actual hemophagocytosis may be viewed as a result of overstimulated macrophages. While blood cells may harbour infectious agents and therefore the infected individual could benefit from the macrophages attacking the blood cells, there is also the possibility that hemophagocytosis benefits the infectious agent. Bacteria in hemophagocytic macrophages could access nutrients from the ingested cells, or hemophagocytic macrophages could reduce bacteria-killing activity by killing the very cells that could attack them. Yet, other macrophages could still be sufficiently activated to generate additional hemophagocytic macrophages. (({{pubmed> |
==== Relation to chronic infection ==== | ==== Relation to chronic infection ==== |