bluuebunny/crossref_metadata_2025_split huggingface dataset:
Neoplastic cells obtained from Hodgkin's disease are potent stimulators of human primary mixed lymphocyte cultures.
Authors: Fisher R I , Bostick-Bruton F , Sauder D N , Scala G , Diehl V 
Published: December 2022

Abstract
Neoplastic cells obtained from the pleural effusion of a patient with Hodgkin's disease have been maintained in culture since 1978. These tumor cells have been shown to have the cytologic features, cytochemical staining, and cell surface markers of Reed-Sternberg cells. In this study we demonstrate that the cell line termed L428 is a potent stimulator of the primary human mixed lymphocyte reaction. Significant proliferation occurred when mononuclear leukocytes obtained from normal donors were stimulated with radiated L428 cells at responder:stimulator ratios varying from 200:1 to 20:1. Proliferative responses occurred between days 3 and 6 of the cultures with maximal proliferation on day 5. Under optimal culture conditions, mean net proliferative response of 14 normal donors was 51,000 +/- 10,600 dpm. The mixed lymphocyte response was totally blocked by concentrations of monoclonal anti-Ia antibody that had no effect on concanavalin A-induced proliferation. However, the mixed lymphocyte response was not blocked by an anti-K562 cell monoclonal antibody of the same immunoglobulin subclass that binds to the L428 cells. Antigen processing by responder monocytes or Ia-positive cells was not required for the MLC. When responder T cells from two normals were depleted of Ia-bearing cells and monocytes, the mixed lymphocyte reaction between the two normals was eliminated, yet the stimulation of each normal by the L428 cells was not reduced. The cells that proliferated in response to stimulation by the L428 cells were T cells, primarily of the helper subset. No IL 1 activity could be detected in concentrated supernatants of L428 cultures after stimulation of L428 cells by mitogens, phorbol esters, or muramyl dipeptide, or in the MLC. All of these cultures contain fetal calf serum. However, the L428 cells are capable of producing IL 1, because IL 1 was detected when the L428 cells were stimulated with LPS in the absence of fetal calf serum. These neoplastic cells, obtained from Hodgkin's disease, have many similarities to the murine as well as human dendritic cells.
Sharing of Ia antigens between species. IV. Interspecies cross-reactivity of monoclonal antibodies directed against polymorphic mouse Ia determinants.
Authors: Lunney J K , Osborne B A , Sharrow S O , Devaux C , Pierres M , Sachs D H 
Published: December 2022

Abstract
The specificity of interspecies Ia cross-reactions has been analyzed by testing a panel of monoclonal antibodies (mAb) to mouse I-E and I-A antigens for reactivity with pig Ia antigens. Our earlier studies showed that mouse anti-I-E alloantisera recognized common determinants on Ia antigens of other species, whereas anti-I-A alloantisera showed much more limited cross-reactivity. These results were confirmed using a panel of 17 anti-I-E mAb, 10 of which were cytotoxic to pig cells. 2D gel electrophoretic analyses of precipitates with these mAb of 35S-labeled, NP40 solubilized pig cells revealed a limited set of protein spots that appeared to be identical to the subset of pig Ia antigens precipitated by A.TH anti-A.TL alloantiserum. Because the cross-reactive mouse sera were produced in mouse strains that do not express an I-E molecule (H-2b and H-2s), it was anticipated that the cross-reacting antibodies would be reactive with the monomorphic determinant of the I-E molecule, Ia.7. However, comparison of the reactivity of these mAb with pig cells and mouse cells revealed that the cross-reactivity on pig cells correlated not with Ia.7 but rather with detection of epitope(s) of the I-E molecule associated with inter-strain polymorphism. Anti-I-A cross-reactions were also detected, but were weaker and more limited. These findings may have implications for the evolution of Ia antigens in mammalian species.
Isolation and identification of the third component of complement of Japanese quails.
Authors: Kai C , Yoshikawa Y , Yamanouchi K , Okada H 
Published: December 2022

