P. D. Issitt

Anti‐IB, an Expected “New” Antibody Detecting a Joint Product of the I and B Genes

Since the original description, in 1956, of the I antigen by WIENER, UNGER, COHEN and FELDMAN [14] it has become increasingly apparent that there is an association between the I and the ABO antigens. The autoimmune anti-I (Steg) described by RACE and SANGER [9] reacts, on an average, more strongly with 0 cells than with cells of other ABO groups. ROSENFIELD, SCHROEDER, BALLARD, VAN DER HART, MOES and VAN LOGHEM [lo] have shown that the antibody with anti-H specificity that is not neutralizable by saliva from a group 0 secretor usually has anti-IH specificity while SCHMIDT and MCGINNISS [12] consider the relationship between I and 0 to be closer than the relationship between I and H from working with anti-0, anti-H and anti-I sera. TIPPETT, NOADES, SANGER, RACE, SAUSAIS, HOLMAN and BUTTIMER [13] describe an anti-IA, formed by a group A, subject which reacts more strongly with A, than with A, or 0 cells while NEWTON [7] has recently found a serum from an A, subject that contains both anti-A, and anti-IA the latter of which reacts much more strongly with A, than with 0 cells. In 1965, SALMON, HOMBERG, LIBERGE and DELARUE [ll] made a series of eluates from red cells of patients with acquired hemolytic anemia. In one instance they found in the eluate of a group A, patient an anti-I that reacted only with cells producing I and H or I and A. In the eluate from the red cells of a group AB patient they found an anti-I which would react with cells producing I and H; I and A or I and B. SALMON et al. interpret these findings as indicating that the

Anti‐IP1: Antibodies that Show an Association Between the I and P Blood Group Systems1

Summary. In a study of four antibodies originally thought to be anti‐P1, two different specificities have been demonstrated. Anti‐P1 agglutinates P1 + bloods whether or not they are I +, while anti‐IP1 reacts with 1 + P1 + but not with I– P1+ cells. It appears that anti‐IP1 is directed not against the P1 antigen but against an antigenic determinant produced by the actions of both the P1 and I genes. Because bloods from newborn infants give weak or negative reactions with anti‐IP1, it is important that ‘anti‐P’ used for testing newborns be shown to be really anti‐P1 and not anti‐IP1.

Further Observations on the Matuhasi‐Ogata Phenomenon

Summary. When a specific antigen‐antibody complex is formed another antibody present at the same time, or introduced to the complex subsequently, can attach to and be eluted from the complex although the antigen to which it is directed is not present. This nonspecific binding of antibody, the Matuhasi‐Ogata phenomenon, has been examined in a series of 45 experiments and has been shown to occur independently of temperature, the strength or specificity of any of the antibodies involved or red cell individuality. The phenomenon is important: in the preparation of blood typing antisera; in the interpretation of antibody significance in eluates from persons with a positive direct antiglobulin test; in the separation, by absorption and elution procedures, of antibodies in multispecific sera; and in the detection of weak isoagglutinins in sensitized patients.

The simultaneous presence of anti-I and anti-i in sera.

The specificity of antibodies that detect the antigens I, i, IT, IH (10), IA, IB, iH (iO), and IP1, [23, 10, 21, 11, 12, 3, 16, 17, 2, 5, 18, 22, 4, 20, 6, 7] can be established with little difficulty. There remain, however, many cold agglutinins that do not have specificity directed against any one of these antigens; this paper describes studies on 22 such sera, 3 of which react equally with I and i cells (regardless of ABO group) and 19 of which have anti‐I specificity but react with significant strength with i cells as compared to a ‘standard’ anti‐I. Absorption and elution experiments with selected erythrocytes show that all 22 sera contain separable anti‐I and anti‐i.

Sj, a new antigen in the MN system, and further studies on Tm.

Summary. A serum containing antibody activity within the MN blood group system is described. Absorption studies showed that the serum detects two new antigenic determinants that have been named Tm and Sj. The results obtained when 1,400 bloods, 500 from Negroes and 900 from Caucasians, were tested for ten antigens in the MN system — M, M1, N, S, s, U, Hu, He, Tm and Sj — are presented. Unlike most of the recently described new antigens in the MN system both Tm and Sj are of fairly high frequency in Caucasians and Negroes. Calculations of gene frequencies from these data are published in an accompanying paper [7].

