The best part about visiting the farm without the boyfriend is that I get to cuddle with the cats. I have Nanner, a petite tortie, on my lap right now and Beezle, the black and white pigeon-eating monster, is making bizarre whistling noises a few feet away. I generally have to watch my cat exposure carefully, lest I convey cat dander to any of my cat-allergic friends.
Since the boyfriend actually like cats, I can conceivably talk him into allergy shots and then we could have a cat. How well do allergy shots really work? We learned about them briefly in immunology: the repeated introduction of small amounts of allergen gradually switch the immune response from TH2 to TH1. The TH2 path involves immunoglobulin E, which triggers histamine release and the well-known effects of allergy, ex. constricted airways, runny nose, swelling, etc. The TH1 pathway, on the other hand, has less drastic effects on the body, since the production of immunoglobulin switches from IgE to IgG. IgG does not trigger histamine release. In addition, T-cells that react to the specific antigen eventually become anergic.
Now if only all autoimmune diseases were so easy to understand, we'd be set.
Showing posts with label immunology. Show all posts
Showing posts with label immunology. Show all posts
Wednesday, January 13, 2010
Thursday, December 10, 2009
Hypersensitivies
Using the blog for notes today. (Why? Because. It's here. I like to try new note taking formats.)
Type I:
antibody: IgE
antigen: foreign
effector mechanism: Activation of mast cells and mediators
skin test is available
Time to onset: seconds to minutes
Examples of the disease: include hay fever and anaphylaxis.
Type II:
antibody: IgG and IgM
antigen: Cell or tissue antigens AND cell surface receptors work as antigens.
Effector mechanisms: Complement activation, which leads to phagocytosis; also, cell signalling altered by antibody.
No skin test available.
Minutes to hours for onset.
Examples of disease: transfusion reactions, autoimmune hemolytic anemia, pemphigus vulgaris, and some drug allergies.
Other diseases include Grave's disease, myasthenia gravis, and type 2 diabetes.
Type III:
antibody: IgG aand IgM
antigen: Immune complexes work as the antigen; they activate complement system and phagocytosis. "Why would phagocytosis or complement activation of immune defenses lead to tissue damage? Why is the pathology of mycoplasma immune-mediated? It's because mycoplasms are bound so tightly to the cells that the immune defense can't differentiate. It's bystander damage."
skin test: Arthus reaction (inject antigen and circulating antibodies bind, forming an immune complex and resulting in 'weal and flare').
Inappropriate immune response to antigen, and also excessive.
How do allergy shots, desensitization, work? Kicks the body into T helper 1 response, with IgG. This moves it away from TH2, where IgE activate mast cells for massive degranulation.
6-8 hours to see reaction.
Examples: rheumatoid arthritis, serum sickness, systemic lupus erythematosus (SLE). What is serum sickness? Let's say someone with hepatitis is discovered to have helped prepare food; everyone who ate some is given a massive dose of anti-serum to mop up the hepatitis. (And yes, I know hepatitis is technically just a word for unhappy livers)
Not all hypersensitivities are auto immune.
Type IV
Antibody: none
antigens: foreign, cell antigen...or cell associated.
Effector mechanism: macrophage activation by TH1, plus inflammation
Or CTL mediated cytotoxicity (and inflammation) (if antigen is cell associated).
Skin test: most certainly. It takes 48-72 hours (though the TB skin test in cattle can be nicely simulated in under an hour by using chicken blood cells. On the other hand, you can also induce anaphylaxis, hypersensitivity type I, with chicken cells...apparently reversible).
Examples: contact dermatitis, tuberculin reaction, type 1 diabetes, multiple sclerosis. CTL mediated: acute graft rejection ("omg alien invasion kill kill kill!" scream the CTLs)
Hemolytic disease in newborns: the mother makes antibodies to the fetal antigens (just think of the fetus as an allograft; this is why pregnant women are immunosuppressed). This is a problem for horses; the mare concentrates antibodies in her colostrum. The foal is born without any problems and nurses, and ingests what is essentially anti-foal colostrum. The complicated bit is that this doesn't happen with the first foal she has by that stallion; it takes that first pregnancy to introduce her immune system to the foreign genetics. By breeding her to a different stallion each time, she never builds up the antibody response. The other option is to feed the foal colostrum from a different mare. HOWEVER, the replacement colostrum should be from a mare on the same farm. Horses develop very localized immunity; the endemic pathogens of one farm are not the same as what may be endemic on a different farm.
Type I:
antibody: IgE
antigen: foreign
effector mechanism: Activation of mast cells and mediators
skin test is available
Time to onset: seconds to minutes
Examples of the disease: include hay fever and anaphylaxis.
Type II:
antibody: IgG and IgM
antigen: Cell or tissue antigens AND cell surface receptors work as antigens.
Effector mechanisms: Complement activation, which leads to phagocytosis; also, cell signalling altered by antibody.
No skin test available.
Minutes to hours for onset.
Examples of disease: transfusion reactions, autoimmune hemolytic anemia, pemphigus vulgaris, and some drug allergies.
Other diseases include Grave's disease, myasthenia gravis, and type 2 diabetes.
