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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 (

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13 Responses to Real examples of hypersensitivity reactions

  1. SALMA says:


  2. Kristine says:

    Yes – Hashimoto’s is an example of type IV. Even though there are antibodies present, the damage is mediated by T cells – so it falls into the type IV category.

    Here’s a great description I found on a USMLE forum:

    Type II hypersensitivity – Humoral antibodies participate directly in injuring cells by predisposing them to phagocytosis or lysis. Antibodies are directed toward antigents on cell surfaces. This can be complement-dependent, antibody-dependent cell mediated, or antibody-mediated cell dysfunction. Graves disease for example is antibody-mediated. Antibodes are directed toward TSH receptor.

    Type IV hypersensitivity – Tissue injury in which cell-mediated immune responses with senstized T lymphocytes are the cause of cellular and tissue injury. Delayed type is initiated by CD4 t cells. Cytotoxic is mediated by CD8 t cells. Hashimotos is a disease mainly reflective of T cell dysfunction. T cells are directed to the thyroid antigens with MHC. Activated T cells will either interact with B cells to secrete antibodies (antithyroid Ab) or the T helpers will promote CD8 formation. (This part is what confuses many, becuase T helpers are always percieved to be associated wih CD4, but it’s important not to forget the intricate mechanism. CD4 can use IL-2 to activate CD8). Autoantibodies in Hashimotos doesn’t arise until B lymphocytes are activated. Antibodies may play a role here but it’s important to know that T cells are what’s really emphasized. the role of T cells in this case supercedes the role of the antibodies.

    I hope this clears up any confusion.

  3. Big Al says:

    Amazing website
    thank you

  4. belete says:

    Thank you very much, it is very interesting, i know a lot from this.

  5. indri says:

    Very interesting…it makes me enjoy learning. Thsnk you very much

  6. rianne says:

    thank you so much! great help.

  7. Med Tech Intern says:

    The way you word things makes everything understandable, so much better than my textbook..thank you!

  8. elizabeth y kelley says:

    I am curious, would gout be an example of hypersensitive reaction 3? I am finding contradicting statements about it.

  9. Kristine says:

    Lupus and post-Streptococcal glomerulonephritis are probably the most common diseases caused by type III hypersensitivity. Here’s a post that lists a bunch of others.

  10. vetstudent says:

    u make things a lot of easier! 🙂 tq

  11. mamo says:

    thanks u ! for great help

  12. Ivy says:

    Thank you!

    I’m just a little confused about PSGN and Arthus reaction. They both seem pretty local and the Abs are just binding the Ag and having a reaction. Why aren’t they considered Type II?

  13. Kristine says:

    I think it is because it’s not just a 1:1 antibody:antigen binding – it’s complexes (multiple antibodies connected together by antigens), and it’s those complexes that do the damage. That’s just my take on it, though – I haven’t seen that question answered in textbooks…

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