Here’s a summary of those four pesky hypersensitivity reactions you will definitely be asked questions on at some point.
Sometimes, the best way to remember things is to boil them down to as few words as possible. For the hypersensitivity reactions, here’s what that might look like:
Type I – allergy
Type II – antibodies
Type III – immune complex
Type IV – T cells
Here’s a little more information:
Type I hypersensitivity is the mechanism underlying the classic allergic response. It’s also called “immediate” hypersensitivity, which makes sense to any allergy sufferer (as soon as you start petting the cat, you start sneezing). It’s caused by an antigen (from an allergen, like cat dander) binding to IgE antibodies that are bound to the surface of mast cells. The antigen bridges the IgE antibodies, triggering release of nasty mediators (like histamine) from the mast cell. The end result: vessels dilate, smooth muscle contracts, and inflammation comes in and makes itself at home.
Type II hypersensitivity is also called “antibody-mediated” hypersensitivity. Which is kind of misleading, because it’s not the only type of hypersensitivity reaction that involves antibodies. Oh well. In this type of hypersensitivity antibodies bind to antigens on a cell surface (any cell surface). Macrophages come in and eat up the cells (they think the Fc fragments of antibodies are yummy). Complement gets activated, inflammation comes in (harming tissue) and cells end up dying. Examples of this type of hypersensitivity include: autoimmune hemolytic anemia, pemphigus vulgaris, Goodpasture syndrome, myasthenia gravis, and Graves disease.
Type III hypersensitivity is also called “immune-complex-mediated” hypersensitivity. In this one, antibodies bind to antigens, forming complexes. These antigen-antibody complexes circulate (either throughout the whole body, or within one area of the body), get stuck in vessels, and stimulate inflammation, the end result being inflammation-mediated tissue damage and necrotizing vasculitis. Examples of this type of hypersensitivity include: systemic lupus erythematosus, post-streptococcal glomerulonephritis, polyarteritis nodosa, serum sickness, and the Arthus reaction.
Type IV hypersensitivity is also called “T-cell-mediated” hypersensitivity. This type of hypersensitivity has two subtypes. In one subtype, called delayed-type hypersensitivity, helper T cells secrete cytokines that activate macrophages (which eat the antigen) and induce inflammation (which damages tissue). A good example of delayed-type hypersensitivity is poison ivy. The other subtype, called T-cell-mediated cytotoxicity, involves cytotoxic T cells coming and killing target cells (like the cells of a transplanted organ, or the pancreatic islet cells in a patient with type I diabetes).
Thanks for making easy to remember…so much easier than my text books..
Awesome! Very clear & concise. Thanks!
These are the best kinds of posts in my opinion. This, nephrotic vs nephritic kidney disease, cardiac biomarkers, etc. So clear and so succinct. Keep them coming!
Nice work,,,,,,,keep the goodwork
made very simple and precise,easy to understand.Remarkable
much easier to learn and understand this complex topic
good n precise work…
thanks for making this lesson interesting
to me. I found it difficult when the tutor was lecturing.
Thanks for this nice intresting presentation.
Thank very much, Æ”â˜ºu made it much easier to understand and remember…
so simple and so easy to understand.thanks
Real nice.. especially for my immunology CAT this morning!
You’ve made it so easy to understand, Am using it in my assignment.
Great! Glad it was helpful!
Precise and concise.God bless!
Hi! My classmates and I were given a case study where a 10 year old patient was diagnosed with Diabetes–Type One and we were asked to determine the type of hypersensitivity the patient had. I guessed type 4 but we were told it was type 2. I read above that it is in fact, type 4. I just wanted to see if anyone could provide an explanation as to why it is type 4 so I can share the info with my group mates? Thanks so much!!
Hi Rahwa – You’re correct: type I diabetes mellitus is mediated by a type IV hypersensitivity reaction. There is a table on page 209 of the new Robbins (9th edition) that lists type I DM under type IV hypersensitivity. The basic mechanisms is destruction of the islet cells by cytotoxic T cells (so it’s an example of T-cell mediated cytotoxicity). The cytotoxic T cells appear to react with antigens on the beta cells of the pancreatic islets, including insulin and glutamic acid decarboxylase. Hope that helps!
Am a Ghanaian , this explanation has really helped me thanks very much
I’ve watched videos, read my textbook and listened to my professor and I still didn’t quite understand this concept. I do now. Thank you!
Great! I’m so glad it helped! A couple more posts that might also help are: Real life examples of hypersensitivity reactions and Are all autoimmune diseases caused by hypersensitivity reactions?.
Wow! Thanks! In NP school — doing pharm, and once again faced with some type of hypersensitivity reaction and thought, “Oh, Godâ€¦which one is that again?” So decided to Google it to refresh my memory, and found this site. I will bookmark, for sure! Have no idea why these concepts, which are not the least bit hard to grasp, are so rarely explained with clarity and precision. Thank you!
Thanks, Julia!! So glad you found it and it was helpful 🙂
this helped me in my microbiology/immunology final exams. thank you
Wow! Good thing I found this! Really helped me a lot! Thanks
thank you, (^_^) it was very helpful
Yay! Glad you liked it! Cute kitty 🙂
Thanks so much…..was really helpful for my seminar work……
Dope!! I love your summary….keep it up
Very simple way to explain. Specifically one word for each hypersensitivity.
simple and brief description, you made the sub-topic easier than in module