Rh Factor in Humans
An isoantigen that can trigger haemolytic disease in newborns due to incompatibility between maternal and infant blood factors.
Rh factor is an RBC antigen of major clinical concern. It is also called the D antigen.
This factor was first discovered in experiments exploring the genetic relationships among animals. Rabbits inoculated with the RBCs of rhesus monkeys produced an antibody that also reacted with human RBCs. Further tests showed that this monkey antigen (termed Rh for rhesus) was present in about 85% of humans and absent in the other 15%.
In simple terms, a person's Rh type results from a combination of two possible alleles a dominant one that codes for the factor and a recessive one that does not. A person inheriting at least one Rh gene will be Rh positive; only those persons inheriting two recessive genes are Rh negative.
This factor is denoted as ‘Rh+’ or ‘Rh-” by a symbol above the blood type, as in O+ or AB+. However, unlike the ABO antigens, exposure to normal flora does not sensitize Rh persons to the Rh factor.
The only way one can develop antibodies against this factor is through placental sensitization or transfusion.
The potential for placental sensitization occurs when a mother is Rh negative and her unborn child is Rh positive. The obvious intimacy between mother and fetus makes it possible for fetal RBCs to leak into the mother's circulation during childbirth, when the detachment of the placenta creates avenues for fetal blood to enter the maternal circulation.
The mother's immune system detects the foreign Rh factors on the fetal RBCs and is sensitized to them by producing antibodies and memory B cells.
The first Rh child is usually not affected because the process begins so late in pregnancy that the child is born before maternal sensitization is completed.
So, this concludes, that the second child that the mother may have, is more prone to risk
The mother's immune system has been strongly primed for a second contact with this factor in a subsequent pregnancy.
In the next pregnancy with an Rh-positive fetus, fetal blood cells escape into the maternal circulation late in pregnancy and elicit a memory response. The fetus is at risk when the maternal anti-Rh antibodies cross the placenta into the fetal circulation, where they affix to fetal RBCs and cause complement-mediated lysis.
The outcome is a potentially fatal hemolytic disease of the newborn (HDN) called erythroblastosis fetalis. This term is derived from the presence of immature nucleated RBCs called erythroblasts in the blood.
They are released into the infant's circulation to compensate for the massive destruction of RBCs by maternal antibodies. Additional symptoms are severe anaemia, jaundice, and enlarged spleen. and liver.
In response to the Rh+ blood of the foetus, the maternal blood develops antibodies of the IgG type. This is the only class of antibodies that can cross the human placenta. Hence, this poses the most risk as these antibodies cross the placenta and attack the blood components of the foetus.
If there is any possibility that the fetus is Rh, the mother must be passively immunized with antiserum containing antibodies against the Rh factor (Rho [D] immune globulin, or RhoGAM*).
This antiserum, injected at 28 to 32 weeks and again immediately after delivery, reacts with any fetal RBCs that have escaped into the maternal circulation, thereby preventing the sensitization of the mother's immune system to Rh factor.
An isoantigen that can trigger haemolytic disease in newborns due to incompatibility between maternal and infant blood factors.
Rh factor is an RBC antigen of major clinical concern. It is also called the D antigen.
This factor was first discovered in experiments exploring the genetic relationships among animals. Rabbits inoculated with the RBCs of rhesus monkeys produced an antibody that also reacted with human RBCs. Further tests showed that this monkey antigen (termed Rh for rhesus) was present in about 85% of humans and absent in the other 15%.
In simple terms, a person's Rh type results from a combination of two possible alleles a dominant one that codes for the factor and a recessive one that does not. A person inheriting at least one Rh gene will be Rh positive; only those persons inheriting two recessive genes are Rh negative.
This factor is denoted as ‘Rh+’ or ‘Rh-” by a symbol above the blood type, as in O+ or AB+. However, unlike the ABO antigens, exposure to normal flora does not sensitize Rh persons to the Rh factor.
The only way one can develop antibodies against this factor is through placental sensitization or transfusion.
The potential for placental sensitization occurs when a mother is Rh negative and her unborn child is Rh positive. The obvious intimacy between mother and fetus makes it possible for fetal RBCs to leak into the mother's circulation during childbirth, when the detachment of the placenta creates avenues for fetal blood to enter the maternal circulation.
The mother's immune system detects the foreign Rh factors on the fetal RBCs and is sensitized to them by producing antibodies and memory B cells.
The first Rh child is usually not affected because the process begins so late in pregnancy that the child is born before maternal sensitization is completed.
So, this concludes, that the second child that the mother may have, is more prone to risk
The mother's immune system has been strongly primed for a second contact with this factor in a subsequent pregnancy.
In the next pregnancy with an Rh-positive fetus, fetal blood cells escape into the maternal circulation late in pregnancy and elicit a memory response. The fetus is at risk when the maternal anti-Rh antibodies cross the placenta into the fetal circulation, where they affix to fetal RBCs and cause complement-mediated lysis.
The outcome is a potentially fatal hemolytic disease of the newborn (HDN) called erythroblastosis fetalis. This term is derived from the presence of immature nucleated RBCs called erythroblasts in the blood.
They are released into the infant's circulation to compensate for the massive destruction of RBCs by maternal antibodies. Additional symptoms are severe anaemia, jaundice, and enlarged spleen. and liver.
In response to the Rh+ blood of the foetus, the maternal blood develops antibodies of the IgG type. This is the only class of antibodies that can cross the human placenta. Hence, this poses the most risk as these antibodies cross the placenta and attack the blood components of the foetus.
If there is any possibility that the fetus is Rh, the mother must be passively immunized with antiserum containing antibodies against the Rh factor (Rho [D] immune globulin, or RhoGAM*).
This antiserum, injected at 28 to 32 weeks and again immediately after delivery, reacts with any fetal RBCs that have escaped into the maternal circulation, thereby preventing the sensitization of the mother's immune system to Rh factor.
