bluuebunny/crossref_metadata_2025_split huggingface dataset:
Immunological Studies in Tuberculosis
Authors: Petroff S. A. , Stewart F. W. 
Published: December 2022

Summary
Five series of experiments with guinea pigs sensitized with dead tubercle bacilli are reported, in which tuberculin hypersensitiveness was induced with dead tubercle bacilli. During the allergic state inoculations of living tubercle bacilli were made, with the use of approximately the same number of normal control animals. The sensitized animals outlived the controls an average of 46 days. The amount of macroscopic disease at autopsy in the former was much less extensive than in the latter, confirming the belief that dead tubercle bacilli can induce some degree of protection. A small series of guinea pigs was sensitized with Dreyer's defatted tubercle bacilli. We produced only a mild skin hypersensitiveness and even that not uniformly. No appreciable resistance could be observed in these animals. The average duration of life was approximately the same as that of the control animals.
Genetic Differences in BCG-Induced Resistance to Schistosoma Mansoni Are not Controlled by Genes within the Major Histocompatibility Complex of the Mouse
Authors: Civil Richard H. , Mahmoud Adel A. F. 
Published: December 2022

Summary
Induction of nonspecific resistance to Schistosoma mansoni infection after the i.v. injection of viable BCG was investigated in outbred mice and a panel of inbred and H-2 congenic strains. Significant protection was induced in CF1, A/J, C57BL/6, C57BL/10, DBA/2, C57BR, and SJL mice. BALB/c mice were not protected whereas CBA and C3H mice expressed intermediate degrees of protection. Expression of the protective phenomenon is not controlled by genes within the MHC as shown by the marked differences in response between BALB/c and DBA/2 (H-2d) as well as between C57BR and C3H (H-2k) mice. H-2 congenic strains with C57BL/10 background (B10.A and B10.D2) were high responders. BALB.B10 mice carrying the high responder (B10) MHC on the nonresponder (BALB/c) background were not protected. The degree of splenic hypertrophy did not correlate with the expression of nonspecific resistance. These results demonstrate that, in addition to controlling specific immune responses, genetic differences influence the nonspecific protective phenomena related to BCG administration as well.
Immune Response to Immunization via the Anterior Chamber of the Eye
Authors: Kaplan Henry J. , Streilein J. Wayne 
Published: December 2022

Abstract
Exposure to alloantigen via the anterior chamber of the eye elicits a transient suppression of cellular immunity, whereas humoral immunity is preserved—i.e. F1 LI-ID. The majority of lymphoid cells inoculated into the anterior chamber are retained within the posterior segment of the eye. The latter serves as a depot of alloantigen, allowing the chronic egress of small numbers of cells into the vascular tree. The persistence of this antigen depot is essential to the development of F1 LI-ID. Since there is a preferential distribution of cells that migrate from the eye to the spleen, the functional integrity of the latter is also necessary to elicit F1 LI-ID. It is concluded that an anatomically intact spleen, i.v. presentation of antigen, and persistence of antigen within the eye are all important to the elicitation of this phenomenon.
Molecular Basis of B Cell Activation: Mitogenicity of Native and Modified Digitalis Glycosides
Authors: Hammarström Lennart L. G. , Smith C. I. Edvard 
Published: December 2022

Abstract
Lanatoside C, a digitalis glycoside, has previously been shown to be a potent polyclonal B cell activator for mouse lymphocytes. Since the chemical structure of lanatoside C is well defined we investigated the effect of different chemical modifications on the mitogenic properties of the glycoside in order to determine the molecular basis of B cell activation. The presence of an OH-group at C12 in the steroid nucleus proved to be essential for activation to occur in serum-free medium. Likewise, an intact carbohydrate side chain at C3 appeared to be necessary for retaining mitogenic properties. In serum-supplemented cultures, however, a much more complex response pattern was observed where the prerequisites for activation were not as distinct as in serum-free medium.
Triggering of Histamine Release from Rat Mast Cells by Divalent Antibodies against IgE-Receptors
Authors: Ishizaka Teruko , Ishizaka Kimishige 
Published: December 2022

