Table 1.
Differences in the pathophysiology of anaphylaxis in murine models compared to humans (adapted from Turner and Campbell113)
| Murine models | Mediators and mechanisms | Humans |
|---|---|---|
| Polymeric IgA (low serum levels) IgD, IgE, IgMIgG1, IgG2a, IgG2b, IgG3 | Immunoglobulins | Monomeric IgA, 2 serotypes (IgA1, IgA2), IgA1 abundant in serumIgD, IgE, IgMIgG1, IgG2, IgG3, IgG4 |
| Yes | High‐affinity IgE receptor (FcεRI) on mast cells and basophils | Yes |
| No | FcεRI receptor on antigen‐presenting cells | Yes |
| Yes | IgE‐dependent anaphylaxis | Yes |
| Yes | IgG‐dependent anaphylaxis | No evidence for IgG‐mediated activation of human mast cells. If present, likely to require very high levels of antigen exposure |
| Very high: in murine models of peanut allergy, dose/weight equivalent to a human eating ≅1000 peanuts! | Allergen dose required through oral exposure to cause anaphylaxis | Very low doses (mgs), for example, for peanut allergy, 10% of individuals react to 1/70 of a peanut |
| + | Sensitivity to histamine | ++++ |
| Yes | Anaphylaxis inhibited by H1‐antihistamines | Little clinical evidence for this. Significant interspecies differences exist in histamine receptor pharmacology. |
| Yes | Basophils secrete Platelet Activating Factor (PAF) | Data inconsistent |