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I had saved this information on my computer in 2014, just found it, and wanted to share it.
The genetic marker:  HLA-B27 is a MHC (Major histocompatibility complex) class I 
molecule consisting of an alpha chain encoded in the MHC region on chromosome 6 
and a non-MHC encoded beta chain I32 microglobulin, and  is highly recognized as 
being associated with certain Rheumatic and Inflammatory Autoimmune Conditions.
Similar information, statistics, geographical similarities and other associations between Rh- individuals and many of the various Autoimmune Conditions.
According to Randall Johnson at the Baylor College of Medicine in Houston, “Only 7% of the US population tests positive for the HLA-B27 gene;  this gene, found only in persons with Rh- blood, can trigger the immune system to operate overtime at WARP SPEED in times of medical emergency.”
Can the HLA-B27 genetic marker be found in Rh+ individuals?
Autoimmune diseases are disorders where the primary cause is an inflammatory
reaction caused by the body’s own immune system attacking the body’s own tissues. 
It has been established that the Rh- factor can be recessive, but it does not disappear. Where do the Rh- cells, that one without the Rh protein go to hide within the body? Could this incompatibility be the result in Autoimmune diseases?  Recessive Rh- blood cells do not just morph into Rh+ blood cells because if they did, a parent could not pass it down from their recessive gene pool.
What is the relationship of Rh- and HLA-B27 Positive?
The HLA profile defines the cells from an individual or “self”, distinguishing them from those from other individuals showing a different HLA profile “non-self”.
Autoimmunity is the failure of an organism to recognize its own constituent parts as “self”, which allows an immune response against its own cells and tissues.
Knowing our true blood type and factors makes a big difference to our health.
This information led me to 23andme.com, looking for the HLA-B27 genetic marker.  My search brought up no results, so I typed in A- Blood.  This search led me to the following information:
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Non-ABO Blood Groups
Most people think of their blood type as A+ or O- (or some other combination of A, B, O, +, and -) but there actually are more than 25 different blood groups that go into your particular "type." All of these blood groups can be important in the event that you need a blood transfusion. Blood type is also important during pregnancy—some types of mismatch between mother and fetus are potentially dangerous to the developing baby. In both cases, reactions to mismatched blood happen because the immune system can't tell the difference between foreign red blood cells and dangerous foreign cells like bacteria.
The following results are based on  Established Research for 4 reported markers.

My Genotype Genetic Marker  rs2285644  is GG   di(a-b+)  on the SLC 4A1 Gene.
The SLC 4A1 determines the "Diego" blood group.

Blood type is high heritable.  Each of the different blood types are determined by genotype at just one or two SNP's.  The Diego, Kidd, and Kell blood types are inherited in a codominant manner.  This means the red blood cells of heterozygotes actually present two different versions of a protein on their surface.  (For example, Diego heterozygotes have the Di)a+b+) blood type - their blood cells have both Di(a) and Di(b) proteins. 

The SLC4A1 gene determines the "Diego" blood group.  It makes a protein that transports ions in and out of red blood cells and plays an essential role in enabling the red blood cells to transport the waste product carbon dioxide to the lungs, where it can be removed from the body.  The different versions of the SLC4A1 protein are call Di(a) and Di(b).  A single SNP that changes the protein sequence determines which one of these blood group antigens will be made.  Immune responses to blood mismatched for the Diego blood group can cause moderate to severe transfusion reactions and mild to severe hemolytic disease of a newborn.
The Diego blood group is interesting to anthropologists because the distribution of the various blood types is different in diverse populations from around the world.  The Di(a) version of this blood group is mainly found in populations of Mongolian descent.  It is found in 36% of South American Indians, 12% of Japanese, and 12% of Chinese, but is rare in Caucasians and Blacks (0.01%).  Interestingly, the Di(a) antigen is less rare in the Polish population (0.47%) compared to most Caucasian populations (0.01%).  This may reflect the invasion of Poland by Tatars (who have Mongolian heritage) many centuries ago.  The Di(b) blood group antigen is found in almost every population.  Frequencies of the Diego blood types:
Di(a-b+) is found in more than 99.9% of Europeans and Africans and >90%of Asians.
Di(a+b+) is found is less than 0.1% of Europeans and Africans and in 10% of Asians.
Di(a+b-) is found in less than 0.01% of Europeans, Africans and Asians.

