bluuebunny/crossref_metadata_2025_split huggingface dataset:
An antigen cross-reactive with gp52 of mammary tumor virus is expressed on a B cell subpopulation of mice.
Authors: Tax A , Ewert D , Manson L A 
Published: December 2022

Abstract
The reactivity of murine lymphoid tissue with biotinylated F(ab')2 fragments of monoclonal antibody VE7 (BIOT VE7), which reacts with gp52 of murine mammary tumor virus (MuMTV), was tested with fluoresceinated avidin in an indirect fluorescent antibody assay on live splenocytes. A small percentage of splenic lymphocytes in C3H/He mice infected exogenously with MuMTV, and in C57BL/6 mice that, like C3H/He, harbor several endogenous MuMTV proviruses in their genomes, were reactive with the monoclonal antibody. The antigen-positive splenocytes were shown to represent a subpopulation of B cells. The possible nature of the B cell-associated antigen recognized by monoclonal antibody VE7 is discussed.
Viral inhibition of lymphocyte mitogenesis: interference with the synthesis of functionally active T cell growth factor (TCGF) activity and reversal of inhibition by the addition of same.
Authors: Wainberg M A , Vydelingum S , Margolese R G 
Published: December 2022

Abstract
We have investigated the mechanisms whereby co-incubation of several types of virus particles with human lymphoid cells in the presence of T cell lectins leads to inhibition of the proliferative response that otherwise ensues. The data indicate that, in the absence of infection, such inhibition can be reversed by the addition to cultures of relatively high concentrations of fluids rich in T cell growth factor (TCGF) activity. The ability of these fluids to achieve such reversal of inhibition is both concentration- and time-dependent. Addition of the factor to virus co-incubated cells more than 26 hr after culture initiation does not restore responsiveness. We have also shown that virus co-incubated cultures are deficient with respect to their ability to synthesize detectable levels of TCGF activity in the presence of phytohemagglutinin. In contrast, the use of relatively dilute virus preparations (less than 10 particles per cell) permits partial responsiveness to lectin as well as the synthesis of moderate levels of TCGF. These finding suggest that viral inhibition of lymphocyte mitogenesis is mediated directly or indirectly by interference with the synthesis of functionally active TCGF activity.
Isolation and characterization of a CNBr cleavage peptide of influenza viral hemagglutinin stimulatory for mouse cytolytic T lymphocytes.
Authors: Wabuke-Bunoti M A , Fan D P 
Published: December 2022

Abstract
A polypeptide fragment obtained by CNBr cleavage of the hemagglutinin from A/JAPAN/305/57 influenza virus has been purified by using high performance liquid chromatography. The first five N-terminal amino acids as determined by sequential Edman degradations have localized this peptide to the HA2 subunit of the hemagglutinin between residues 103 and 123. This peptide, denoted HA2(103-23), can generate both proliferative and cytolytic responses from spleen cells of BALB/c mice previously immunized with A/JAPAN/305/57. These results demonstrate that a single nonglycosylated fragment of the influenza hemagglutinin as small as 21 amino acid residues is capable of being recognized as an antigenic determinant to generate influenza CTL from primed precursors.
Immunologically specific direct T lymphocyte-mediated killing of Nocardia asteroides.
Authors: Deem R L , Doughty F A , Beaman B L 
Published: December 2022

Abstract
Macrophage-depleted populations of splenic lymphocytes obtained from immunized and nonimmunized BALB/c mice were tested to determine their ability to kill Nocardia asteroides GUH-2 in vitro. Nocardia-primed lymphocytes, but not normal lymphocytes, killed N. asteroides. The ability of these lymphocytes to kill N. asteroides could be further enhanced by in vitro activation of the lymphocytes with nocardial cell wall fragments 12 to 48 hr before challenge. The nocardicidal activity of the lymphocytes was greater in populations enriched in T cells and was eliminated by lysing the lymphocytes with anti-Thy-1.2 plus C. N. asteroides-primed T cells were unable to kill a distantly related actinomycete, Rothia dentocariosa, and killed other species of Nocardia (N. brasiliensis and N. caviae) poorly or not at all, indicating that the microbicidal activity was immunologically specific. Light microscopy and electron microscopy revealed a close association between the T cell membrane and the cell wall of N. asteroides, with possible damage to the latter structure. The ability of immunologically specific T cells to recognize, bind, and kill Nocardia may be an important mechanism of host defense, because these microorganisms often are able to escape intracellular killing by macrophages.
In vitro growth of B lymphocytes infiltrating human melanoma tissue by transformation with EBV: evidence for secretion of anti-melanoma antibodies by some transformed cells.
Authors: Watson D B , Burns G F , Mackay I R 
Published: December 2022

