We only do screen for ABO and Rh systems and do blood matching between donor and recipient during blood transfusion, while nothing is done for screening HLA which are important target molecules in transplanted tissue rejection.
Because blood for transfusion only has RBCs and soluble proteins/compounds, RBCs don't express HLAs. ALL the WBCs are removed before the blood can be used for a donor.
Dear Ali,
The given answers from Shen-An Hwang are not completely correct.
There is small number of HLA-molecules on RBCs, too!
We call them Bennett-Goodspeed (Bg) blood group molecules (Bga = HLA-B7, Bgb (HLA-B17 [→ HLA-B57 & HLA-B58] and Bgc = HLA-A28 [→ HLA-A68 & HLA-A69]).
Every blood preserve contains a small number of HLA-bearing leukocytes, too!
We have only a leukocyte depletion, not a complete leukocyte reduction!
If a patient get a lot of blood preserves, the patient can build anti-HLA-antibodies!
In blood transfusion, the other blood groups, like ABO and rhesus, are much more important than HLA.
In platelet transfusion, HLA matching is more important!
Best regards,
Thomas
Dear Ali Bayati,
It is a very good basic question....
I will try to explain in a simpler way. Production of antibodies in the recipient against alloantigens (HLA) molecules received from donor while transfusion is well recognized phenomena. However, the question is whether it causes serious reactions as in GVHD.
In general, blood bags stored for certain duration before transfusion procedures. Available evidences indicated that storage of WBCs beyond the threshold ( 72 hrs at 20C and/or 13 days at 4C) resulted in loss of co-stimulatory capacity and HLA-DR. Hence, the antigens remains in blood bag becomes weakly immunogenic or non-immunogenic which depends on the HLA status of the donor and recipient. Strong immunological responses (in case of transfusion or transplantation) often related with HLA Class II molecules. Sharing of any one HLA Class II allele reduces the formation of antibodies (or rate of synthesis) in the recipient system.
Hence, it can be concluded that the magnitude (strength) of the immune response mounted in the recipient body remains at very lower levels or at negligible proportion.
Patients whom undergoes very frequent transfusion (as in case of thalassemia or similar clinical conditions) certainly produces wide range of antibodies against several HLA antigens. In such conditions, certainly we can see a greater degree of immune response….
Other cells present in blood also carries HLA molecules (at different surface level expression), free HLA molecules in plasma also come into the play. At this moment, I can say that the strength of immune response against alloantigens is very weak or under subclinical to cause a strong antigenic response like graft rejection...
Dear Narayanan,
Thank you for valuable inputs.
But sometimes, blood is not stored for long time, then there is remote chance of weak immunogenicity of HLA molecule.
What happens then
Dear DS Rahalkar,
If you refer any classic immunology books it denotes "the magnitude of the immune response which depends on the affinity and avidity of an antigen".
Hence, the chances of transfusion associated/induced GVHD is veray rare. If my meory is correct, one case study was reported from Japan about such rare phenomena.
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