canola fields

Sometimes we (okay, I) get so caught up in describing pathologic mechanisms that real-life examples get the short end of the stick. Let’s look at some real diseases in which the underlying problem is a hypersensitivity reaction.

Type I (allergic) hypersensitivity
The big example (obviously) of this type of hypersensitivity is allergy. Pollen, cat dander, peanuts – they all have the same mechanism and this is it.

Type II  (antibody-mediated) hypersensitivity
There are a ton of diseases that have an underlying type II hypersensitivity reaction going on. Here’s a partial list:

1. Autoimmune hemolytic anemia: the patient makes antibodies to red cell antigens for some reason (not a good thing to do) which end up causing hemolysis.
2. Pemphigus vulgaris: the patient makes antibodies against the proteins connecting epithelial cells together, resulting in epithelial cell discohesion and bullae formation.
3. Goodpasture syndrome: the patient makes antibodies that react against proteins in both the glomeruli and the alveoli, leading to nephritis and lung hemorrhage.
4. Myasthenia gravis: the patient makes antibodies that bind to the acetylcholine receptor (on the muscle end plate), preventing acetylcholine from binding and doing its job; the end result is muscle weakness.
5. Graves disease: the patient makes antibodies that bind to the TSH (thyroid-stimulating hormone) receptor on thyroid epithelial cells, causing excessive stimulation of the receptor (just the opposite of what happens in myasthenia gravis!), leading to excessive production of thyroid hormone (hyperthyroidism).

Type III (immune-complex-mediated) hypersensitivity
There are a ton of diseases in this category too.

1. Lupus: the patient makes antibodies that bind to certain nuclear antigens; complexes lodge anywhere they please but especially in the kidneys, skin, and joints.
2. Post-streptococcal glomerulonephritis: in fighting a strep infection, the patient makes an antibody that reacts against the strep bug but also cross-reacts with some antigen in the glomerulus; antigen-antibody complexes lodge there and cause nephritis.
3. Serum sickness: after injection of foreign proteins into the patient (e.g., like they did in the old days when they used horse serum in vaccines!), the patient makes antibodies against the foreign proteins, and the resulting complexes lodge anywhere they want, but especially in the joints, kidneys, and vessels.
4. Arthus reaction: after injection of foreign protein into the skin, the patient (the original patient in Arthus’ 1903 experiments was a poor little bunny – but the same thing happens in humans) makes antibodies against this protein, and the resultant complexes stay in the skin, eliciting a nasty localized vasculitis and a big owie on the skin.

Type IV (T-cell-mediated) hypersensitivity
There are two kinds of this one (after all, there are two kinds of T cells!).

Delayed-type hypersensitivity
A good example of this is poison ivy exposure (patient gets exposed to poison ivy, helper T cells respond and some become memory cells; upon repeat exposure the memory T cells rush to the site, activating macrophages and causing inflammation). Another example is the Mantoux test; same principle.

T-cell-mediated cytotoxicity
Type I diabetes is a good example of this one. In this disease, cytotoxic T cells kill pancreatic islet cells. That’s not very nice. They are supposed to be killing infected cells, or tumor cells – not the patient’s own normal cells.

Photo credit: Joe Shlabotnik (