Abstract
Epstein Barr virus was used to transform the B lymphocytes infiltrating metastatic tumor tissue from seven patients with melanoma. In this way it was possible to establish continuously growing B lymphoblastoid cell lines (LCL) derived from the tumor-infiltrating B lymphocytes from each of the seven patients. Antibody production of up to 50 micrograms/ml could be achieved by such cultures, and the lymphoblastoid cells could be cloned readily by limit dilution on a feeder layer of irradiated fetal fibroblasts. Preliminary analysis of the antibodies produced by lymphoblastoid cell lines established from tumors from two of the patients indicated that most were of IgM type and bound to a panel of melanoma cell target cells, as well as to some nonmelanoma tumor cell lines. Cloned LCL were produced from the tumor-infiltrating B cells from one of the patients, and of 100 such clones tested, 9% secreted antibody that bound to autologous tumor cells, and one of these clones produced antibody that appeared to be melanoma specific.
Suppression and elimination of BCL1 leukemia by allogeneic bone marrow transplantation.
Authors: Weiss L , Morecki S , Vitetta E S , Slavin S 
Published: December 2022

Abstract
Mice carrying the B cell leukemia (BCL1)+ were successfully treated by total lymphoid irradiation (TLI), cyclophosphamide, and allogeneic bone marrow (BM) transplantation. Long-term survivors were examined for residual BCL1 cells and for the ability to transfer adoptively graft vs. leukemia (GVL) activity. Residual BCL1 cells could not be detected in the allogeneic BM chimeras (greater than 14 to 16 months) with the use of indirect immunofluorescent staining with anti-idiotype antibody. However, residual tumor cells were present in 50% of the "cured" chimeric mice since adoptive transfer of 10(6) spleen cells from 50% of the treated chimeric mice caused leukemia in BALB/c recipients. In order to determine whether leukemia had been prevented in the "cured" chimeras by a persistent cell-mediated mechanism, BALB/c mice were injected with 10(6) spleen cells from the "cured" BM chimeras together with a dose of 10(2) or 5 x 10(5) BCL1 cells. Onset of leukemia was delayed or completely abolished in a significant proportion of recipients receiving the cell mixtures, suggesting the presence of anti-tumor immunity in the cured mice. The data suggest that a persistent active immune mechanism may be responsible, in part, for the significant antileukemic effects observed in mice tolerant to donor alloantigens.
Expression of common acute lymphoblastic leukemia antigen (CALLA) on human malignant melanoma cell lines.
Authors: Carrel S , Schmidt-Kessen A , Mach J P , Heumann D , Girardet C 
Published: December 2022

Abstract
Fifteen human melanoma cells lines were tested by an antibody-binding radioimmunoassay using a monoclonal antibody (A12) directed against the common acute lymphoblastic leukemia antigen (CALLA). Cells from six melanoma lines were found to react with this antibody. The level of antigen and the percentage of positive cells in these six melanoma lines showed wide variation, as demonstrated by analysis in the fluorescence-activated cell sorter (FACS). Immunoprecipitation of solubilized 125I-labeled membrane proteins from CALLA positive melanoma cells with A12 monoclonal antibody revealed a major polypeptide chain with an apparent m.w. of 100,000 daltons, characteristic for CALLA as determined on SDS-polyacrylamide gel electrophoresis. The expression of CALLA on MP-6 melanoma cells was modulated when the cells were cultured in the presence of A12 antibody. Reexpression of CALLA on these cells occurred within 5 days after transfer of the modulated cells into medium devoid of monoclonal antibody.
Independent immunodominant and immunorecessive tumor-specific antigens on a malignant tumor: antigenic dissection with cytolytic T cell clones.
Authors: Wortzel R D , Urban J L , Philipps C , Fitch F W , Schreiber H 
Published: December 2022