Abstract
The identification of the third component of complement (C3) of Japanese quails was attempted by using rabbit antiserum prepared against quail serum-treated zymosan (ZX) as an initial reagent. This antiserum (anti-ZX) had agglutinating activity on rabbit erythrocytes reacted with quail antibody and quail complement (EACq) but not on EAq, and developed two precipitin lines against quail serum at beta- and gamma-regions in crossed immunoelectrophoresis. Subsequently, monospecific antisera to each of these precipitin lines were prepared in rabbits, and quail serum proteins reactive with these antisera were purified by salt precipitation followed by Sephadex gel filtration and DEAE cellulose column chromatography. One protein with a m.w. of 184,000 (184K) resembled mammalian C3 in that: 1) monospecific antiserum (anti-184K protein serum) agglutinated EACq but not EAq; 2) treatment of fresh quail serum with either inulin or zymosan resulted in the conversion of the precipitin line developed against 184K protein from gamma to beta in crossed immunoelectrophoresis; 3) the 184K protein was shown to consist of two polypeptide chains of 110K and 73K linked by disulfide bonds. Furthermore, the 184K protein in serum was cleaved through the incubation with inulin to 174K and 140K proteins that might correspond to C3b and C3c of human complement; 4) the 184K protein bound to zymosan was eluted with hydrazine or methylamine but not with Nonidet P-40, indicating that 184K protein binds to zymosan by a covalent bond but not by a hydrophobic one; and 5) by treatment of fresh quail serum with methylamine, complement reactivity was reduced, although its activity was restored by the addition of purified 184K protein. These results suggest the 184K protein is the quail's equivalent to mammalian C3. When quail serum was reacted with cells that had complement-activating capacity, quail C3 deposited on their membrane as in mammalians; however, no conversion of quail C3 was noted by the reaction with CVF. Antibody to quail C3 failed to cross-react with that in mammals.
The biologic activity of mast cell granules. VI. The effect of vinblastine-induced neutropenia on rat cutaneous late phase reactions.
Authors: Lemanske R F , Guthman D A , Oertel H , Barr L , Kaliner M 
Published: December 2022

Abstract
Type I immediate hypersensitivity reactions in human and rat skin may be followed by late phase reactions (LPR). A consistent feature of both human and rat LPR is the early histologic appearance of neutrophils, which, in rats, is followed by the later appearance (8 to 24 hr) of mononuclear cells. To determine the importance of the neutrophil in the development of LPR, rats were depleted of neutrophils using parenteral injections of vinblastine sulfate (VS). VS produced a dose-dependent neutropenia, with the maximal effect on day 4. LPR that were induced with anti-IgE, isolated mast cell granules (MCG), or purified high (greater than 10,000 daltons) and low (500 to 10,000 daltons) m.w. fractions obtained from MCG were significantly abrogated in VS-treated rats. In neutropenic rats previously immunized with complete Freund's adjuvant, the intensity of inflammatory reactions produced by skin testing with purified protein derivatives was also significantly reduced. Administration of exogenous neutrophils to neutropenic animals partially reconstituted the reduced LPR. These data confirm and extend previous observations on the contribution of neutrophils to delayed hypersensitivity reactions and provide evidence that the neutrophil is critical for the development of rat cutaneous LPR as well.
A phenotypically normal revertant of an adenosine deaminase-deficient lymphoblast cell line.
Authors: Uberti J , Peterson W D , Lightbody J J , Johnson R M 
Published: December 2022

Abstract
Two lymphoblast lines from a patient with partial adenosine deaminase deficiency have been obtained. The patient has a T cell deficiency, with normal B cell function, and has been successfully treated by multiple partial exchange transfusions with normal erythrocytes. The patient's lymphocytes have about 8% of normal adenosine deaminase activity. The derived lymphoblast line that initially had low adenosine deaminase activity has undergone spontaneous reversion to normal enzyme activity. The HL-A types remain the same as the patient's. Both cell lines have the same HL-A types, and eight isoenzymes are identical. In addition, the isoenzymes of a fibroblast line derived earlier, GM-2445, are identical with those in our lymphoblast lines. The following characteristics of the enzyme in the cell lines are normal: Km, Vmax, inhibitor sensitivity, heat sensitivity, and m.w. This suggests, but does not prove, that the low adenosine deaminase activity in this patient is caused by underproduction of a normal enzyme, and the observed reversion to normal activity in one line is a correction of this regulation defect.
Resistance to Streptococcus pneumoniae is induced by a phosphocholine-protein conjugate.
Authors: Wallick S , Claflin J L , Briles D E 
Published: December 2022

