"red cell antigens cause the production of antibodies"
and
"In general, antigens are composed of carbohydrates, lipids, and proteins, usually a combination of any two. For example, ABH antigens are glycosphingolipids (sugars attached to a lipid backbone) and glycoproteins (sugars attached to a protein backbone)
Rh antigens are lipoproteins."
As many of you may already know...if a mom is Rh negative and her baby is Rh postitive, she forms antibodies to the fetus and can kill it in utero.
So...they give IgG.
"IgG anti-D antibodies "
Now...about IgG...
Here is another GREAT interactive website to help understand the differences between our 2 major immune system pathways:
"Prior exposure to uninfected vector ticks protects residents of disease-endemic sites from Lyme disease."
Why?
(Watch carefully for the mention of IgE below.)
"These observations suggest that residents of disease-endemic sites who experience persistent tick-associated itch are less likely to develop Lyme disease than are those who do not experience this reaction.
Itch was reported at the site of tick bite, and the frequency of itch increases as the number of reported tick bites increase, which strongly suggests that tick-associated itch is associated with an acquired cutaneous hypersensitivity response.
Such a relationship has definitively been established in the case of I. ricinis, the European analog of the North American deer tick.
After having been bitten by these ticks repeatedly, persons experience both immediate and delayed cutaneous hypersensitivity reactions.
They express tick-specific IgE antibodies, as well as dermal and perivascular infiltrates of CD8+ T lymphocytes and Langerhans' cells (13).
Additional studies of other tick species also suggest that tick-associated itch is mediated by tick-specific antibody or cellular infiltration (12,18,19).
People in our study who reported a single episode of tick-associated itch were more likely to acquire Lyme disease than those who did not report itch, probably because tick-associated itch is a marker for tick exposure.
In contrast, persons who had repeated tick-associated itch were protected from developing Lyme disease.
We are confident, therefore, that the people in our study who described repeated episodes of tick-associated itching were experiencing cutaneous hypersensitivity and that this immune reaction protected them from acquiring Lyme disease."
Don't wait for someone to take you under their wing. Find a good wing and climb up underneath it~ Frank C. Bucaro Posts: 80 | From Desert Southwest | Registered: Nov 2006
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Marnie
Frequent Contributor (5K+ posts)
Member # 773
posted
I was hoping it would be simple...!
"The Rh(D) antigen is inherited on one locus (on the short arm of the first chromosome, 1p36.13-p34.3)
with two alleles, of which Rh+ is dominant and Rh− recessive .
The gene codes for a polypeptide on the red cell membrane. Rh− individuals (dd genotype)
do not produce this antigen,
and may be sensitized to Rh+ blood."
I was wondering if the dd genotype gave Rh negative persons some "added protection".
It appears the "allergic response" is more "protective" i.e., IgE, in the long run.
Histidine (in Zinc fingers)...converting to histamine?
What's missing?
Posts: 9424 | From Sunshine State | Registered: Mar 2001
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posted
I am also Rh neg and my son is Rh pos. I had to get the shot after I had him. I always felt like the Rh-/Rh+ thing set me up for a worst case of autoimmune problems. Just another trigger in the DR4 picture.
Posts: 315 | From USA | Registered: May 2005
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I got the Rhogam shot after my children were born--my husband is A+, so is my daughter. My son is 0+.
I tested positive on a RAST for allergies (it tests for specific IgEs) and also had extensive skin reactions to testing in 2005 before I realized that my symptoms WEREN'T from allergies.
Later in 2005, my total IgE tested well within normal range.
I did experience itching at my EM site in 1989, although it was more of a burning, irritating feeling.
My HLA testing was negative for DR4, although my mother had RA and I always test positive for RA factor.
I do have "Lyme knees" and skin problems, but most of my symptoms are neurological.
Posts: 353 | From Florida boonies | Registered: Nov 2005
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posted
I am blood type O-. I received the Rhogam shot after my children were born.(starting in 1977) I am HLA positive for DR4.(recent test) Tested positive for Lyme first time with PCR '04 Misdiagnosed for 20+ years. CD 57 is 1. White blood cell count dropped from 8.4 to 3.7 since sept.'05.
-------------------- Corinne Posts: 529 | From Raleigh, NC | Registered: Jun 2006
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posted
B- here...had the shot after ectopic preg then again later after 1st daughter who is rh+; second daughter is also B-....and also a Lymie. Can't remember if I got a 3rd shot after misscarriage which was my last preg - but I'm assuming I must have.
Both of us had EM rashes - hers was small & pale, maybe the size of a plum & no itching....mine was huge,hickey red/purple & close to frizbee size - itched like crazy.(Let me take a moment to personally thank Dr General Practioner who gave me that steroid cream!)
Neither of our rashes was the typical bullseye.
Of course being young teen daughter hasn't had any pregnancies so she has never had the shot, if this is significant.
Hope this helps w/ your research, Marnie.
Now if I may ask - what does this all mean? You are way smarter than me & I have too much of a headache to try to comprehend it. (Friends funeral today-on emotional overload)...
If you pretend your explaining it to a 6th grader, I'll prolly be able to grasp it!
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