Type III:
antibody: IgG aand IgM
antigen: Immune complexes work as the antigen; they activate complement system and phagocytosis. "Why would phagocytosis or complement activation of immune defenses lead to tissue damage? Why is the pathology of mycoplasma immune-mediated? It's because mycoplasms are bound so tightly to the cells that the immune defense can't differentiate. It's bystander damage."
skin test: Arthus reaction (inject antigen and circulating antibodies bind, forming an immune complex and resulting in 'weal and flare').
Inappropriate immune response to antigen, and also excessive.
How do allergy shots, desensitization, work? Kicks the body into T helper 1 response, with IgG. This moves it away from TH2, where IgE activate mast cells for massive degranulation.
6-8 hours to see reaction.
Examples: rheumatoid arthritis, serum sickness, systemic lupus erythematosus (SLE). What is serum sickness? Let's say someone with hepatitis is discovered to have helped prepare food; everyone who ate some is given a massive dose of anti-serum to mop up the hepatitis. (And yes, I know hepatitis is technically just a word for unhappy livers)
Not all hypersensitivities are auto immune.
Type IV
Antibody: none
antigens: foreign, cell antigen...or cell associated.
Effector mechanism: macrophage activation by TH1, plus inflammation
Or CTL mediated cytotoxicity (and inflammation) (if antigen is cell associated).
Skin test: most certainly. It takes 48-72 hours (though the TB skin test in cattle can be nicely simulated in under an hour by using chicken blood cells. On the other hand, you can also induce anaphylaxis, hypersensitivity type I, with chicken cells...apparently reversible).
Examples: contact dermatitis, tuberculin reaction, type 1 diabetes, multiple sclerosis. CTL mediated: acute graft rejection ("omg alien invasion kill kill kill!" scream the CTLs)
Hemolytic disease in newborns: the mother makes antibodies to the fetal antigens (just think of the fetus as an allograft; this is why pregnant women are immunosuppressed). This is a problem for horses; the mare concentrates antibodies in her colostrum. The foal is born without any problems and nurses, and ingests what is essentially anti-foal colostrum. The complicated bit is that this doesn't happen with the first foal she has by that stallion; it takes that first pregnancy to introduce her immune system to the foreign genetics. By breeding her to a different stallion each time, she never builds up the antibody response. The other option is to feed the foal colostrum from a different mare. HOWEVER, the replacement colostrum should be from a mare on the same farm. Horses develop very localized immunity; the endemic pathogens of one farm are not the same as what may be endemic on a different farm.
Wednesday, October 7, 2009
Immunology, you're not my friend*
*to the tune of Rubber Ducky
I came to the conclusion half way through the immuno exam that the only way I was going to survive the post-exam anxiety was to not think about it. Actually, I have this nice rationalization about how the professors gave us absolutely no direction for studying, and the exam was written a bit erratically and may have completely missed important points (that I knew) while focusing on silly little things (that I may not have known) like whether the membrane attack complex uses C5b, C6, C7, C8, or if it uses C4a, C6, C7, C8. The latter incidentally, and I got it wrong. Same thing with convertases of the classical and alternative pathways.
So I made chocolate cake.
Then I came back to it, and now I see: How could I have been so foolish? The right answer was so easy to arrive at, and so completely necessary to a sound understanding of immunology!
After all, the pathway goes along the lines of:
C1 cleaves itself. C1s cleaves C2 and C4. C4 is now C4b. C4b and C2b make C3.
Meanwhile, C4b2b cleaves C3!
C3b joins C4b2b to be C4b2b3b...did we mention C5 yet? Well, OBVIOUSLY C4b2b3b cleaves C5, and now we have C5b, which clearly shows why the answer to the other question was C5b, C6, C7, C8, and C9. And since this was the classical pathway, that's why you were wrong. The alternative pathway uses C3bBb. That's a B, not a 2. (sheesh, get it right)
But I was a silly student and didn't realize that we were supposed to know the alphabet in this new, convoluted form. I just had it summarized in my notes as "Legos."
Probably it would help if our prof used something other than the detailed diagrams from our textbooks. Lecture becomes exponentially harder to follow when you don't know which part of the twenty-piece jigsaw you're on.
(In case you were wondering what this was all about, the C#letters are tiny molecules in your bloodstream that eventually assemble themselves into the molecular equivalent of an awl, and then they go punch holes in bacteria. It's wonderful.)
Meanwhile, C4b2b cleaves C3!
C3b joins C4b2b to be C4b2b3b...did we mention C5 yet? Well, OBVIOUSLY C4b2b3b cleaves C5, and now we have C5b, which clearly shows why the answer to the other question was C5b, C6, C7, C8, and C9. And since this was the classical pathway, that's why you were wrong. The alternative pathway uses C3bBb. That's a B, not a 2. (sheesh, get it right)
But I was a silly student and didn't realize that we were supposed to know the alphabet in this new, convoluted form. I just had it summarized in my notes as "Legos."
Probably it would help if our prof used something other than the detailed diagrams from our textbooks. Lecture becomes exponentially harder to follow when you don't know which part of the twenty-piece jigsaw you're on.
(In case you were wondering what this was all about, the C#letters are tiny molecules in your bloodstream that eventually assemble themselves into the molecular equivalent of an awl, and then they go punch holes in bacteria. It's wonderful.)
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