THE ANTIBODY RESPONSE OF RABBITS TO INJECTIONS OF EMULSIONS AND EXTRACTS OF HOMOLOGOUS BRAIN

Rabbits injected with fresh emulsions of homologous brain developed few or no antibodies capable of fixing complement in the presence of aqueous emulsions or alcoholic extracts of rabbit brain. Complement-fixing antibodies, however, were produced in rabbits by means of injections (1) of sterile emulsions of homologous brain which had been allowed to stand at room temperature for 5 to 30 days and (2) of emulsions of homologous brain experimentally infected with vaccine virus. The antisera that were produced following injections of emulsions of autolyzed homologous brain were shown by absorption tests to contain both specific and non-specific antibodies. The specific brain antigen was found to be approximately six times as abundant in the white matter as in the grey. It was almost absent from the brain of fetal and newly born rabbits, but increased in amount with the age of the animal to reach a maximum concentration at maturity. The specific antigen seemed to parallel the myelin content of brain tissue.     

QUANTITATIVE ASPECTS OF HOMOLOGOUS AND HETEROLOGOUS ACTIVE IMMUNITY TO STRAINS OF THE VIRUS OF EPIDEMIC INFLUENZA

When mice are immunized by one intraperitoneal inoculation with active or inactive influenza virus (strain PR8, W.S., and Melbourne) the quantity required for protection against heterologous strains is about 10 times the homologous minimal immunizing dose. Three injections increase the immunity to all strains, but the ratio between the homologous and heterologous minimal immunizing dose is not altered. Swine influenza virus given intraperitoneally fails to immunize against human strains unless the quantity injected is 1,000 times the minimal amount required for homologous immunity. Intranasal immunization of mice with 1/100 M.L.D. of attenuated ferret passage strains PR8 and Philadelphia, or the tissue culture strain of swine influenza, gives a solid resistance to infection with heterologous strains. When smaller amounts of virus are given intranasally, strain specificity becomes more apparent, and with minimal doses the immunity may be effective only against the homologous and closely related strains.     

THE MECHANISM OF TOLERANCE PRODUCED IN RATS TO SHEEP ERYTHROCYTES : I. PLAQUE-FORMING CELL AND ANTIBODY RESPONSE TO SINGLE AND MULTIPLE INJECTIONS OF ANTIGEN

Previous studies suggested that an active immune response was partially responsible for maintaining immunological unresponsiveness to sheep erythrocytes. Measurement of the plaque-forming (antibody-releasing) cell response proved to be a sensitive indicator of an immune response to sheep erythrocytes in the absence of detectable circulating antibody to the antigen. The present studies were undertaken to determine whether an active immune process, measured by the plaque-forming cell response, was partially responsible for induction and maintenance of tolerance. Rats injected intraperitoneally with large doses of sheep erythrocytes beginning at the day of birth develop tolerance to the antigen. In this paper, the plaque-forming cell and antibody response to sheep erythrocytes was characterized for rats receiving a single antigen injection at various ages and for rats which received repeated antigen injections as adults. The dose of antigen was the same as that used to produce tolerance; the injection schedule for repeated immunizations was also the same as that used to produce tolerance. Rats receiving a single antigen injection on the day of birth or at age 7 days had no measurable response to the antigen. Rats receiving a single antigen injection at age 17 days and sacrificed 4 days later had an unequivocal response to the antigen. The spleens had about one-tenth as many plaque-forming cells as spleens of adult animals immunized similarly, but the antibody titers were as high as titers for adult animals. Presumably the high titers of these young animals resulted from the high ratio of plaque-forming cells to body weight and blood volume. Adult animals receiving a single antigen injection had a peak or near peak plaque-forming cell response 4 days after immunization; at this time, sera contained high titers of 19S antibody and the numbers of plaque-forming cells in spleens correlated reasonably well with circulating antibody titers. 7S antibody appeared in serum 5 or 6 days after immunization. The numbers of plaque-forming cells declined progressively 2 and 3 weeks after immunization. Repeated twice weekly, injections of the antigen in adult rats produced a marked decline and then stabilization of numbers of plaque-forming cells in spleens. Although the numbers of plaque-forming cells were fewer, titers of 19S and 7S antibody stabilized at high levels. A progressive recovery of the plaque-forming cell response and a rise in antibody titer occurred when the interval between the last 2 injections was increased from 3 to 10, 17, or 32 days. These findings suggested that repeated closely spaced antigen injections interfered with either cell division or maturation of antibody-forming cells. As the interval between injections was increased, additional antibody-forming cells matured or were formed through cell division. Thus, relatively constant antigenic stimulation provided a mechanism for controlling or limiting the response of antibody-forming cells. In the following paper, it will be shown that this mechanism operating together with a homeostatic mechanism which prevents induction of new antibody-forming cells serves to regulate the immune response to repeated injections of antigen.     