Abstract
Previous studies demonstrated that naturally occurring antibodies to the pneumococcal cell wall hapten phosphocholine (PC) are important for the survival of mice against infection with Streptococcus pneumoniae, and that passively administered hybridoma antibody to PC results in added resistance. To determine if a PC-protein conjugate could elicit protective levels of anti-PC antibody, mice were immunized with PC-keyhole limpet hemocyanin (KLH) and tested for their ability to resist challenge with virulent S. pneumoniae. PC-KLH-immunized mice were observed to be resistant to 10- to 1000-fold more organisms than unimmunized control animals. The levels of protection were comparable to those induced with capsular polysaccharide antigens, but had the advantage of not being type-specific; immunization with PC-KLH protected mice against both type 1 and type 3 organisms. The induced immunity appeared to be antibody-mediated; it could be passively transferred with immune serum, and absorption of the immune serum with PC-Sepharose removed its protective capacity. Anti-PC antibodies in the serum of immunized mice were primarily IgM and IgG3 and possessed predominantly the T15 idiotype. Antibodies with these particular isotypes and this idiotype also arise after immunization with heat-killed rough pneumococci and recently were shown to be important in the resistance of mice to pneumococcal infection.
IgA blocks IgM and IgG-initiated immune lysis by separate molecular mechanisms.
Authors: Griffiss J M , Goroff D K 
Published: December 2022

Abstract
Circulating IgA which does not bind the first component of complement (C) and does not activate the classical C pathway, blocks the initiation of C-mediated immune effector mechanisms. In at least two clinical situations, epidemic meningococcal disease and severe hepatic dysfunction, IgA blockade of one such mechanism, immune lysis, results in susceptibility to hematogenous bacterial dissemination. The presence of strain-specific IgM, but not IgG, in the sera of susceptibles at the time of dissemination suggested that IgA blockade of IgM-initiated lysis involves a separate mechanism more sensitive to quantitative changes than that involved in IgA blockade of IgG-initiated lysis. We report here that whereas IgA blockade of IgG-initiated immune lysis is a competitive function of the ratio of IgA to IgG, the blocking of IgM-initiated lysis is a noncompetitive function of the ratio of IgA to target cells, independent of the concentration of IgM. In the presence of sufficient IgA to saturate binding sites, IgM is an impotent bystander unable to compete for sites or initiate lysis. Therefore, C-mediated effector mechanisms are more sensitive to quantitative changes in circulating IgA and target cells (binding sites) in the absence of IgG than in its presence. Neither mechanism appears related to binding kinetics.
Infection of a macrophage-like cell line, P388D1 with reovirus; effects of immune ascitic fluids and monoclonal antibodies on neutralization and on enhancement of viral growth.
Authors: Burstin S J , Brandriss M W , Schlesinger J J 
Published: December 2022

Abstract
We studied the effect of antibody on the growth of reovirus, serotypes 1 and 3, in P388D1, a continuous mouse macrophage-like cell line. Enhanced growth of virus was observed when cells were infected in the presence of nonneutralizing monoclonal antibodies or subneutralizing concentrations of either immune ascitic fluids or neutralizing monoclonal antibodies. Both enhancement of viral growth and neutralization were accompanied by an antibody-mediated increase in binding of radiolabeled virus to P388D1 cells. Although neutralization was seen only with monoclonal antibodies directed toward the sigma-1 surface protein of the virus, enhancement was observed with two monoclonal antibodies directed toward other surface proteins. Trypsin treatment of P388D1 cells abrogated enhanced growth of virus mediated by a mouse IgG2a antibody; preincubation with P388D1 with human IgG1 but not IgG2 myeloma proteins also abrogated enhancement by immune ascitic fluid or monoclonal antibody. These observations are compatible with known properties of P388D1 Fc receptors and support the role of the Fc receptor in antibody-mediated infection.
T cell allotypic determinants encoded by genes linked to the immunoglobulin heavy chain locus. I. Establishment of monoclonal antibodies against allotypic determinants.
Authors: Aihara Y , Tadokoro I , Katoh K , Minami M , Okuda K 
Published: December 2022

