carmenburana
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C3b???
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| bm
Forum Elite
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disease?
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| carmenburana
Forum Newbie
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You've stumped me, bm. I looked it up in a bunch of places with no luck. I just remembered that C3b is responsable for the appearance of opsonization receptores on phagocytes. C3 deficiency is asoc with recurrent pyogenic infections (sinus, ear, resp tract).
What's the answer?
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| bm
Forum Elite
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sorry about that. i encountered it in nbme. i'm thinking that it might be SCID.
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| meghana jadhav
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hey bm
as t and b cell r normal how can we say SCID
can it be severe liver disease in which comlement formation is not there...
just want to ask????
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megha
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| bm
Forum Elite
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not sure. here are the choices:
a)affinity maturation of Ig
b)immunoglobulin isotype switching
c)recombination of heavy chain variable region genes
d)recombination of light chain variable variable region genes
e)somatic mutation of Ig genes
as i don't know what dse they're refering to, i don't know which one is correct :cry:
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| mani
Forum Guru
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i would say "A" bcoz pt cannot make IgG (that is an opsonin". but there is some information missing in the question stem. I have a similar question that mght be helpful:
A 5 y/o boy with a hx of recurrent ear infections receives his preschool booster immunization of DTP. He is participated in a community-sponsored study to determine the humoral immune response to tetanus toxoid (tt). His response is well below normal for age- & sex-matched children. Peripheral B & T lymphocyte count and function are within the reference range. The antibody he makes is positive in both the passive hemagglutination and complement-mediated lysis of tt-coated erythrocytes. His antibodies do not opsonize tt-coated latex particles for phagocytosis and do not directly precipitate tt efficiently. This child most likely has a defect in which of the following processes?
A.) Affinity maturation of immunoglobulins
B.) Immunoglobulin isotype switching
C.) Recombination of heavy chain variable region genes
D.) Recombination of light chain variable region genes
E.) Somatic mutation of immunoglobulin genes
Since complement is activated, it could be IgG or IgM. But since it does not opsonize, the antibody he is producing is only IgM. So I think the answer is B.
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| mani
Forum Guru
Topics: 104
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i would say "A" bcoz pt cannot make IgG (that is an opsonin". but there is some information missing in the question stem. I have a similar question that mght be helpful:
A 5 y/o boy with a hx of recurrent ear infections receives his preschool booster immunization of DTP. He is participated in a community-sponsored study to determine the humoral immune response to tetanus toxoid (tt). His response is well below normal for age- & sex-matched children. Peripheral B & T lymphocyte count and function are within the reference range. The antibody he makes is positive in both the passive hemagglutination and complement-mediated lysis of tt-coated erythrocytes. His antibodies do not opsonize tt-coated latex particles for phagocytosis and do not directly precipitate tt efficiently. This child most likely has a defect in which of the following processes?
A.) Affinity maturation of immunoglobulins
B.) Immunoglobulin isotype switching
C.) Recombination of heavy chain variable region genes
D.) Recombination of light chain variable region genes
E.) Somatic mutation of immunoglobulin genes
Since complement is activated, it could be IgG or IgM. But since it does not opsonize, the antibody he is producing is only IgM. So I think the answer is B.
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| whereami
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I think it's B, too.
On a related note, IgM may not participate in opsonization, but it can still cause complement-mediated lysis.
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| Malaysian
Forum Guru
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Hi I wanted to ask you....which Ig activates the complement.....and which component of the comPliment?If I'm not mistaken Ig M and G activate it.....am I on the right path?
From the question above I get the impression that the Fab part of the Ig is fine but the Fc portion is not functioning properly.The reason why I feel it isn't class switching is because you still would have got precipitation of the tt right?Can it be somatic mutation of the Ig gene.....involving the C region of the chromosome?
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| Dr. Hussam
Forum Junior
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the question is describing Hyper IgM disease, in which there's a defect in isotype switching of Ig.
the scenario describes that the complement can be activated but opsonization isn't taking place, which means that IgG is absent and IgM is present.
so the answer is B
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