THE ANTIBODY RESPONSE TO SWINE INFLUENZA

Antibodies that neutralize swine influenza virus became detectible in the serum of swine on the 6th or 7th day after infection with swine influenza. Their appearance corresponded rather closely with clinical recovery. In swine with the milder filtrate disease, neutralizing antibodies did not appear until sometime between the 7th and 10th days. The maximum antibody titers ranged from 1:60 to 1:160 and were attained on from the 14th to the 27th days after infection.     

EXPERIMENTAL IMMUNOLOGIC ADRENAL INJURY : A RESPONSE TO INJECTIONS OF AUTOLOGOUS AND HOMOLOGOUS ADRENAL ANTIGENS IN ADJUVANT

Twenty-three unilaterally adrenalectomized guinea pigs were injected with autologous and homologous adrenal tissue homogenates respectively, in Freund's adjuvant. Widespread adrenal lesions were found in 10 of 12 animals receiving auto-antigen and to a lesser extent in 6 of 11 animals injected with homologous pooled antigen. Widespread systemic lesions were present in both these and in control animals receiving Freund's adjuvant alone. These latter animals showed no adrenal involvement. The early changes within the adrenal consisted of perisinusoidal cellular proliferations in the deeper layers of the cortex. Focal granulomata developing at a later stage tended to become confluent and to displace cortical cells. Some loss of these cells was attributable to ischemic injury. The localization in the deep fasciculata and reticularis was thought to depend (a) on the varying antigenicity of adrenal cortical components, (b) the possible inhibitory effect of antiphlogistic adrenal cortical hormones on the development of lesions in the outer cortex, and (c) the presence of littoral cells in the deep cortex. These cells are thought to be involved in the mediation of the stimulus initiating differentiation of primitive mesenchymal cells in response to a circulating auto-antigen. The medullary lesions may be related to the presence of ectopic reticularis cells in this location. It was suggested that the cellular response in the target organ to injections of adrenal homogenates may denote a specific "organ-self" recognition mechanism involving an immune (i.e. defensive) reaction. It was postulated that this may be an accentuation of the physiological function of immunologically competent cells. Their proliferation, under normal circumstances, would prevent by means of production of "binding" globulins, the escape and dissemination of endogenous freed adrenal antigens into the circulation. Although the experimental stimulus arose from without the gland, by virtue of the presence of a circulating adjuvant-bound antigen, the adrenal reaction followed the same pattern as would obtain if the antigen was liberated within the suprarenal cortex.     

THE ANTIBODY RESPONSE OF HUMAN SUBJECTS VACCINATED WITH THE VIRUS OF HUMAN INFLUENZA

Human influenza virus cultivated in tissue culture medium may be administered subcutaneously or intradermally to human individuals without causing evidence of infection. Subjects so treated develop a good titer of circulating antibodies effective against mouse passage virus and, if antibodies were previously present, vaccination stimulates the production of more antibody. The antibodies so induced persist for at least 5 months, although in this period of time some decline in titer may have begun. The antibody response to vaccination parallels both in extent and persistence that occurring as a result of the naturally acquired disease. The available data do not enable one to evaluate the effect of vaccination in preventing human infection with influenza. It seems not unlikely that the increase in circulating antibody will be accompanied by an increased ability to combat the natural infection.     

A COMPLEX VACCINE AGAINST INFLUENZA A VIRUS : QUANTITATIVE ANALYSIS OF THE ANTIBODY RESPONSE PRODUCED IN MAN

A quantitative study of the antigenicity of various vaccines containing influenza A virus has been made in human beings. A complex vaccine prepared from chick embryos inoculated with both influenza A virus and the X strain of canine distemper virus was found to be more effective than other vaccines in stimulating the production of neutralizing antibodies against the former virus. The increased antibody levels which resulted from the administration of this vaccine remained almost unaltered for at least 5 months.     

