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A few hypersensitivity rxns questions

  1. Apr 21, 2004 #1
    Hey guys, I have a few questions regarding hypersensitivity reactions in the immune system. We covered the four types today, but I wrote down a few questions in my notes that I wanted to ask to verify my understanding of what we learned. I will ask the questions as statements of what I have learned to make sure I have no gaps.

    I appreciate if someone may reply with answers, or just to say if my understanding is correct.

    1. Ok, with regards to Type 2 (cytotoxic) rxns, we discussed how the blood type B is rare in Caucasians (European decent). This was because the organism that caused the (name?) plague had a surface antigen that was similar to the antigen on type B blood. This means that the body would recognize the plague organism as "self" and not attack it. The organism killed the people with blood type B, so that is why the type is rare. So how did the organism kill the people?

    2. This next part refers to Rh factor and hemolytic disease of the newborn. I have in my notes that blood ABO antibodies are IgM. What does this mean? I also have that Rh factor antibodies are IgG. I see that the IgM antibodies won't cross the placenta, but the IgG will (because of size?) Do the IgG antibodies (the anti-Rh antibodies) cross the placenta while the fetus is in utero? So the sensitization happens during the first child birth, and the anti-Rh antibodies cross the placenta during a 2nd pregnancy? What causes them to cross the placenta? Is this just after fertilization?

    3. What is the advantage of becoming sensitized to things? Like if someone has an allergy to saw dust. From what I know now, it seems like on their first exposure to sawdust that they would have no reaction. But on their second exposure they would have a Type 1 (anaphylactic) reaction. That means that each time they encounter sawdust, they would have the IgE's bound to basophils with the antigen on the IgE antibody, and then the basophils degranulate. What is the advantage of this? Is the basophil degranulation what gives the chemotaxis for the appropriate WBCs to come fight the foreign particle? From what I see, that is just harmful to the person, and that the sawdust is benign. I guess the advantage is that if the foreign body is a pathogen that you become sensitized to, that your body will fight it off.

    4. For things like bacteria, sawdust, penicillin, etc, anything that gets in your blood circulation that causes any type of reaction, where do these foreign objects leave the blood? What filters them out? How do they exit the body?

    5. In the text, it mentions that some people are allergic to penicillin. I thought penicillin (a fungus, right?) was some type of wonder drug? If it is, how does it help the body? The text states that penicillin is a hapten that must combine with a carrier serum protein. That makes it immunogenic. How does this help a person that is not allergic to penicillin?

    6. The text states that allergy desensitizations aim to cause the production of IgG antibodies rather than IgE antibodies. How does this happen? How does the repeated presence of an antigen gradually make IgG be produced over IgE?

    7. Where does all this fit in with the thing about if you get sick once with a disease (like chicken pox), that you can not get sick with it again? Why for some things if you are exposed once you are immune from it forever, but for other things if you are exposed a second time you could die (anaphylactic shock)? In addition, what makes a person hypersensitive to something whereas another person isn't?

    I thank you very much if you may help me out with these questions. I find this area really interesting, but I know my knowledge has huge, gaping holes in it. My professor this semester was, well, horrible. The only way to pass the class was to memorize his old tests that you had to get from people in previous semesters (this is true, his tests had probably 25% questions on material we didn't cover, and 15% questions on material we covered the days AFTER the test!!). But my professor had rheumatic fever and endocarditis. Had just had his bicuspid and aortic semilunar valves replaced. So,, we have a new guy, and now we are kind of learning!
  2. jcsd
  3. Apr 21, 2004 #2


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    The organism is called Yersinia pestis and the mechanism employed by the bactirium to kill is host is not fully understand but septicimia seem to be a part of it. The bacteria is not killed therefore it over mutiplies and cause cellular damage.

    Yes the size of Ig matters. IgM is a pentamer whereas IgG is a 150 kDa. IgG cross the when the fetus is in utero. Crossing of the placenta is done by diffusion because IgG is small and the crossing must start occuring after the umbilical cord is developed. Sensitization and crossing happens during the first pregnancy but during the 2nd pregnancy, the immune system reacts the antigen (crossing still occurs).

    You are not supose to be come oversensitized to things. Sometimes the immune system goes awire. You got most of the answers in your question. The basophil degranulation cause the release of factor that are chemotactic factors for eosinophils and neutrophils

    They get filter out by lymph node because during immune responce the blood vessel and the lymphatic capillary become dilated and the exchange of fluid is easier. The filter are usually macrophage (lymph nodes are full of them).

    Penicillin is antibitotic produce by the fungus Penicilium. Penicillin is good but again the immune system overreactes on occassion in certain individuals. Penicillin does not always combine to the serum protein sometimes it get to site of infection and attack the bacteria.

    Different immune responce are targetted. Hypersensitivity was cause by IgE but you can stimulate an immune responce that is byas toward IgG. IgG is present in your mucosa therfore it is the first Ig to be in contact with external factors. The immune reaction will be started at the IgG level and avoid the IgE reaction. Also there IgG is the most prominent Ig and IgE is least present. This desensitization does not always work. sometimes, immune memory disapear and you lose the hypersensitivity after a couple of years.

    Immune system memory such as memory T and b cells and cirulating Ig.

    Immune system over reacts because it is not perfect. Sometimes over reaction occure the first time. for many infection people die because the bacteria cause an over reaction. The immune system act with the principal "Kill first although i migth not get out of it".

    It is not fully understand why some people of hypersensitive but there migth genetic and environmental reason. Some people are more prone to develop an IgE responce and some have higher count of basophiles and esinophiles than the normal average. There is also the oversanitation of our household as an environmental factor.

    Edit is in bold.
    Last edited: Apr 21, 2004
  4. Apr 21, 2004 #3
    Hey ian smith!

    Thank you for that reply! That answered my questions, and has made clear a handful of points! My I ask what your area of exerptise is?
  5. Apr 21, 2004 #4


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    For now I study a bovine/ovine pathogen, so I have to know a bit about immunology. I also had to take two immunology class during my undergrad
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