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To my understanding, an allergic response is a non-adaptive response of the immune system to some molecule. The molecule in question is therefore "thought by the immune system" to be infectious although it is not. An allergic response is triggered by immunoglobulin of type E ($IG_E$) and causes an immune reaction.

I'd expect immune responses to not be instataneous, that is I would expect that it takes some time in order for the immune system to achieve some reaction peak. In consequences, I have been wondering whether someone that is under an allergic reaction is more resistant to early development of infectious disease because the immune system is already "switched on" prior to the infection. On the other hand, I would have thought that the body resistance to anything is lowered during an allergic reaction 1) because the allergy diminishes "general health" and 2) because allergic response may kill body cells.

Are we more/less resistant to infectious diseases during an allergic reaction?

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  • $\begingroup$ An allergic reaction is caused by by IgE antibodies - which are part of the adaptive immune system. When you are allergic, the reaction happens very fast after the exposure to the antigen. $\endgroup$ – Chris Dec 25 '14 at 11:57
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There are a number of issues with your question, and the short answer is no.

Immunity to pathogens is conferred by antibodies, but not usually of the IgE group. Pathogens usually stimulate IgM -> IgG; IgAs are present in mucosal surfaces.

There are multiple kinds of "allergic responses", and each carries its own risks.

  • Type I reactions (ie, immediate hypersensitivity reactions) involve immunoglobulin E (IgE)–mediated release of histamine and other mediators from mast cells and basophils.
  • Type II reactions (ie, cytotoxic hypersensitivity reactions) involve immunoglobulin G or immunoglobulin M antibodies bound to cell surface antigens, with subsequent complement fixation.
  • Type III reactions (ie, immune-complex reactions) involve circulating antigen-antibody immune complexes that deposit in postcapillary venules, with subsequent complement fixation.
  • Type IV reactions (ie, delayed hypersensitivity reactions, cell-mediated immunity) are mediated by T cells rather than by antibodies.

Limiting ourselves to allergic responses mediated by IgE, we have anaphylaxis, allergic asthma, urticaria, angioedema, allergic rhinitis, some types of drug reactions, and atopic dermatitis. These reactions can result in something as mild as urticaria or as life-threatening as anaphylaxis. None of these conditions carries an increased or decreased general immunological response to pathogens.

If allergy affected immunocompetency, one would expect to see, for example, an increased incidence of fungal infections in allergic individuals, but this is not the case. Allergy does not result in an immunocompromised condition, nor does it result in a primed response (an idea popular in the 90's). They are mediated by different pathways.

Effector mechanisms in allergic reactions
The production of IgE
Allergy, Parasites, and the Hygiene Hypothesis
Immunocompetence and allergy

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  • $\begingroup$ I also had this doubt once; is it not possible that there is a general hyperactivity irrespective of the antigen involved (Something like excess interleukin signaling. I don't know if there is a condition like that). $\endgroup$ – WYSIWYG Dec 27 '14 at 7:09
  • $\begingroup$ @WYSIWYG - There are 37? ILs now which do different things. If you're referring to autoimmune disorders, then yes, it's a "hyperimmune" IL- mediated response of a certain kind (or, better, kinds). That's a huge can of worms (or maybe chicken-and-eggs). Some kinds of autoimmune disorders carry an increased risk of infections, but this is usually due to tissue damage, not decreased responsiveness to pathogens. Maybe I'm not understanding the deeper issues here (more likely they're too complex for me). But I don't see much in the literature about protective effects with autoimmune disease. $\endgroup$ – anongoodnurse Dec 27 '14 at 7:42
  • $\begingroup$ Isn't allergic rhinitis compromising the mucociliary escalator? $\endgroup$ – abukaj Apr 9 '18 at 13:07
  • $\begingroup$ @abukaj - allergic rhinitis affects the nasopharynx, not the trachea, so, no. $\endgroup$ – anongoodnurse Apr 9 '18 at 14:08
  • $\begingroup$ @anongoodnurse I am sorry but I see no connection with trachea... One of causes of common cold is a malfunction of the escalator in nasopharynx due to a sudden change of temperature. Why then rhinitis has no similar effect? Or am I extrapolating meaning of the mucociliary escalator? $\endgroup$ – abukaj Apr 9 '18 at 14:25
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This is a very good question which is an active research topic! I can just say that we do not know the correct answer to it but we have some evidences that some allergies are connected with autoimmune diseases. You called this

1) the allergy diminishes "general health" and 2) because allergic response may kill body cells.

I would say that there can be a mechanism between allergies and autoimmune diseases.

  • IgE Mediated allergy to wheat in a child with celiac disease. There has been later found other cases on this but not published in PubMed. The link between coeliac disease and IgE-mediated allergy is not very clear. Pharmacological intervention with Montelukast (a leukotriene-antagonist) can possibly in all sorts of ways. However, research is going on about this because the mechanism is unknown.

I picked celiac disease here because it is been connected to many other autoimmune diseases and is the most undiagnosed disease. I consider Montelukast because its mechanism in IgE and because of its latest research findings with childhood asthma (about 2001), see this search in PubMed, and in successful treatment of opportunistic diseases in HIV/AIDS, see this publication.

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