REACTIONS OF RABBITS TO INTRACUTANEOUS INJECTIONS OF PNEUMOCOCCI AND THEIR PRODUCTS : I. THE ANTIBODY RESPONSE

1. Sixty rabbits were immunized by the repeated injections into the skin of small doses of suspensions of heat-killed Type I pneumococci. In 53 of the rabbits no type-specific antibodies appeared in the serum, and in the remaining seven the titre of these antibodies in the serum was very low. In all cases, however, the sera possessed a high titre of species-specific antibodies. 2. Forty-five rabbits similarly immunized by injections of heat-killed Type III pneumococci also failed to form type-specific antibodies but did form species-specific antibodies. 3. Suspensions of heat-killed R pneumococci and solutions of bacterial substances when injected into the skin stimulated the production of species-specific antibodies, although they failed to stimulate the production of any type-specific antibodies. 4. Animals which had been immunized by intracutaneous injections still possessed the ability to form type-specific antibodies when they were subsequently given intravenous inoculations of type-specific pneumococci.     

THE MECHANISM OF TOLERANCE PRODUCED IN RATS TO SHEEP ERYTHROCYTES : II. THE PLAQUE-FORMING CELL AND ANTIBODY RESPONSE TO MULTIPLE INJECTIONS OF ANTIGEN BEGUN AT BIRTH

An active immune response to sheep erythrocytes was demonstrated in rats made "tolerant" to sheep erythrocytes by twice-weekly antigen injections beginning on the day of birth. Groups of tolerant rats were sacrificed 4 days after they had received 5 to 42 antigen injections; spleens were sampled for plaque-forming (antibody-releasing) cells and sera were titrated for antibody to sheep erythrocytes using a sensitive "plate hemolysin" technique. During the 3rd week of life and after the 5th antigen injection, the tolerant rats had an immune response equivalent to that of rats of similar age which had received a single antigen injection, but spleens contained only about one-tenth as many plaque-forming cells as adults animals receiving similar antigen injections. Continued antigen injections produced a marked decline and stabilization of this relatively small population of antibody-forming cells; however, the number of plaque-forming cells in the tolerant rats remained considerably elevated above the numbers of plaque-forming cells present in the spleens of non-immunized animals. The sera from all but 1 tolerant rat had demonstrable antibody to sheep erythrocytes in low titer. A progressive recovery of the plaque-forming cell response and rise in antibody titers occurred in adult tolerant rats when the interval between the last 2 antigen injections was increased from 3 days to 14 or 28 days. The decline and stabilization of numbers of plaque-forming cells occurring with continued injections after the 3rd week of life paralleled a similar decline and stabilization in rats receiving similar antigen injections as adults. Also, the recovery of the plaque-forming cell and antibody response of tolerant animals paralleled the recovery observed when the interval between injections was increased in rats receiving similar antigen injections as adults. These findings suggested that the same mechanism controlled numbers of antibody-forming cells in tolerant and normally responsive adult animals. Repeated closely spaced antigen injections presumably interfered with either cell division or maturation of antibody-forming cells. As the interval between injections was increased, additional antibody-forming cells matured or were formed through cell division. Relatively constant antigenic stimulation provided a mechanism for controlling or limiting the response of antibody-forming cells. The mechanism controlling or limiting the response of antibody-forming cells would not account for the stabilization of numbers of antibody-forming cells at high levels for normal animals and at low levels for the tolerant animals. Passive immunization of growing rats with homologous anti-sheep erythrocyte serum markedly inhibited the plaque-forming cell response of growing rats. It was proposed that antibody produced by the small population of antibody-forming cells in the tolerant rats provided a feedback or homeostatic mechanism which inhibited transformation of potential antibody-forming cells to antibody-forming cells. Thus, tolerance to sheep erythrocytes was induced and maintained by two mechanisms. One mechanism, dependent on relatively constant antigenic stimulation, limited or controlled the numbers of antibody-forming cells. The other, dependent on the production of small quantities of antibody by a few antibody-forming cells, limited or controlled the transformation of potential antibody-forming cells to antibody-forming cells.     