Abstract
We have analyzed the complexity of a unique tumor-specific transplantation antigen expressed by the murine ultraviolet light-induced fibrosarcoma 1591-RE. This tumor is highly immunogenic and is regularly rejected by normal mice. We have derived a cloned cytolytic T cell line showing a reactivity pattern representative of the cytolytic response of the host rejecting this regressor tumor. Using this T cell line (anti-A), variants of 1591-RE (1591-A-) were selected in vitro that had lost the same antigen as progressor variants of 1591-RE selected by the host in vivo. The in vitro derived variant was then used to generate a second T cell clone (anti-B) that recognized an antigen on the parental tumor that had been retained by the variants derived in vitro. Host-selected progressor variants were also found to have retained this antigen. By selecting for variants in vitro from the parental tumor with the anti-B T cell line, it was shown that the two different antigens (A and B) present on the parental tumor were lost independently of each other. Despite the independence of these two antigens, the host T cell response to the parental regressor tumor was invariably restricted to only the "immunodominant" A antigen.
Ultraviolet radiation inhibits human natural killer activity and lymphocyte proliferation.
Authors: Schacter B , Lederman M M , LeVine M J , Ellner J J 
Published: December 2022

Abstract
Exposure to ultraviolet radiation (UVR) has been implicated in the predisposition to certain neoplasms and leads to viral reactivation. Natural killer (NK) activity may play a role in immunosurveillance and response to certain viral infections. We have evaluated the sensitivity to UVR of human NK activity, a nonproliferative function, and the proliferative response to the mitogen phytohemagglutinin (PHA). In vitro exposure to UVR resulted in a dose-dependent inhibition of NK activity and response to PHA. The wavelength dependence for UVR inhibition of NK activity and of the PHA response of lymphocytes were virtually superimposable at wavelengths at or above 300 nm, but NK activity was less sensitive to UVR at 260 and 280 nm. Maximal sensitivity for both functions was found at 260 nm, consistent with a nucleic acid chromophore mediating UVR inhibition of both activities. The DNA-directed drugs mitomycin C, acridine orange, and adriamycin at concentrations that inhibit proliferation are poor inhibitors of NK activity. These results suggest that UVR inhibition of NK activity as well as proliferation may be mediated by a nucleic acid chromophore. NK activity, however, is less sensitive to direct damage of DNA by alkylation, distortion, or oxidation. At 300 nm, the amount of radiation required to inhibit NK activity and proliferation is within the range penetrating to the dermis and capillaries during environmental exposure to sunlight.
Identification of circulating maternal T and B lymphocytes in uncomplicated severe combined immunodeficiency by HLA typing of subpopulations of T cells separated by the fluorescence-activated cell sorter and of Epstein Barr virus-derived B cell lines.
Authors: Geha R S , Reinherz E 
Published: December 2022

Abstract
Circulating maternal T cells were sought in a child with severe combined immunodeficiency (SCID) and no evidence of acute graft-vs-host disease, but who had small numbers (9 to 11%) of circulating T3-positive cells. HLA typing of unfractionated peripheral blood lymphocytes (PBL) and of isolated E rosette-forming cells (37 to 44% of PBL) failed to reveal the presence of maternal lymphocytes. T3-positive cells isolated by the fluorescence-activated cell sorter, however, expressed exclusively maternal HLA antigens. A lymphoblastoid B cell line established by infecting the patient's PBL with Epstein Barr virus then expressed exclusively maternal HLA antigens. The presence of maternal T and B cells in uncomplicated SCID may be more common than thought previously and calls for a careful assessment of the origin of any mature T cells that are present in affected infants. In addition, the presence of maternal cells in SCID may complicate the infant's therapy.
Hapten-specific responses to the phenyltrimethylamino hapten. IV. Occurrence of mechanistically distinct idiotypic suppressor T cells before the appearance of anti-idiotypic suppressor T cells induced by the monovalent antigen L-tyrosine-p-azophenyltrimethylammonium.
Authors: Jayaraman S , Bellone C J 
Published: December 2022