Abstract
Antibodies against receptor molecules for IgE on rat basophilic leukemic (RBL) cells were prepared by immunization of a rabbit with immune precipitates composed of IgE-receptor complexes and anti-IgE. Antibodies against cell surface components were specifically purified by using RBL cells and rendered specific for mast cells by appropriate absorption. The major antibodies in the final preparation (anti-RBL) were directed against receptor molecules. It was found that the F(ab′)2 fragments of anti-RBL induced histamine release from rat mast cells and caused immediate skin reactions in normal rats. These reactions by anti-RBL or its F(ab′)2 fragments were inhibited if the receptors on mast cells had been saturated with IgE. The Fab′ fragments of anti-RBL could bind with receptors on RBL cells and blocked passive sensitization of mast cells with IgE antibodies, but failed to induce skin reactions and histamine release from normal mast cells. Sensitization of normal rat skin with the Fab′ fragments followed by an i.v. injection of anti-rabbit IgG induced skin reactions. The results indicated that bridging of receptor molecules by divalent anti-receptor antibody triggered mast cells for histamine release.
Structural and Genetic Studies on Chicken 7S Immunoglobulin Allotypes
Authors: Foppoli James M. , Wakeland Edward K. , Benedict Albert A. 
Published: December 2022

Abstract
Low concentrations of allotypic specificity CS-1.1 were detected in the sera of two inbred chicken lines [University of California, Davis (UCD) 7 and Regional Poultry Research Laboratory 15I4] previously reported to lack this specificty. The CS-1.1 alloantigen in 15I4 chickens has the same specificity as the major allotype in a line of chickens (UCD 2) in which it was initially defined. In 15I4 chickens, CS-1.1 allotype is present on a population of molecules distinct from those which carry the major allotype; thus a second 7S Ig H chain locus, CS-2, is proposed.
The concentration of CS-1.1-bearing molecules determined by two different methods was 7 µg/ml and 230 µg/ml in 15I4, whereas UCD 2 chickens had 4 mg/ml of CS-1.1 molecules. The levels of CS-1.1 inhibitory activity in 15I4 birds remained relatively constant over a 30-day period.
The presence of two 7S Ig populations in 15I4 chickens may be interpreted as evidence either for 7S Ig subclasses with shared allotypes or for a pseudoallelic organization of genes controlling expression of 7S Ig H chains. The results were consistent with the presence of redundant C region genes, differing in allotypes, whose expression is under the control of an as yet undefined regulatory mechanism.
Suppressor T Cells for IgE and IgG in Peyer's Patches of Mice Made Tolerant by the Oral Administration of Ovalbumin
Authors: Ngan Johnson , Kind Leon S. 
Published: December 2022

Abstract
A single oral dose of ovalbumin (Ov) resulted in inhibition of IgE formation in mice subsequently immunized i.p. with Al(OH)3-Ov. Repeated feeding of Ov (on alternate days for 2 weeks) induced the formation of detectable suppressor cells in Peyer's patches and spleen. Suppression was demonstrated by the ability of adoptively transferred Peyer's patch or splenic lymphocytes from Ov-fed tolerant mice to inhibit IgE formation in Ov-immunized syngeneic recipients. Suppressor cells could be induced by feeding mice as little as 100 µg of Ov on alternate days for 2 weeks. Suppression was specific and Peyer's patch lymphocytes were shown to be more effective suppressors than splenic lymphocytes.
Potentiation of Mast Cell Mediator Release by Adenosine
Authors: Marquardt Diana L. , Parker Charles W. , Sullivan Timothy J. 
Published: December 2022

Abstract
Since extracellular adenosine can alter adenylate cyclase activity and cell function in a variety of tissues, the effect of adenosine on mediator release was studied with isolated rat mast cells. Adenosine did not alter the rate of spontaneous release, but histamine release induced by anti-IgE, concanavalin A (Con A), 48/80, or the calcium ionophore A23187 was markedly enhanced by 1 nM to 0.1 mM adenosine. Mast cells preincubated in the presence of 10 µM adenosine and then challenged with 0.1 µg/ml of A23187 released 71.5% (± 7.4 SEM) of the cellular histamine compared to a 38.2% (± 3.0 SEM) release from control cells. Adenosine caused a 3.0-fold (± 0.2 SEM) increase in the rate of release occurring 30 to 60 sec after A23187 addition, but did not change the duration of mediator release. Adenosine did not appear to decrease the minimum concentration of ionophore required to stimulate release. The poorly metabolized adenosine analog 2-chloroadenosine (100 µM) potentiated release approximately 2-fold whereas dipyridamole, an inhibitor of mast cell uptake of adenosine, did not inhibit adenosine potentiation suggesting that adenosine actions on mast cells may be mediated by direct activation of cell-surface receptors. Adenosine modestly potentiated the fall in cyclic AMP levels occurring 30 to 60 sec after ionophore challenge, raising the possibility that potentiation may be mediated by alterations in cyclic AMP metabolism. Mast cells suspended in media containing 1 mM EGTA and no added calcium demonstrated adenosine potentiation of A23187-induced release indicating that the adenosine effect was not mediated by increased translocation of calcium into the cells. Adenosine potentiation was completely blocked by 100 µM theophylline, a known inhibitor of adenosine binding, with 50% inhibition of release occurring at 3 µM theophylline. These studies indicate that adenosine may be an important modulator of mast cell function in complex tissues and that part of the pharmacologic action of theophylline in human bronchial asthma may be through inhibition of adenosine binding, rather than direct effects on cyclic AMP metabolism.
Membrane Receptors of Mouse Leukocytes
Authors: Rabellino Enrique M. , Ross Gordon D. , Polley Margaret J. 
Published: December 2022