MULTIPLE VIRUS INFECTION OF SINGLE HOST CELLS

Evidence is presented to show that two or more viruses can simultaneously manifest their characteristic activities within individual epithelial cells of the normal rabbit''s cornea. This evidence, together with that previously presented (1, 5, 6), makes plain that multiple virus infection of a single host cell can take place in corneal cells, in the cells of chick embryos, and in those of rabbit tumors, both benign (Shope''s papilloma) and malignant. Certain implications of the findings are discussed.     

ACTION ON FIBROBLASTS OF EXTRACTS OF HOMOLOGOUS AND HETEROLOGOUS TISSUES

Extracts of homologous adult tissues detemine an increase in the mass of pure cultures of chicken fibroblasts nourished thereon comparable to that resulting from embryonic tissue juice. But the effect of these extracts differs markedly from that of the latter, since cell multiplication does not continue indefinitely. After a few passages, the fibroblasts cultivated in adult tissue extracts grew more slowly than in Tyrode solution. The cytoplasm became dark and filled with fat granules, and death followed. It is possible that the tissues of adult animals contain, as does the serum, substances which are toxic for the homologous cells, and which progressively overcome the effect of the growth-activating substances. The effect of heterologous adult tissue extracts did not differ markedly from that of homologous tissues. The chicken connective tissue increased slightly in mass, but died sooner than the controls in Tyrode solution. By contrast, tissue juices derived from the embryos of mice, guinea pigs, and rabbits acted on chicken fibroblasts in the same manner as chick embryo juices. The increase in mass of the cultures was regular and rapid. They doubled in size every 48 or 72 hours, and the rate of growth did not decrease after 30 days. It appears that embryonic tissue juices are not necessarily toxic for heterologous fibroblasts, and that they can be used in the building up of protoplasm in the tissues of a different species. In experiments made long ago, the action of tissue juice was described as being specific. The premature death of the fibroblasts cultivated in heterologous juices at that time would now appear to have been due to spontaneous changes in the pH and the deterioration that even normal chick embryo juice at a pH of 7.8 undergoes spontaneously. In the recent experiments, when freshly prepared homologous and heterologous juices were used, their action on chicken fibroblasts in pure culture was identical. However, the fibroblasts produced in cultures nourished by rabbit juice grew better when transferred to rabbit serum than did ordinary chicken fibroblasts. It has not been determined as yet whether this effect is due to an immunization of the fibroblasts against rabbit humors, or to some decrease in the specificity eventuating in cells intermediate between rabbit and chicken fibroblasts. It may be concluded that, under the conditions of the experiments : 1. Pure cultures of chicken fibroblasts increase in mass under the influence of extracts of adult homologous tissues. But they ultimately die while the fibroblasts cultivated in embryonic tissue juices live indefinitely. 2. The increase in mass of chicken fibroblasts cultivated in the juices of mouse, guinea pig, rabbit, and chick embryos is about identical. 3. Chicken fibroblasts produced in cultures nourished by rabbit embryonic tissue juice are less sensitive to the inhibiting action of rabbit serum than ordinary chicken fibroblasts. 4. Cultures of chicken fibroblasts in extracts of adult tissues of mice, guinea pigs, and rabbits increase slightly in mass, but the increase is temporary and death occurs after a few passages.     

CUTANEOUS REACTIVITY OF IMMUNE AND HYPERSENSITIVE RABBITS TO INTRADERMAL INJECTIONS OF HOMOLOGOUS INDIFFERENT STREPTOCOCCUS AND ITS FRACTIONS

Rabbits were immunized intravenously with intact indifferent streptococci, with homologous P fraction, and with an emulsion of mechanically ground cocci; others were sensitized by intravenous injection of the intact microorganisms. Their serologic and dermal reactions to these materials and to the homologous S fraction were compared with those of normal animals. The dissociation, in certain instances, between circulating antibody and dermal reactivity was noteworthy. From the results the following conclusions were drawn. 1. Intradermal injection of a soluble streptococcal protein into a rabbit immunized intravenously with that protein leads to the immediate anaphylactic type of skin response; while similar dermal testing of a rabbit sensitized by intracutaneous inoculation of the intact microorganism induces the delayed (tuberculin) type of response. 2. The induction of the immediate type of dermal reaction to streptococcal protein requires more than the mere presence of a high serum precipitin titer to that protein. 3. Lesions of the immediate type can be induced by the intradermal injection of a streptococcal carbohydrate into rabbits immunized intravenously with intact cocci and showing a high serum precipitin titer to that carbohydrate. 4. Intravenous immunization of rabbits with an emulsion of mechanically ground indifferent streptococci leads to the production of only non-type-specific antibodies. 5. It is possible that carbohydrate as well as protein fractions of indifferent streptococci are capable of eliciting the delayed type of dermal response in rabbits intracutaneously sensitized with that microorganism.     

