Serum IgA deficiency with anti IgA antibodies at the high titer was found in a patient with renal failure due to SLE. Before detection of anti IgA antibodies, she had experienced severe anaphylactoid reactions at the start of the plasma exchange therapy. Afterwards anti IgA antibodies were found by double diffusion in agarose gel and in the IgG fraction of the patient serum, and were directed against only IgA1 subclass. IgA2 was detected by double diffusion method with commercial anti IgA2 antisera. The patient was lacking in IgA, but had secretory component in her saliva.
The patient is now well controlled by hemodialysis three times a week for renal failure and by transfusion of washed red blood cells without leukocytes for anemia. Accordingly, irk case of a patient who has little amount of serum IgA requires blood or blood products, anti IgA antibodies should be investigated carefully before administration to avoid anti IgA mediated transfusion reactions.

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An anti-Jk3 was identified in the serum of a healthy 35-year-old female donor who had not been transfused. The proposita (Mrs. Suzu.) has two children and a histry of three stillbirths. The serum of Mrs. Suzu. was reacted with all the cells tested except three Jk (a- b-) cells by anti-globulin test, but it very weakly reacted with the dominant Jk (a- b-) cells. The antibody was only active in the antiglobulin test phase and was of the IgG1 subclass. Proposita's red cells were resistant to urea lysis using the Groupamatic-360 GMP III system. Her red cells failed to react either with anti-Jk^a, anti-Jk^b or anti-Jk3 as expected. These negative reactions were reconfirmed by absorption-elution tests.
The anti-Jk3 was absorbed by cells from the lymphocytes and granulocytes layer, but both the anti-Jk^a and anti-Jk^b were not.

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