Abstract
Mouse leukocytes were studied for membrane receptors for the third C component by rosette formation with C coated erythrocytes (EAC). Methods were devised for the preparation of EAC complexes containing either mouse C3b or mouse C3d. EAC 1-3dmo were prepared from EA treated with whole mouse serum while EAC 1-3bmo were produced from EAC 142hu treated with whole mouse serum containing sodium suramin. The specificity of the EAC complexes for mouse leukocytes was confirmed by inhibition experiments using fluid phase human C3d. Low concentrations of fluid phase human C3d inhibited EAC1-3dmo rosettes but failed to inhibit EAC 1-3bmo rosettes. Eight-fold higher concentrations of fluid phase C3d caused partial inhibition of EAC1-3bmo rosette formation with lymphocytes, but not with other types of murine leukocytes. Thus mouse leukocytes apparently contain the same two types of C receptors as do human and guinea pig leukocytes. Mouse CR1 is specific for a non-C3d region of C3b, (possibly analogous to human C3c) whereas mouse CR2 is specific for both C3d and the C3d region of C3b.
Selective IgA Deficiency Associated with Total Villous Atrophy of the Small Intestine and an Organ-Specific Anti-Epithelial Cell Antibody
Authors: McCarthy D. M. , Katz S.I. , Gazze L. , Waldmann T. A. , Nelson D. L. , Strober W. 
Published: December 2022

Abstract
A patient with total villous atrophy of the small intestine, associated with selective IgA deficiency, presented after an acute febrile illness. Gluten-free diet and other standard treatments were without benefit. Studies revealed that T cell function, serum antibody production, delayed hypersensitivity, mixed leucocyte reaction, antibody-dependent and cell-mediated cellular cytotoxicity, and general immune responsiveness seemed intact. However, IgA could not be detected in serum, tissues, or external secretions and, cultured with poke weed mitogen, the patient's B cells failed to produce IgA. In addition, the patient's cells suppressed IgA production by control cells co-cultured in the presence of mitogen. Indirect immunofluorescent studies revealed in his serum an IgG-class organ-specific antibody which bound to villus cells in control intestine, obtained from normal and diseased subjects, but not to cells in the patient's diseased mucosa. After low dose cyclophosphamide therapy, IgA remained absent but suppressor activity disappeared, intestinal villi regenerated fully, cellular cytotoxicity was reduced, and the antibody titer in serum slowly declined. The antibody bound strikingly to mature cells in the patient's regenerated villi, on indirect but not direct immunofluorescence. These unique findings suggest an autoimmune aetiology. No such antibodies were found in other IgA-deficient subjects.
Structural Studies of Rabbit IgA Allotypes: Partial Amino Acid Sequences of α-Chain Allotypes Controlled by Alleic Genes at the Cαg Locus
Authors: Malek Thomas R. , Peterson Bruce E. , Hanly W. Carey , Knight Katherine L. , Friedenson Bernard 
Published: December 2022