ANTIBODY RESPONSE OF HUMAN BEINGS FOLLOWING VACCINATION WITH INFLUENZA VIRUSES

Eleven different preparations of influenza virus were used to vaccinate large groups of human beings. The antibody response to these vaccines was measured by means of the in vitro agglutination inhibition test, and the geometric mean titers of sera taken 2 weeks after vaccination were compared. From these comparisons the following conclusions were drawn: 1. There was a wide individual variation in the antibody response of human beings to the same preparation of influenza virus administrated subcutaneously. The amount of antibody produced by a group with a low prevaccination antibody level was very nearly the same as the amount produced by groups that had higher initial levels. 2. The use of the X strain of distemper virus in the preparation of an influenza vaccine did not enhance the antigenicity of the influenza virus present. 3. Within certain limits the mean antibody response of human beings increased as the amount of virus injected was increased. When large amounts of influenza A virus were given, the antibody response was of the same order of magnitude as that which occurred following actual infection by this virus. 4. When the vaccine was prepared from allantoic fluid, there was no significant difference in the antibody response of human beings given active virus, formalin-inactivated virus, heat-inactivated virus, or virus inactivated by the drying process. 5. Ground infected chick embryos, when diluted with infected allantoic fluid, gave a greater antibody response than allantoic fluid alone (when the virus remained active). The antigenicity of such a preparation was diminished when the virus was inactivated by formalin. 6. Antibody levels 6 and 9 weeks after vaccination showed a marked drop from the 2-week postvaccination levels. In a small group the antibody levels at 5 months were still further reduced. Those individuals who possessed the higher titers tended to lose their antibodies faster than did those at a lower level.     

THE CATABOLISM OF HOMOLOGOUS AND HETEROLOGOUS 7S GAMMA GLOBULIN FRAGMENTS

The catabolism of homologous and heterologous 7S gamma globulin fragments obtained by pepsin and papain digestion was studied in rabbits, guinea pigs, and mice. The elimination from the circulation of I* labeled gamma globulin fragments was followed and the urinary excretion of the total and protein-bound I* activity determined. Evidence is presented that the molecular structure responsible for the catabolism of 7S gamma globulin is located in papain fragment III. The elimination of papain fragment III was slow and closely related to the intact gamma globulin, whereas the pepsin fragment and papain fragments I and II were rapidly eliminated and catabolized in all species examined. Prolonged incubation with cysteine altered papain fragment III as shown by a rapid catabolism of a large portion of incubated fragment III within 24 hours after injection. Small amounts of intact RGG and RGG papain fragment III were excreted as protein-bound I* activity in the urine. On the other hand, large amounts of the pepsin fragment and papain fragments I and II of RGG were excreted as protein-bound I* activity in the urine. The possibility of a molecular structure present in papain fragment III, which may be responsible for tubular reabsorption in the kidney, is discussed. The rate of urinary excretion of fragments obtained from RGG was different from that of fragments obtained from gamma globulin of several other species. In general, small amounts of the pepsin fragment and papain fragment III obtained from gamma globulin other than RGG were excreted as protein-bound I* activity. The amounts of fragment I* excreted as protein-bound I* activity depended on the species in which it was injected, as well as the source of the gamma globulin. The rapid catabolism of the pepsin fragment and papain fragments I or II which bear antibody-combining sites suggest that their use for the prophylactic treatment of tetanus and diphtheria in man is limited.     