Rapid in vivo Destruction of Yt(a+) Red Cells in a Patient with Anti-Yta1

In 1956, EATON, MORTON, PICKLES and WHITE [2] discovered anti-Yta, which detects an antigen, Yta, present on the red cells of most individuals. In 1964, GILES and METAXAS [3] and in 1965, IKIN, GILES and PLAUT [4] reported the first two examples of anti-Ytb which detects the antithetical antigen t o Yta. From the work on the two antigens it can be calculated that about three in every one thousand persons are of type Yt(a-bf) and thus able to form anti-Yta. However, in spite of this low figure, the antibody is not infrequent, suggesting that Yta is a ‘strong’ antigen. Since 1956, six examples of anti-Yta have been identified at the Memorial Hospital and in a two-year period ending December 1966 six other examples have been encountered at the New York Blood Center. Of the 12 examples, seven were present in sera that had many other antibodies while five were seen in the ‘pure’ state. Anti-Yta was demonstrated in EATON’S patient four days after a second series of transfusions. Sixty days later Yt(a+) cells were thought still t o be present since there was a weakly positive direct antiglobulin test suggesting that although ‘coated‘, the Yt(a+) cells were not destroyed prematurely. The direct antiglobulin test was negative 102 days after transfusion. Thus, although the reactions of anti-Yta in vitro suggest it t o be a dangerous antibody as far as transfusion is concerned, it has been concluded that in EATON’S patient the anti-Yta ‘apparently failed t o reduce the survival of transfused red cells’ [5]. In 1962, STERN [7], in a review of unusual blood types listed anti-Yta as a cause of cross-matching difficulties

Another Example of a “Naturally-Occurring” Anti-Kl*

Most antibodies in the Kell blood group system are produced by immunization of the subject, by accidental exposure to foreign erythrocytes during transfusion or pregnancy. The antigenicity of K:l (K) has been studied by ALLEN and WARSHAW [l] who found that anti-Kl was more likely to result from transfusion than pregnancy. Rarely anti-Kl is found in the serum of persons who have had neither transfusions nor pregnancies and the source of the immunizing agent is not known. Two such cases were described by MORGAN and BOSSOM [5]. The purpose of this report is to describe another such 66 naturally-occurring ” example of anti-Kl ; in this instance, however, the exact time at which the antibody was produced is known but again the causative agent is obscure. Mr. H. Kav. was a 34-year-old Caucasian male suffering from Lymphosarcoma and Pulmonary tuberculosis, he had never received a blood transfusion or a parenteral injection of blood. His blood was first studied by us in 1963 at which time no atypical antibodies were present. Between 1963 and May 1966 when the current investigation was undertaken, his blood was tested on five different occasions. Each time antibody screening, including tests against K :1 red cells was negative. The last tests to give negative reactions were carried out in March 1966, then in May 1966 his serum was found to agglutinate the test cells at room temperature (22°C) and 37°C. Subsequent investigations, to be described in detail below, revealed the presence of an unusual form of anti-Kl. It was noted in 1963 that the direct antiglobulin test on the patients cells was weakly positive, this finding was a constant feature of his disease. Two eluates from the

A Second Example of Anti‐Lan

Summary. An antibody in the serum of a recently transfused woman has been shown to be an IgG anti‐Lan, active in albumin and by the antiglobulin technique.

Anti‐Vel 2, a New Antibody Showing Heterogeneity of Vel System Antibodies

Anti‐Vel 2 is a newly recognized antibody in the Vel system. Two anti‐Vel sera have been shown to contain anti‐Vel 2, while 4 others have anti‐Vel 1 plus anti‐Vel 2. The new phenotype Vel: 1, ‐2 is twice as common (frequency about 0.00053) as Vel: ‐1, ‐2 (frequency about 0.00025). Tests with the original Vel serum of Sussman and Milleh [8] show that the phenotype Vel: ‐1, ‐2 corresponds to the original Vel‐negative type.