Abstract
We have previously shown that a single i.p. injection of the monovalent synthetic antigen, L-tyrosine-p-azophenyltrimethylammonium [tyr(TMA)] in complete Freund's adjuvant induces an anti-idiotypic T suppressor cell (Ts2) population that can be detected 6 wk later by its ability to shut down delayed-type hypersensitivity (DTH) specific for the TMA hapten. In this paper we present evidence that 2 wk after tyr(TMA) administration, a subset of Ts, termed Ts1, appears that is both functionally and phenotypically distinct from the late appearing Ts2 population. The early occurring Ts1 act only at the induction phase of the DTH response and can also suppress this response intrinsically. This latter point is in marked contrast to our previous observation that the tyr(TMA)-induced anti-idiotypic Ts2 fail to function intrinsically and can only be detected upon adoptive transfer into naive mice. Ts1 bear idiotypic receptors and are Ly-1+,2- in contrast to the anti-idiotypic Ly-1-,2+ Ts2 population. In addition, unlike the Ts2 population, Ts1 are comparatively nylon wool-adherent. Adsorption of Ts1 on either antigen- or idiotype-coated petri dishes indicate that the suppressor activity can be transferred only by antigen-binding cells. Cellfree factors prepared from spleens containing the Ts1 population can suppress DTH only if administered at the induction phase of the response, in contrast to the factors derived from the Ts2 population that act both at induction as well as effector phases, suggesting that Ts1 and Ts2 can function via soluble mediators. Finally, we show that when Ts1-bearing mice are primed and boosted for anti-TMA antibody formation, the resulting response was overall reduced with respect to the idiotype-positive and negative plaque-forming cells that differs from the Ts2-bearing hosts wherein the idiotypic component is preferentially suppressed. The appearance of Ts1 before the detection of Ts2 in the same experimental animals is discussed with reference to a normal physiologic sequence of events involved in suppressor pathways.
Ontogeny of con A and PHA responses of chicken blood cells in MHC-compatible lines 6(3) and 7(2).
Authors: Fredericksen T L , Gilmour D G 
Published: December 2022

Abstract
The development of T cell responsiveness to Con A and PHA was examined in two MHC-compatible inbred chicken lines, RPRL 6(3) and 7(2), at ages 2 to 118 days posthatching. These lines are respectively resistant or susceptible to Marek's disease, a naturally occurring, virally induced T cell lymphoma. Between-line comparisons were made of optimal in vitro responses of diluted serum-free blood cells to each mitogen in two groups of chicks tested over ages 2 to 63 and 41 to 118 days. Over 2 to 63 days, Con A responses increased with age at the same rate in each line, but 7(2) responses averaged 2.3 times higher than 6(3). The increase with age was dependent on blood lymphocyte counts, which also increased with age in parallel in both lines. In contrast, the between-line difference in responsiveness was dependent on intrinsic reactivity of cells as well as lymphocyte counts. Covariance analysis was used to estimate that line 7(2) was 1.4 times higher than 6(3) in intrinsic cell reactivity, after accounting for the effect of the twofold higher blood lymphocyte counts in 7(2), and that this intrinsic difference contributed almost one-half the total difference. Over 41 to 118 days Con A responses no longer increased with age, although lymphocyte counts were still increasing, and the line difference (2.6 times) was now almost entirely contributed by a 2.3-fold superiority of 7(2) blood cells in intrinsic reactivity. The line difference in PHA responses was the reverse of the above in young chicks, with 6(3) responses greater than 7(2) in spite of lower lymphocyte counts. In additional chicks tested over 5 to 26 days, intrinsic reactivity of 6(3) cells to PHA averaged 4.5 times higher than 7(2). There was an abrupt decline in intrinsic reactivity of line 6(3) blood cells between 26 and 41 days to a level equal with 7(2). After this age, line 7(2) responses were 1.8 times greater than those of 6(3), and this difference was dependent solely on lymphocyte count differences. The results suggest that different gene systems mediate blood cell responses to PHA as compared with Con A. The pattern of developmental differences between inbred lines indicates the existence of distinct or partly overlapping T cell subsets with different reactivities to PHA or Con A, and of higher suppressor activity of adherent cells in line 6(3) blood. Both these differences may be related to line 6(3) inherited resistance to Marek's disease.
Phospholipid synthesis by activated human B lymphocytes.
Authors: Chien M M , Ashman R F 
Published: December 2022