Di(a-b+) is found in more than 99.9% of Europeans and Africans and >90% of Asians.
Di(a+b+) found in less than 0.1% of Europeans and Africans and in 10% of Asians.
Di(a+b-) found in less than 0.01% of Europeans, Africans, and Asians.
My Genotype Genetic Marker  rs8176058   is GG K-k+ for the KEL Gene.

The KEL gene determines the Kell blood group.  It encodes a protein that cuts another protein called endothelin-3, producing a short form of endothelin-3 that causes blood vessels to constrict.  Several different antigens are determined by the KEL gene. (23andMe reports data on 2 of these.)  SNP  rs8176058 determines the K/k antigen.  SNP rs817059 determines the Kpa/Kpb antigen.  In both cases the SNPs are affecting the sequence of the protein made by the KEL gene.
Immune responses to blood mismatched for the Kell blood group can cause severe transfusion reactions and severe hemolytic disease of the newborn (reactions against K are stronger than against k, Kpa, or Kpb).  In the case of hemolytic disease of the newborn, the mother's antibodies prevent red blood cells from being made in the fetus.
The k version of this blood group antigen is much more common than the K version in most populations.  The K-k+ blood type is found in 98% of Africans and 91% of people of European ancestry.  25% of people with Arabic ancestry have the K version on their red blood cells.  The Kp(a-b+) blood type is found in 97.7% of Europeans and 100% of Africans.
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My Genotype Genetic Marker  rs1058396 is GG k(a+b+) on SLC14A1 Gene.
The SLC14A1 Gene determines the Kidd blood group.
This gene encodes a protein that transports a chemical called urea in and out of red blood cells, keeping the ion concentration of the cells balanced, and maintaining the shape of the red blood cells.  The different versions of the SLC14A1 protein are called Jka and Jkb.  A single SNP that affects the protein sequence determines which one of these blood group antigens will be made.
Immune responses to mismatched blood for the "Kidd" blood group can cause moderate transfusion reactions and mild hemolytic disease of the newborn.  In fact, the reactions are so mild that antibodies against Kidd blood group antigens can be difficult to detect when a doctor does a cross-matching test, so transfusion reactions due to Kidd group mismatches end up happening more often that with other blood groups.

23andme use a set of 11 SNPs in the ABO gene to determine our ABO blood type:
rs8176719, rs1053878, rs785389, rs8176740, rs8176743, rs8176746, rs41302905, rs41302905, rs8176747, i4000504, rs8176749, i4000505.
However, there are many other mutations and deletions in the ABO gene that can affect blood type.  If you have one of these more rare mutations, your actual blood type could be different than that predicted by these SNPs.
It often takes more than a single mutation to differentiate between the A, B, and O versions of the ABO gene.  This complicates the analysis of probable blood type.  Take for example, a SNP that distinguishes between the A and B versions of the gene.  If you have a copy of the "A" version from parent and a copy of the "B" version from the other parent, it would seem obvious that you have type AB blood.  But if you also have a variant that indicates an O version of the gene (O SNPs make the protein encoded by the ABO gene non-functional, effectively cancelling out A and B versions), things get complicated.  That "O" SNP could be in the A copy of the gene, or the B copy of the gene.  In the first case, you would be "B/O", or type B.  In the latter case, you would be "A/O", or type A.
Knowing for sure which versions of different SNPs are in the same copy of a gene thakes complicated calculations that 23andMe does not currently perform.  To make this experimental feature work, 23andMe has implemented a simplified version of the procedure, which is known as phasing.  However, this method may introduce errors into your predicted blood type.
There are multiple subtypes of the A,B,  and O families.  My data indicates that I probably have either the subtyp
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Went to the hospital today for RA meds blood work.  Went to see Dr. McMath at 10:30, and picked up the Zocor Dr. Hall had prescribed.  Worried about starting it, but I guess if my cholesterol is so out of wack, I need to do something.  
Later tonight, Ron and I met Ron and LeeAnn at Casey's Pizza and we got to meet Darren McCarty.
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My Dr. appointment was at 9:45, but I arrived at 9:35.  Didn't even get back to see him until 10:00, and sat in his room for another 1/2 hour.  He came in at 10:30.  Asked him if I could get out of my pain management contract for Norco so I could have Dr. VanDellen prescribe it for me.  He is so Frustrating, but on a good note, today was his last day at this office.  Thanks for the heads up Doc.  Whatever.  I never liked him anyway.  So I left there at 10:50.  Was late for my chiropractor appointment which was at 10:45, but I went and got in right away.  I Felt So Much Better after seeing Dr. McMath.  I Always Do!  Don't know what I would do without Dr. McMath!
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I have always loved the taste of watermelon, but watermelon has never liked me.  And to be honest, I believe that Watermelon could have been the trigger to my auto immune response which led me to being struck done with Rheumatoid Arthritis over 25 years ago.  Here is some interesting information about watermelon:

 The lycopene in watermelon is a well-documented inhibitor of many inflammatory processes, including the production of pro-inflammatory messaging molecules, the expression of enzymes like cyclo-oxygenase and lipoxygenase that can lead to increased inflammatory response, and the activity of molecular signaling agents like nuclear factor kappa B (NFkB).  Lycopene is also a well-known antioxidant, with the ability to neutralize free radical molecules.
 
One study showed red watermelon to contain over 600 micrograms of beta-carotene per 3.5 ounces of melon and over 6,500 micrograms of lycopene.

Watermelon is a unusual fruit source of the carotenoid lycopene and a rich source of phenolic antioxidants.  Watermelon containscucurbitacin E, a triterpene anti-inflammatory phytounutrient, and unusual amounts of the amino acid citruline.

Citrulline is alpha amino gamma ureidovaleric acid.  It is formed from ornithine and takes part in the synthesis of urea.  It donates one of its nitrogen for the systhesis of urea.  Arginine is synthesized from citrulline in presence of aspartic acid, ATP and Mg ++ Citrulline  is found in high concentration in the liver.  Citrulline is not a component of any major proteins or enzymes.

In the mitochondria, the ‘power house’ of cells, ammonia combines with carbon dioxide and ornithine to form citrulline.  Citrulline is then transported out of the mitochondria into the cytoplasm where it is then converted to yet another amino acid called arginine. Thus citrulline is essential to detoxify and remove ammonia from muscle and liver cells.

Citrulline is a non-essential amino acid and plays a role in nitrogen balance and
metabolic processes.  Although not a component of most proteins in the body, citrulline is found in some specialized proteins in the hair, skin and neural cells.  It is primarily synthesized from glutamine in the intestines but is also found naturally in trace amounts in some foods.

Citrulline supplied by the diet is efficiently absorbed from the stomach and enters the blood via the major vein draining the digestive system that empties into the liver.  Much of it bypasses uptake in the liver and is then circulated for distribution to the kidneys, brain, muscle and other tissues for conversion to arginine.
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Left today at 7:15 to go to Dr. Frascones.  I arrived at 8:15 even though my appointment was at 8:45, and got right in.  Had shots in both feet. The right one hurt, but not as bad as yesterday's transferaminals, so I was happy.  Came right home, and vacuumed the living room and kitchen.
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Lori came to pick me up at 11:15 and drove me to Dr Turk's to have Dr. Schuato give me my second series of Transferaminals.  We arrived at 11:30, so had time to go to his other office to pee in a cup and get my Norco prescription, then to the other office to have the shots.  I know the injections help, but they sure do hurt!  After getting them, Lori brought me to the pharmacy so I could get my script filled, the home.  Felt good when I got home, just sore.  But I vacuumed the entry and fireplace rooms.
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Arrived at Dr. Frascone's at 9:00.  Appointment at 9:15.  Shots in both feet again, but they didn't hurt at all.  Nothing compared to yesterdays.  Right foot burned afterwards, but I know the shots are working.

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My name is Karen.  I was diagnosed with Rheumatoid in the fall of 1990 when I was almost 22 years old.