Abstract
Monoclonal alloantibodies for T cell allotypic determinants were obtained by hybridizing SP-2 tumor cells with BALB/c (H-2d, Igh-1a) spleen cells, which had been repeatedly immunized with Con A-stimulated CB-20 (H-2d, Igh-1b) spleen cells. It was found that these monoclonal anti-CB-20 antibodies detect the new allotypic determinants (distinct from the B cell Igh-C region determinant) expressed only on the augmenting or suppressor T cells. Genetic analysis of these antigenic determinants revealed these antibodies react with the gene products located on the telomeric side chromosome of the Igh variable region gene (Igh-V) cluster. These antibodies when given in vivo caused a modification of antibody production. The antibody activity was absorbed by Con A-stimulated B10.BR (H-2b, Igh-1b), C57BL/6 (H-2b, Igh-1b), CWB (H-2b, Igh-1b), CB-20 (H-2d, Igh-1b), and BAB-14 (H-2d, Igh-1b) spleen cells, but not by Con A-stimulated C3H.SW (H-2b, Igh-1j), BALB/c (H-2d, Igh-1a), A/Sn (H-2a, Igh-1e), and C.AL-20 (H-2d, Igh-1d) spleen cells. In addition, in vivo these monoclonal antibodies modified anti-SRBC antibody production only in Igh-1b allotype-bearing mice. One monoclonal antibody reacted with 4-hydroxy-3-nitrophenyl acetyl- (NP) hapten-specific augmenting T cells, and the other two batches of monoclonal antibodies reacted with NP-specific suppressor T cells of NP-mediated cutaneous responses. A mapping study with these recombinants limits the gene coding for the T cell-specific determinants to a gene within the variable region to the telomeric side of NP-VH and to the centromeric side of prealbumin. This segment is inclusive of all immunoglobulin genes, the region Owen named IgT-C, and a histocompatibility gene (H-Ig).
Establishment of human cytotoxic T cell lines specific for human adult T cell leukemia virus-bearing cells.
Authors: Kannagi M , Sugamura K , Sato H , Okochi K , Uchino H , Hinuma Y 
Published: December 2022

Abstract
Human cytotoxic T cells (Tc) specific for autologous adult T cell leukemia virus- (ATLV) bearing cells were induced in vitro. Peripheral blood leukocytes (PBL) from healthy donors were stimulated repeatedly with autologous ATLV-bearing T cells. In two out of four seropositive donors and one out of two seronegative donors, the responder cells showed cytotoxicity for autologous ATLV-bearing cells, but not for autologous PBL, autologous cloned T cell lines, Epstein Barr virus-transformed autologous lymphoblastoid B cell line (LCL) cells, or various ATLV-negative cell line cells. The effector cells induced were cytotoxic T cells possessing Leu-1 and Leu-2a antigens that were able to proliferate continuously in vitro with periodic restimulation by appropriate cells and supplementation with partially purified T cell growth factor (TCGF). Of three Tc lines tested, one exhibited significant cytotoxicity against allogeneic ATLV-bearing cells that shared HLA-A2 antigen with the effector cells, possibly indicating HLA-restriction of ATLV-specific Tc. HLA-restriction was also suggested by cold target inhibition of cytotoxicity. Interestingly, Tc from this individual could also kill fresh adult T cell leukemia cells that were not expressing the ATLV surface antigens. These results, together with the target specificities of other Tc lines, suggest the possibility of at least two distinct target antigens recognized by ATLV-specific Tc, with one of these antigens differing from the ones detected by serologic methods.
Circadian rhythm of thymosin-alpha 1 in normal and thymectomized mice.
Authors: McGillis J P , Hall N R , Goldstein A L 
Published: December 2022

Abstract
Studies by many investigators have demonstrated that the immune system is subject to regular circadian fluctuation. Some rhythms that have been reported include circadian changes in components of the immune system, e.g., lymphocytes, and circadian variation in primary and secondary immune responsiveness. The observation that many of these rhythms are inversely correlated to the glucocorticoid rhythm has led to the suggestion that fluctuations in the immune system may be a result of the glucocorticoid circadian rhythm. This study was designed to see if thymosin-alpha 1 (Tsn-alpha 1), a 28-amino acid polypeptide isolated from bovine thymus that has been reported to influence thymocyte differentiation, might follow a circadian rhythm, and thus play a role in the periodicity of the immune system. In these experiments, groups of 10 C57BL/6 or Swiss Webster mice were sacrificed at 4- or 6-hr intervals over a 24-hr period. Serum Tsn-alpha 1 and corticosterone levels were determined by radioimmunoassay. Results from the first experiment showed that Tsn-alpha 1 undergoes a circadian rhythm (p less than 0.001) with an acrophase (time of peak levels) 1.5 hr after the onset of light, and an amplitude (amount of maximum variation from the 24-hr mean) of 0.493 ng/ml Tsn-alpha 1-like immunoreactivity. These results were confirmed in an experiment in which the animals were placed on a reversed light cycle. In a separate experiment, the Tsn-alpha 1 circadian rhythm persisted in mice thymectomized 6 mo. earlier. In this latter experiment, a significant increase in the amplitude of the corticosterone rhythm in the thymectomized relative to sham-operated controls was also observed. Although these experiments do not imply casuality, it is interesting that the time of peak Tsn-alpha 1 levels can be correlated with the time of optimal immune function.
Human T lymphocyte proliferation induced by a pan-T monoclonal antibody (anti-Leu 4): heterogeneity of response is a function of monocytes.
Authors: Kaneoka H , Perez-Rojas G , Sasasuki T , Benike C J , Engleman E G 
Published: December 2022

