Farmasevtika instituti farmakologiya va klinik farmatsiya kafedrasi



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Fiziologiya

 


Rh Immune Response 
Formation of Anti-Rh Agglutinins. 
When red blood cells containing Rh factor are injected into a 
person whose blood does not contain the Rh factor—that is, into an Rh-negative person—anti-Rh 
agglutinins develop slowly, reaching maximum concentration of agglutinins about 2 to 4 months later. 
This immune response occurs to a much greater extent in some people than in others. With multiple 
exposures to the Rh factor, an Rh-negative person eventually becomes strongly ―sensitized‖ to Rh 
factor.
Sera Red Blood Cell Types 
Anti-A Anti-B
O − − A + − B − + AB + + 
Table 35-2 
Blood Typing, Showing Agglutination of Cells of the Different Blood Types 
with Anti-A or Anti-B Agglutinins in the Sera 
Unit VI Blood Cells, Immunity, and Blood 
Coagulation 
448 
bilirubin, which causes the baby‘s skin to become yellow (jaundiced). The 
antibodies can also attack and damage other cells of the body. 
 
Clinical Picture of Erythroblastosis. 
The jaundiced, erythroblastotic newborn baby is 
usually anemic at birth, and the anti-Rh agglutinins from the mother usually circulate in the infant‘s 
blood for another 1 to 2 months after birth, destroying more and more red blood cells. The 
hematopoietic tissues of the infant attempt to replace the hemolyzed red blood cells.
 
Prevention of Erythroblastosis Fetalis. 
The D antigen of the Rh blood group system is the 
primary culprit in causing mmunization of an Rh-negative mother to an Rh-positive fetus. In the 
1970s, a dramatic reduction in the incidence of erythroblastosis fetalis was achieved with the 
development of 
Rh immunoglobulin globin, an anti- D antibody 
that is administered to the expectant 
mother starting at 28 to 30 weeks of gestation. The anti-D antibody is also administered to Rh-negative 
women who deliver Rh-positive babies to prevent sensitization of the mothers to the D antigen. This 
greatly reduces the risk of develop ng large amounts of D antibodies during the second pregnancy.The 
mechanism by which Rh immunoglobulin globin prevents sensitization of the D antigen is not 
completely understood, but one effect of the anti-D antibody is to inhibit antigen-induced B 
lymphocyte antibody productionin the expectant mother. The administered anti-D antibody also 
attaches to D-antigen sites on Rh-positive fetal red blood cells that may cross the placenta and enter 
the circulation of the expectant mother, thereby interfering with the immune response to the D antigen.

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