The IgE system exists because the same events which lead to often-life threatening complications of allergy, in presence of parasites are helpful in their elimination.

The tissue injury mediated via this hypersensitivity (type I) occurs due to the mediators released by mast cell degranulation due to IgE being synthesised in atopic individuals towards normal environmental particles. The effects are also due to further immune cells being recruited by the mediators. In case of parasites, this IgE is supposed to help in their elimination and not cause tissue injury, justifying its evolution as a defence mechanism.

How does this happen? If release of the mediators is a part of the pathway, even if the degranulation is localised in the vicinity of the parasite, the mediators will spread systemically or atleast in the nearby tissues with the same consequences as in the case of non-parasite activation of these events.

What then is the ultimate cause beneath there being tissue injury if the stimulation is unintended but there being none when the stimulation is directed and intended? Or is there some injury in the latter case also, in which case the classification of this response in absence of a parasite into hypersensitivity i only because there is no positive effect in this case, while there was some benefit accompanying the deleterious effects in the former case? Is the presence of a parasite and possible localised degranulation the only difference between these cases?

  • $\begingroup$ I think it does help in case of the intestinal parasites. By purging them out. I am not too sure about it though. $\endgroup$ – WYSIWYG Nov 27 '15 at 14:53
  • $\begingroup$ IgEs are generated by B-cells as a result of activation and antigen presentation. They associate with Fc receptors of mast cells and it is only when IgE is bound to antigen that the degranulation can occur . In the case of parasites, the antigen on the parasite would have generated those specific IgEs. It is the specific binding of the IgE to the surface of the parasite that causes the Mast cell to degranulate directly onto the parasite. There may be some diffusion, but most will find its target. In allergy, IgEs are produced against harmless compounds and mast cells respond in appropriately. $\endgroup$ – AMR Nov 27 '15 at 16:11
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    $\begingroup$ Also is your BlockQuote a direct quote, in which case, can you provide the citation, or is it to highlight your question, it which case you should probably just use Bold Text? $\endgroup$ – AMR Nov 27 '15 at 16:13
  • $\begingroup$ @AMR Can you elaborate on "Find its target". Is not the effect of these mediators on vasculature and musculature the part of their anti-parasite effect? $\endgroup$ – stochastic13 Nov 27 '15 at 16:15
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    $\begingroup$ To answer the title: Histamine has a host of beneficial effects that assist the body in inhibiting and expelling parasites. Consider a parasite that's been ingested: (1) Histamine increases gastric H+ production, (2) promotes peristalsis, mucus production and vasodilation in the intestine. This causes bowel movements, diarrhea, and the mucus is a defense from the parasite. Of course, things tend to go overboard and mass degranulation does cause a lot of damage, but objectively the parasite is removed. The injury is largely unintended, or collateral damage. $\endgroup$ – CKM Nov 27 '15 at 19:01

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