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In the immunology section on pg. 223, it says splenic dysfunction = decreased IgM->decreased complement activation->decrease C3b opsonization->increased susceptibility to encapsulated bacteria.
I remember Goljan saying the splenic macrophages bind up IgG and C3b (extravascular hemolysis) while IgM in the blood causes intravascular hemolysis. Don't recall anything IgM-related to the spleen. I assumed this same mechanism accounted for why encapsulated bacteria clearance depends on the spleen. The capsule is tagged by IgG or C3b and then picked up by the splenic macrophages? I also recall in my school classes that the reason asplenic pts are susceptible to encap bacteria is because the capsule is only sensitive to IgG2 (special kind of IgG I guess) which is only made by the spleen. That was the explanation by my immunology teacher.
So, basically, I've heard different explanations on this. Which one is correct?
I remember Goljan saying the splenic macrophages bind up IgG and C3b (extravascular hemolysis) while IgM in the blood causes intravascular hemolysis. Don't recall anything IgM-related to the spleen. I assumed this same mechanism accounted for why encapsulated bacteria clearance depends on the spleen. The capsule is tagged by IgG or C3b and then picked up by the splenic macrophages? I also recall in my school classes that the reason asplenic pts are susceptible to encap bacteria is because the capsule is only sensitive to IgG2 (special kind of IgG I guess) which is only made by the spleen. That was the explanation by my immunology teacher.
So, basically, I've heard different explanations on this. Which one is correct?