Abstract
Four α-chain allotypic specificities of the IgA-g subclass of rabbit IgA are controlled by allelic genes at the Cαg locus. The structural basis for three of these allotypic specificities, g74, g75, and g76, was investigated by amino terminal sequence analysis. α-Chain fragments were isolated from Fc2α fragments which were obtained by tryptic digestion of g74, g75, and g76 secretory IgA. Amino acid sequence data for the chains were obtained for 92 positions; comparison of these sequences with the sequence of human α1-chain revealed approximately 70% homology with the Cα2 domain. The results indicated that g74 α-chains were cleaved 60 residues N-terminal to the cleavage site in g75 and g76 α-chains.
By comparison of sequences of 24 residues of g75 and g76 α-chains, one allotype-related difference was observed (a cys/ser interchange at position 311). Based on homologies with the human α1-chain, a model for the arrangement of disulfide bonds in rabbit α-chains is proposed; several differences between rabbit and human are indicated, as are differences among the rabbit allotypes. The most striking difference is the apparent presence of the “extra” intradomain disulfide bond in the Cα2 domain of g74 molecules and its absence in g75 and g76 molecules.
Cellular Immunity in Infectious Mononucleosis
Authors: Nikoskelainen Jukka , Ablashi Dharam V. , Isenberg Richard A. , Neel Elizabeth U. , Miller Rupert G. , Stevens David A. 
Published: December 2022

Abstract
Infectious mononucleosis (IM) patients, Epstein-Barr virus (EBV)-seropositive and seronegative healthy donors, and patients with other viral infections were tested for lymphocyte blastogenesis (LB) with phytohemagglutinin and six EBV (virus concentrate, culture supernatant, and soluble [S] antigen) or control antigens. Fluorescent antibodies to EBV viral capsid antigen of IgG, IgM, IgA specificities, to nuclear antigen (EBNA), and heterophile antibodies were also assayed. These were correlated with clinical parameters (fever, pharyngitis, adenopathy, hepatitis, splenomegaly, atypical lymphocytes, and total mononuclear cell counts).
EBV viral and S antigen-induced LB was significantly greater in seropositive donors. IM patients had antigen specific LB below that of seropositive donors initially and low responses for the acute phase of illness when clinical symptoms were present and antibody titers were maximal. Specific LB rose to a peak at 3.5 to 9 weeks when the patients had recovered, most laboratory findings had returned to normal, and antibodies had declined. At peak, specific LB in IM patients exceeded that of seropositive donors, but later declined.
These results demonstrate specific cell-mediated immunity (CMI) to EBV, and indicate that this develops slowly in IM and contrasts with the evolution of the clinical events and humoral immunity. This correlation supports the hypothesis that CMI is the mechanism of terminating lymphoproliferation in IM.
Radiochemical Characterization of Hemoglobins Lepore and Kenya: Unique Antigenic Determinants Located on Hybrid Hemoglobins
Authors: Garver Fred A. , Altay Gultekin , Baker Marilyn M. , Gravely Marsha , Huisman Titus H. J. 
Published: December 2022

Abstract
Antisera were produced in rabbits to the three known types of Lepore hemoglobins, which contain hybrid δ-β non-α-chains, and to hemoglobin Kenya, which has a hybrid γ-β non-α-chain. By using a sensitive radioimmunoassay technique, the absorbed antisera were shown to contain an antibody population that was specific for the hybrid hemoglobin and did not cross-react with normal hemoglobins. However, with the absorbed Lepore-specific antisera, the three known types of Lepore hemoglobins were antigenically indistinguishable from each other, suggesting that antibodies are not produced to the primary structural differences which define the three non-α-chains of the Lepore hemoglobins. These studies demonstrate that the non-α-subunits of hemoglobins Lepore and Kenya possess unique antigenic determinant sites, evidently resulting from an altered polypeptide conformation.
Impairment of Host vs Graft Reaction in Pregnant Mice
Authors: Clark David A. , McDermott Mark R. 
Published: December 2022

Abstract
The fetus resulting from an allogeneic (interstrain) mating represents a type of graft that is not rejected by the mother. Nevertheless, the maternal immune system seems to recognize and to react to the presence of the fetus in a number of ways. One such manifestation is significant enlargement of the lymph nodes that drain the uterus (DLN) of pregnant rodents. We have tested the DLN lymphocytes of mice for reactivity to paternal H-2 alloantigens after interstrain mating. The DLN lymphoid cells obtained from pregnant mice killed fewer newborn F1 recipients in a graft-vs-host mortality assay, and generated less cytotoxic T cell activity against paternal H-2 antigens both in vivo and in vitro. In vitro mixing experiments demonstrated the presence of a cell-associated suppressor activity in the DLN of pregnant mice. This suppressor proved resistant to treatment with mitomycin C, and appeared in the DLN early in pregnancy.
Release of Arylsulfatase A but Not B from Rat Mast Cells by Noncytolytic Secretory Stimuli
Authors: Lynch Susan M. , Austen K. Frank , Wasserman Stephen I. 
Published: December 2022