流感病毒对两种细胞敏感性的比较

目的比较流感病毒对Vero细胞和MDCK细胞敏感性的差异及影响敏感性的因素,寻找流感病毒灭活试验的最佳细胞。方法用测定两种细胞感染病毒后TCID50值和血凝效价值的方法,了解流感病毒对两种细胞敏感性的差异。结果Vero细胞和MDCK细胞接种流感病毒72 h,测得血凝效价分别为1:64和1:128;MDCK细胞的病变较Vero细胞明显。终浓度为5μg/ml的胰酶可提高两种细胞增殖流感病毒的血凝效价,但对TCID50值的大小无明显的影响。随着维持液中血清浓度的升高,两种细胞增殖病毒的血凝效价逐渐降低,MDCK细胞染毒后的TCID50值也明显减小。结论流感病毒对MDCK细胞的敏感性高于对Vero细胞的敏感性,胰酶和血清能影响病毒对细胞的敏感性。     

STUDIES ON INFLUENZA VIRUS : THE COMPLEMENT-FIXING ANTIGEN OF INFLUENZA A AND SWINE INFLUENZA VIRUSES

Influenza complement fixation tests designed for use with ferret serum are described. Complement-fixing antigens derived from influenza ferret lungs were unsatisfactory due to their low content of soluble antigen; those prepared from mouse lungs or developing chick embryo membranes proved to be better antigenically and were reliable when the various reagents in the test were properly adjusted to eliminate non-specific fixation of complement. The results of cross complement fixation tests indicated that the soluble antigens of the PR8 and W.S. strains of influenza A virus were closely similar, if not identical. They indicated also that the soluble antigen of swine virus possessed components present in the antigens of the human strains of virus.     

THE EFFECT OF TOLERANCE ON THE SPECIFICITY OF THE ANTIBODY RESPONSE AND ON IMMUNOGENICITY : ANTIBODY RESPONSE TO CONFORMATIONALLY AND CHEMICALLY ALTERED ANTIGENS

Animals were rendered tolerant to human albumin and were then immunized with azo derivatives of human albumin which differed in the number of hapten groups per molecule and in the extent of conformational change. The incidence and specificity of the resulting antibody response was studied and the presence of antibody to azo groups and to conformationally altered protein determinants was demonstrated. Reactivity with the tolerance-inducing antigen was shown to be due to antibodies directed against conformationally altered protein determinants. The difference in the response of tolerant animals to hapten-poor and hapten-rich derivatives was attributed to the extent of conformational alteration. A genetic factor appeared to be implicated in the capacity of tolerant animals to respond to an antigen which cross-reacts with tolerance-inducing macromolecules.     

THE SUSCEPTIBILITY OF SWINE TO THE VIRUS OF HUMAN INFLUENZA

Swine inoculated intranasally with human influenza virus alone develop an ill defined, mild, and usually afebrile illness of short duration. At postmortem the anterior lobes of the lungs of such animals contain scant, scattered areas of lobular atelectasis. Transmission of the virus for 5 serial passages through two groups of swine failed noticeably to enhance its pathogenicity for this species. The disease produced in swine by infection with human influenza virus alone is indistinguishable clinically and pathologically from that caused by infection with swine influenza virus alone. Transmission of human influenza virus from swine to swine by contact succeeded in only one of four attempts. Swine inoculated intranasally with a mixture of human influenza virus and H. influenzae suis usually develop a febrile, depressing illness similar to mild swine influenza. The pneumonia encountered in such animals at autopsy is similar to but less extensive than that seen in swine influenza. In some animals H. influenzae suis fails to become established and the disease then seen is identical with that caused by human influenza virus alone. The human influenza virus recovered after 5 serial transfers in swine was immunologically the same as that with which the experiments were begun.     

APPEARANCE OF ISOAGGLUTININS IN INFANTS AND CHILDREN

1. The isoagglutination reaction of 131 infants and children from birth to 10½ years was examined by testing their serum and washed corpuscles microscopically against the serum and corpuscles of each of the four adult groups. 2. The grouping as present in adults is rarely present in blood from the umbilical cord. 3. At birth and during the 1st month of life isoagglutination is rarely present, but the percentage of infants in whom the isoagglutinin group is established increases with age, so that after 1 year the group is usually established, and after 2 years is always present as in adults. 4. The grouping is established in the corpuscles before it is established in the serum; i.e., the corpuscles acquire agglutinophilic receptors before the serum acquires agglutinin. Therefore, Group I is the first group to be formed and Group IV is the last. 5. The early grouping in the corpuscles before the group is established in the serum is liable to change by the acquisition of new receptors. 6. When the grouping has been established in both serum and corpuscles it does not change. 7. Isoagglutinins are present in mother''s milk and the grouping is identical with that in the mother''s blood. These agglutinins are probably not transmitted to the nursing infant through the milk. 8. On account of the differences between the agglutination reactions in the blood of mother and child it is not safe to transfuse an infant from its mother without making the preliminary tests.