Abstract
Pokeweed mitogen- (PWM) stimulated DNA and Ig synthesis in human B cells is dependent on the presence of T cells and adherent cells, but the influence of these regulatory cells on earlier activation events is unknown. We have studied the T cell and monocyte influence on the incorporation of [methyl-14C]choline chloride into B cell phospholipids (PL) after varying periods of in vitro culture with or without pokeweed mitogen (PWM). By separating B and T cells after choline pulsing, a peak in PWM-induced PL synthesis of B cells at days 1 to 2 was revealed, whereas the T cell response was later (days 2 to 3). In the first 4 hr of culture, the purified B cell plus monocyte fraction incorporated choline four to six times faster than the T cell fraction, but PWM did not increase choline incorporation, whether these fractions were cultured separately or together. When cultures were pulsed with choline between 16 and 20 hr with or without PWM, monocytes incorporated choline six to nine times faster than T cells, and B cells were intermediate. Also at 16 to 20 hr of culture, a significant PWM-induced increase in choline incorporation by B cells was evident and was dependent on the presence of T cells and monocytes. The monocytes showed no increased choline incorporation due to PWM. Thus, the influence of regulatory cells on the PWM response in B cells is evident within the first 24 hr.
Defective in vitro production of influenza virus-specific cytotoxic T lymphocytes in ataxia-telangiectasia.
Authors: Nelson D L , Biddison W E , Shaw S 
Published: December 2022

Abstract
Peripheral blood mononuclear cells (PBMC) from patients with ataxia-telangiectasia (A-T) were studied for their capacity to proliferate and to generate influenza virus-specific cytotoxic T lymphocytes (CTL) after in vitro stimulation with influenza A/Hong Kong (A/HK (H3N2)) virus. PBMC from 11 patients proliferated poorly to A/HK and 10 of the 11 patients failed to exhibit significant CTL effector activity when tested on influenza A/HK virus-infected autologous target cells. In contrast, PBMC from each of 18 simultaneously studied, unrelated normal individuals proliferated to A/HK and generated influenza-immune CTL. In each of the 10 A-T patients, deficient CTL activity was shown to be due to a lack of generation of CTL and not to target cell resistance to lysis, because the virtually infected target cells of the patients were lysed by parental influenza-immune CTL. Determinations of T cell numbers and existing serum antibody titers to H3N2 influenza virus suggest this nonresponsiveness cannot be simply explained by a lack of T cells or the absence of exposure to type A (H3N2) influenza virus. Studies in which CTL were generated in A-T plasmas and during co-culture of PBMC from an A-T patient and an MHC-matched sibling failed to demonstrate either plasma or cellular suppression as a mechanism for the lack of CTL production in A-T patients. This immune defect in the production of cytotoxic effector T cells may be a cause of the increased frequency of infections and neoplasms observed in A-T patients.
High incidence of free monoclonal lambda light chains in the sera of patients with Sjogren's syndrome.
Authors: Moutsopoulos H M , Steinberg A D , Fauci A S , Lane H C , Papadopoulos N M 
Published: December 2022

Abstract
Sjogren's syndrome presents a wide spectrum of disease manifestations ranging from benign to malignant lymphoproliferation. Sera from 21 patients with primary Sjogren's syndrome, 63 patients with other autoimmune rheumatic diseases, and 140 normal controls were studied by using high-resolution gel electrophoresis combined with immunofixation and specific absorption studies. Two-thirds of the sera from Sjogren's syndrome patients contained free monoclonal lambda light chains. In addition, one patient with Sjogren's syndrome and pseudolymphoma had a circulating monoclonal IgM-lambda immunoglobulin. In contrast, only 16% of the patients with other autoimmune diseases and 5% of normals had monoclonal bands; none of the other patients studied exhibited monoclonal-free lambda light chains in their serum. Our findings suggest that the monoclonal process in Sjogren's syndrome starts early in the disease process in a subset of B cells.