Rh blood group system
This system is based on the theory that there is one gene at a single locus on each of the two copies of chromosome 1, each contributing to production of multiple antigens.
The CDE notation used in the Fisher–Race nomenclature is sometimes rearranged to DCE to more accurately represent the co-location of the C and E encoding on the RhCE gene, and to make interpretation easier.
The allele was thus often assumed in early blood group analyses to have been typical of populations on the continent, particularly in areas below the Sahara.
Ottensooser et al. (1963) suggested that high R0 frequencies were likely characteristic of the ancient Judean Jews, who had emigrated from Egypt prior to their dispersal throughout the Mediterranean Basin and Europe[7] on the basis of high R0 percentages among Sephardi and Ashkenazi Jews compared to native European populations and the relative genetic isolation of Ashkenazim.
If anti-E is detected, the presence of anti-c should be strongly suspected (due to combined genetic inheritance).
When any incompatibility is detected when she conceives the second time in less than two years then, the mother often receives an injection at 28 weeks' gestation and at birth to avoid the development of antibodies towards the fetus.
Here, sensitization to Rh D antigens (usually by feto-maternal transfusion during pregnancy) may lead to the production of maternal IgG anti-D antibodies which can pass through the placenta.
This is of particular importance to D negative females at or below childbearing age, because any subsequent pregnancy may be affected by the Rh D hemolytic disease of the newborn if the baby is D positive.
The vast majority of Rh disease is preventable in modern antenatal care by injections of IgG anti-D antibodies (Rho(D) Immune Globulin).
The incidence of Rh disease is mathematically related to the frequency of D negative individuals in a population, so Rh disease is rare in old-stock populations of Africa and the eastern half of Asia, and the Indigenous peoples of Oceania and the Americas, but more common in other genetic groups, most especially Western Europeans, but also other West Eurasians, and to a lesser degree, native Siberians, as well as those of mixed-race with a significant or dominant descent from those (e.g. the vast majority of Latin Americans and Central Asians).
What differs between Rh disease and NI is the pathogenesis of hemolysis between human fetuses and the animal species.
With human mothers, the maternal antibodies are formed from the sensitization of foreign antigens of her unborn fetus’s red blood cells passing through the placenta causing hemolysis before birth.
After 48 hours of birth, the newborn may be allowed to nurse from its mother as her antibodies can no longer be absorbed through the neonate’s intestines.
Because the most active newborn animals consume the most colostrum, they may be the ones who are most affected by the blood incompatibility of antigen and antibody.
[16] According to a comprehensive study, the worldwide frequency of Rh-positive and Rh-negative blood types is approximately 94% and 6%, respectively.
[17] The frequency of Rh factor blood types and the RhD neg allele gene differs in various populations.
The polypeptides produced from the RHD and RHCE genes form a complex on the red blood cell membrane with the Rh-associated glycoprotein.
And conversely, RhD-negative subjects with anamnestic titres (i.e. with latent toxoplasmosis) exhibited much longer reaction times than their RhD-positive counterparts.
[citation needed] Rh-like proteins can be found even in species other than vertebrates (which have red blood cells) – worms, bacteria, and algae.
[39][40][41] Before the advent of modern medicine, the carriers of the rarer allele (e.g. RhD-negative women in a population of RhD positives or RhD-positive men in a population of RhD negatives) were at a disadvantage as some of their children (RhD-positive children born to preimmunised RhD-negative mothers) were at a higher risk of fetal or newborn death or health impairment from hemolytic disease.
[42] Natural selection aside, the RHD-RHCE region is structurally predisposed to many mutations seen in humans, since the pair arose by gene duplication and remain similar enough for unequal crossing over to occur.
[29] In addition to the case where D is deleted, crossover can also produce a single gene mixing exons from both RHD and RHCE, forming the majority of partial D types.
Simply put, the weak D phenotype is due to a reduced number of D antigens on a red blood cell.
It was discovered in 1939 by Karl Landsteiner and Alexander S. Wiener, who, at the time, believed it to be a similar antigen found in rhesus macaque red blood cells.
The significance of their discovery was not immediately apparent and was only realized in 1940, after subsequent findings by Philip Levine and Rufus Stetson.
[42] The serum that led to the discovery was produced by immunizing rabbits with red blood cells from a rhesus macaque.
The antigen that induced this immunization was designated by them as Rh factor to indicate that rhesus blood had been used for the production of the serum.
In 1940, Landsteiner and Wiener made the connection to their earlier discovery, reporting a serum that also reacted with about 85% of different human red blood cells.
[51] In 1941, Group O: a patient in Irvington, New Jersey, US, delivered a normal[clarification needed] infant in 1931; this pregnancy was followed by a long period of sterility.
[52] Based on the serologic similarities, 'Rh factor' was later also used for antigens, and anti-Rh for antibodies, found in humans such as those previously described by Levine and Stetson.
2. This is the Rh-negative blood cell.
3. These are the antigens on the Rh-positive blood cell that make it positive. The antigens allow the positive blood cell to attach to specific antibodies.