Abstract
Anti-Leu-4 is a murine monoclonal antibody that defines a molecule of 20,000 to 25,000 daltons present on all mature T lymphocytes in man. When cultured in the presence of 10 to 1000 ng/ml anti-Leu-4, the T cells of most individuals proliferate with peak responses on the third day of culture. T cells of both helper and suppressor lineages proliferate, but only in the presence of monocytes. Approximately 40% of individuals tested responded weakly or not at all to anti-Leu-4, despite normal responses to other stimuli. The variation in responsiveness between individuals could not be explained by differences in Leu-4 antigen density on the surface of T cells, differences in the rate of Leu-4 antigen modulation, or structural differences in the Leu-4 molecule as defined by the method of two-dimensional polyacrylamide gel electrophoresis. In the presence of monocytes from high responders, the T cells from low responders proliferated vigorously to anti-Leu-4, whereas monocytes from low responders failed to support proliferation by high responder T cells. On the other hand, low responder monocytes did not prevent T cells from proliferating in the presence of high responder monocytes. These results suggest that the failure of some individuals to respond to anti-Leu-4 is due to the absence or dysfunction of an essential monocyte population.
Selective failure of accessory cell function in Moloney murine leukemia virus-tolerant mice.
Authors: Biasi G , Collavo D , Chieco-Bianchi L 
Published: December 2022

Abstract
Accessory cell activity of spleen cells from M-MuLV neonatally injected (tolerant) mice was studied to evaluate their ability to take part in in vitro CTL generation against tumor-associated antigens induced by M-MSV. In contrast with accessory cell activity in normal spleen cells, spleen cells from M-MuLV-tolerant mice are unable to reconstitute the in vitro virus-specific CTL generation of M-MSV immune, Ia-depleted spleen cells. A selective defect seems to characterize M-MuLV-tolerant mice as their spleens constitute a good source of accessory cells for alloantigen CTL generation.
Proliferative responses to a nonspecific factor produced by irradiated stimulating cells can simulate antigen-specific secondary responses in the primed lymphocyte test.
Authors: Reitnauer P J , Brown L R , Hank J A , Sondel P M 
Published: December 2022

Abstract
The primed lymphocyte test (PLT) was utilized to investigate the biologic relationship between alloantigens and soluble environmental antigens. Human lymphocytes primed in vitro to the soluble antigens Candida (CAN), Tetanus (TET), or Purified Protein Derivative of Tuberculin (PPD) gave a strong proliferative response when restimulated with the initial soluble antigen in the presence of irradiated peripheral blood lymphocytes (PBL) acting as antigen-presenting cells (APC). Surprisingly, the soluble antigen-primed cells as well as alloantigen-primed cells responded to other soluble antigens in the presence of APC. By testing primed cells with supernatants derived from irradiated lymphocytes plus soluble antigen, it was apparent that the responses observed were in part due to stimulation by a soluble factor produced by the irradiated "APC" in response to the soluble antigen rather than to recognition of widespread cross-reactivity by the primed cells. This "nonspecific" factor production could be diminished by increasing the dose of irradiation to the APC or by using a T lymphocyte depleted- (SRBC-E-) APC population. In addition, certain antigen-reactive T cell clones did not respond to the nonspecific factor to the same degree as the primed bulk cultures. Nevertheless, the recognition of nonspecific stimulation induced by factors produced by irradiated lymphocytes is critical in the interpretation of primed lymphocyte responses to alloantigens or soluble antigens.