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By the end of this section, you will be able to:
  • Explain why blood typing is important and what happens when mismatched blood is used in a transfusion
  • Describe how tissue typing is done during organ transplantation and the role of transplant anti-rejection drugs
  • Show how the immune response is able to control some cancers and how this immune response might be enhanced by cancer vaccines

The immune responses to transplanted organs and to cancer cells are both important medical issues. With the use of tissue typing and anti-rejection drugs, transplantation of organs and the control of the anti-transplant immune response have made huge strides in the past 50 years. Today, these procedures are commonplace. Tissue typing is the determination of MHC molecules in the tissue to be transplanted to better match the donor to the recipient. The immune response to cancer, on the other hand, has been more difficult to understand and control. Although it is clear that the immune system can recognize some cancers and control them, others seem to be resistant to immune mechanisms.

The rh factor

Red blood cells can be typed based on their surface antigens. ABO blood type, in which individuals are type A, B, AB, or O according to their genetics, is one example. A separate antigen system seen on red blood cells is the Rh antigen. When someone is “A positive” for example, the positive refers to the presence of the Rh antigen, whereas someone who is “A negative” would lack this molecule.

An interesting consequence of Rh factor expression is seen in erythroblastosis fetalis    , a hemolytic disease of the newborn ( [link] ). This disease occurs when mothers negative for Rh antigen have multiple Rh-positive children. During the birth of a first Rh-positive child, the mother makes a primary anti-Rh antibody response to the fetal blood cells that enter the maternal bloodstream. If the mother has a second Rh-positive child, IgG antibodies against Rh-positive blood mounted during this secondary response cross the placenta and attack the fetal blood, causing anemia. This is a consequence of the fact that the fetus is not genetically identical to the mother, and thus the mother is capable of mounting an immune response against it. This disease is treated with antibodies specific for Rh factor. These are given to the mother during the subsequent births, destroying any fetal blood that might enter her system and preventing the immune response.

Erythroblastosis fetalis

This figure shows the progression of thedisease called erythroblastosis fetalis. The top panel shows the umbilical artery and vein and the placenta. The center panel shows the response in the immune system of a first Rh+ infant. The bottom panel shows the response in the case of a second exposure for a Rh+ infant.
Erythroblastosis fetalis (hemolytic disease of the newborn) is the result of an immune response in an Rh-negative mother who has multiple children with an Rh-positive father. During the first birth, fetal blood enters the mother’s circulatory system, and anti-Rh antibodies are made. During the gestation of the second child, these antibodies cross the placenta and attack the blood of the fetus. The treatment for this disease is to give the mother anti-Rh antibodies (RhoGAM) during the first pregnancy to destroy Rh-positive fetal red blood cells from entering her system and causing the anti-Rh antibody response in the first place.
Practice Key Terms 6

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Source:  OpenStax, Mrs. browne's immune modules. OpenStax CNX. Apr 27, 2015 Download for free at https://legacy.cnx.org/content/col11783/1.1
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