A girl with severe combined immunodeficiency and pronounced malnutrition from chronic diarrhoea is presented. Immunological reconstitution was attempted by transplantation of bone marrow cells from the HL‐A hemiallogeneic father. An initial transplant failed to induce a permanent take of the graft, whereas a second transplant with an increased cell dose ensured a take, which was followed by reconstitution of cell‐mediated immune functions. Fractionation of the transplanted bone marrow cells apparently led to a delay in development of graft‐versus‐host symptoms. Germ‐free isolation and extensive bacterial decontamination markedly reduced the microbial flora and was highly protective against contaminating microorganisms but failed to eradicate completely one strain of Escherichia coli that had invaded the child before institution of this regimen. During a moderate, delayed graft‐versus‐host reaction this strain caused widespread severe infection, to which the child succumbed 10 weeks after the second transplantation. This child presented some additional features, the most conspicuous being a deficiency of erythrocyte adenosine deaminase.

Abstract. Some Rhesus antibodies are demonstrable only by enzyme technique and not by indirect Coombs' technique. An experiment has been carried out, showing that the most likely explanation, why the positive reaction with enzyme technique becomes negative with the indirect Coombs' technique, is that the antibody is simply washed off.

Abstract. An antibody, anti‐A1 Leb, has been found in the serum of a person belonging to group A1h, with complete depression of H on the red cells as well as in the saliva. It differs from earlier examples of the antibody in that it can be neutralized by A1 nL, secretor saliva as well as O Leb secretor saliva in addition to A1 Leb secretor saliva. Although the proposita secretes A substance, she only secretes Lea substance and not Leb substance. No such abnormalities were found in the family investigated. An interpretation of the case is given according to the classical hypothesis of ABO and Lewis system development.

The earlier reported investigations of the red cells of a pair of twins in whom blood group chimerism has been demonstrated (2) have now been extended to investigations of the HL-A system. Chimerism within the HL-A antigens on the lymphocytes of the chimeric twins has been demonstrated. Previous attempts by other authors to prove HL-A chimerism have been unsuccessful (1 ) . Lymphocyte chimerism concerning XX/XY chimerism has been reported (5), (6).The investigations were made using the lymphocytotoxic microtechnique (3). Besides the lymphocytes from the twins T S and MR, lymphocytes from the wife (BS) of TS and their son HS were tested and from the husband (ER) of M R and their daughter HR.TS, MR and their family were tested for the following HL-A antigens: HL-AL, HL-A2, Ba* ( = W28), HL-A3, HL-All, HL-AS, HL-A10, Da25 ( = W19), and HL-Al2, R* ( = W5), HL-A5, TT,The majority of the test sera used came from multiparous women and the remainder from immunized volunteers.Two to four test sera were used for each antigen and, with the exception of the TT antigen, it was possible to test all the antigens listed above with at least one monospecific serum. The HL-A antigens demonstrated on the lymphocytes of T S and MR were tested with specially selected test sera which gave only positive reaction. ( i . e. 75-100 % of the cells were stained by trypan blue) with lymphocytes carrying the corresponding antigens, whereas a negative result ( i. e. less than 1 % of the cells were stained) was obtained with lymphocytes lacking the corresponding antigens. HL-A13, HL-A7, HL-A8, FJH ( = W27), BB ~~ ~ ~ Received 30.xi.71 from Blood Bank, Blood 152The anti-TT has a special status. The antigen TT is closely linked to the HL-A12 antigen and anti-TT has only been found in sera containing ant-HL-A12 (4). Three sera containing anti-HL-12 and anti-TT gave positive reactions with T S and MR cells, but two monospecific anti-HL-A12 sera both gave negative results with the lymphocytes of T S and MR. Thus T S and MR must be HL-A12 negative and TT positive. Table I shows the strength of the reactions of the test sera which reacted with the lymphocytes of T S and MR. Inactivated AB serum from a donor without lymphocytotoxic antibodies was used as negative control. Less than 1 % of the cells was stained by trypan blue. The genotypes of T S and M R can be decuded from Table 1. The genotypes were confirmed by HL-A typing of the members of the family. The results of the HL-A typing of the members of the family are shown in Table 2. CommentsThe test sera used in the lymphocytotoxic test (Table 1 ) were selected in order to give less than 1 70 killed cells with lymphocytes lacking the corresponding antigens, and more than 76 % killed cells with lymphocytes carrying the corresponding antigens. For that reason, T S must have the antigens Ba*, HL-AS, LND and TT, because 7 5 % or more of his cells are killed by the corresponding antiserum. Likewise, MR must have the antigens HL-A2, Ba* and TT.Since reactions of the anti-LND and the anti-HL-A9 sera against...

Abstract. A group B variant, lacking B antigen on the red cells, but secreting small amounts of B substance in the saliva is described. Family investigation showed both parents and three sibs to be normal B. Among six children no normal or abnormal B occurred. It is discussed whether the B variant is due to mutation of the B gene or to the effect of a recessive suppressor gene.