dove02
Forum Senior

Topics: 18 Posts: 126
| | 07/27/10 - 09:45 AM  
 
|   #1 |
Hi: Please if any one knows the concept of IgE hypersensitivity 1 & in hypersensitivity 2. Thanks in advance. Goljan 3rd edition in his 3rd chapter , page 40 has • Helminth in tissue is coated by IgE antibodies —> eosinophil lgE receptors attach to the IgE —> eosinophils release major basic protein, which kills the helminith"
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| indsha008
Forum Junior
Topics: 8 Posts: 60
| | 07/27/10 - 11:55 AM  
 
|   #2 |
Can u elaborate on what u exactly need to know ? The excerpt of RR Goljan what u have written is simply saying IgE binds to the helminths. Eosinophils have F(ab) receptors for IgE which ataches to the IgE (on helminth) -> this causes release of MBP -> toxic for helminth.
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| dove02
Forum Senior

Topics: 18 Posts: 126
| | 07/27/10 - 12:01 PM  
 
|   #3 |
Thanks for the reply, I wanted to know , how helminths killed by IgE by type one hypersensitivity and also helmiths get targeted by type 2 hypersensitivity ? Please explain the mechanism of both hypersensitivities killing helminths. Thanks.
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| indsha008
Forum Junior
Topics: 8 Posts: 60
| | 07/29/10 - 02:29 AM  
 
|   #4 |
Helminths are dealt with by our body only by type I hypersensitivity. Helminths are too big to be killed by other cytopathic or other immune processes. Hence, in helminth infection, there is class switching to IgE by Th2 cells as they secrete IL-4 -> B cells produce IgE -> IgE sits on mast cell and gets cross-linked -> degranulation of mast cell -> release of eosinophil chemotactic factor -> eosinophils are recruited and release MBP which is toxic to helminths.
This is the reason that in those helminthic infections in which helminths traverse blood vessels and migrate to various organs such as lungs, eosinophilia is seen.
There is no type II hypersensitivity involved in helminthic infection. Remember that, type II hyperesenstivity causes release of tissue-specific autoantibodies (IgG or IgM but not IgE). Hence, it will cause diseases like Goodpasture, Acute rheumatic fever, HDNB, etc.
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| dove02
Forum Senior

Topics: 18 Posts: 126
| | 07/29/10 - 11:43 AM  
 
|   #5 |
Thanks for the reply and responding in deltail. Please see page 40 of Goljan rapid review 3rd edition. He is explaining heminth killing by two mechanism .1: Type 1 hypersensitivity as you have described and the other by 2: antibody dependent cell mediated cytotoxicity. Type 2 hypersensitivity. Please , I am still confused b/c of goljan .
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| radoss
Forum Newbie
Topics: 8 Posts: 26
| | 07/29/10 - 07:59 PM  
 
|   #6 |
Hi,
I think both of you guys are partly correct. But my understanding of what Dr Gj told was, Eosinophils are NOT the primary mediators of Type 1 Hypersensitivity but only Mast cells and Basophils. But Eosinophils help to REGULATE (not mediate) type 1 Hypersensitivity reactions because they contain histaminase (that neutralizes Histamine) and arylsulfatase B that neutralize leukotrienes and thus help limit reaction following mast cell degranulation. They have Eosinophylic chemotactic factor.
Regarding helminths, I understand from UW Q bank that Eosinophils' defense against helminths is by Type 2 antibody mediated cytotoxicity (ADCC) which DOES NOT involve complement. i.e when a helminth enters the blood stream it is surrounded by IgE antibody. This pathogen (Antigen) and the IgE forms an Antigen/Antibody complex which gets attached to the IgE Fc receptor on the cell surface of the Eosinophil, which then releases 'Major basic protein' from its granule that eventually destroys and kills the helminths.
In a nutshell, Eosinophils' first response to Helminths' presence in the blood steam is via type 1 hypersensitivity but the mechanism by which they actually kill them is via type 2 hypersensitivity reaction.
I hope this helps but Please anyone can feel free to correct me if I am wrong.
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| radoss
Forum Newbie
Topics: 8 Posts: 26
| | 07/29/10 - 08:27 PM  
 
|   #7 |
Also, regarding the involvement of IgE in Type 2 Hypersensitivity reaction, They ARE involved in type 2 reactions but it DOES NOT involve complement, because only IgG and IgM can fix complement.
Indsha008 is right in saying that the helminths are too big to be phagocytosed but that's why Eosinophils destroy them by degranulation method. This is also the explanation for high IgE levels in parasitic infections (because helminths are surrounded by free IgE) and high eosinophil count (because many eosinophils are needed to release more Major Basic protein from their granules in order to kill the helminths.
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| dove02
Forum Senior

Topics: 18 Posts: 126
| | 07/30/10 - 03:24 PM  
 
|   #8 |
radoss : Thanks for the detailed explanation and clearing the concept.
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