Abstract
The net percentage of release of arylsulfatase activity from purified rat mast cells induced by rabbit anti-rat F(ab′)2 was consistently only about ⅓ that of histamine. Isoelectric focusing of the released and residual arylsulfatase activities demonstrated specific release of the A type without B and a net percentage of immunologic release of arylsulfatase A equivalent to that of histamine. When the net percentage of histamine and arylsulfatase A release were nearly maximal (88 and 76%) in response to the calcium ionophore A23187, specific release of arylsulfatase B did not occur. Thus, arylsulfatase A and not B was associated with the secretory granule released from the rat mast cell by reversed anaphylaxis or the calcium ionophore. In contrast, subcellular fractionation of water-lysed mast cells yielded arylsulfatase B with the heparin- and chymase-containing granule fraction and arylsulfatase A in the aqueous fraction comprised of cell sap and granule water eluate. It may be that arylsulfatase B resides in a minor second granule, whereas arylsulfatase A is loosely associated with the predominant secretory granule of the rat mast cell.
Production of Antisera Specific for Idiotype(s) of Murine Anti-(T,G)-A--L Antibodies
Authors: Pincus Seth H. , Sachs David H. , Dickler Howard B. 
Published: December 2022

Abstract
Antibodies to the synthetic polypeptide (T,G)-A--L were raised in C57BL/10 and C3H.SW mice. For each strain, the anti-(T,G)-A--L antibodies from 10 animals were pooled, affinity purified on a (T,G)-A--L-Sepharose column, and used to immunize Lewis rats. The resulting rat antisera were adsorbed with insolubilized normal mouse globulin in order to remove anti-isotypic and antiallotypic antibodies. The residual antibodies specifically inhibited the binding of (T,G)-A--L by anti-(T,G)-A--L as measured by a radioimmunoassay. The specificity of this inhibition was demonstrated as follows: 1) failure of the anti-(T,G)-A--L anti-idiotype to inhibit the binding of nuclease to anti-nuclease antibody of the same allotype; 2) failure of Lewis anti-[B10 anti-(T,G)-A--L] to inhibit C3H.SW anti-(T,G)-A--L and vice versa; 3) ability to absorb anti-C3H.SW anti-idiotypic activity on insolubilized C3H.SW anti-(T,G)-A--L but not on B10 anti-(T,G)-A--L. The same or cross-reactive idiotype(s) was present in the majority of individuals of each of these strains.
Immunoregulatory Aberrations in Systemic Lupus Erythematosus
Authors: Fauci Anthony S. , Steinberg Alfred D. , Haynes Barton F. , Whalen Gail 
Published: December 2022

Abstract
This study was undertaken to delineate the nature of the immunoregulatory defect in patients with systemic lupus erythematosus (SLE). Thirty-eight SLE patients were studied and it was found that in addition to an absolute T lymphocytopenia, these patients had a selective proportional and quantitative deficiency (P &lt; 0.01) of a subpopulation of T cells possessing a receptor for IgG (TG). This T cell subpopulation has been previously demonstrated to be the suppressor cell population in pokeweed mitogen (PWM)-driven intracytoplasmic Ig production. T cells with a receptor for IgM (TM) which have been shown to be the helper T cells for Ig production were not significantly different from normals in proportion or absolute numbers.
By employing a PWM-induced plaque-forming cell (PFC) assay against sheep red blood cells (SRBC), it was shown that SLE patients had a markedly reduced response of 18 (±4.2) PFC/106 lymphocytes compared to normals with 153 (±18.4) PFC/106 lymphocytes (P &lt; 0.001). This suppressed PFC response was felt to result from in vivo polyclonal activation associated with the autoimmune state.
SLE patients had a marked defect in the ability of their lymphocytes after Con A activation to generate suppressor cells of the PWM-induced PFC response, whereas their ability to be suppressed by suppressor stimuli appeared intact. Despite considerable variability from patient to patient, lymphocytes from SLE patients in general had adequate T helper cell function and could be helped by normal allogeneic T helper cells. Thus, this study demonstrates that SLE patients have a quantitative defect in a subpopulation of T cells with suppressor capability. In addition, they have a defect in the ability to generate suppressor cell function upon appropriate activation. These findings may lend further insight into the understanding of the immunoregulatory defect in SLE.