bluuebunny/crossref_metadata_2025_split huggingface dataset:
Stimulation of mouse lymphocytes by a mitogen derived from Mycoplasma arthritidis. III. Ir gene control of lymphocyte transformation correlates with binding of the mitogen to specific Ia-bearing cells.
Authors: Cole B C , Daynes R A , Ward J R 
Published: December 2022

Abstract
The supernatant from Mycoplasma arthritidis broth cultures (MAS) contains a T cell mitogen that is under Ir gene control. Responsiveness to this mitogen is dictated by the I-E/I-C subregion of the major histocompatibility complex and is dependent upon adherent radioresistant Ia+ accessory cells from responding haplotype animals. In this study, we established that MAS could be removed from culture supernatants by absorption with spleen cells from mice that themselves are responsive to the mitogen (k and d haplotypes), but activity is not removed by spleen cells from mouse strains that are nonresponsive to the mitogen (b, q, and s haplotypes). Absorption studies with lymphoid cells from congenic and recombinant strain mice established that absorption of the mitogen was itself linked to the I-E/I-C subregion of the major histocompatibility complex. Thymocytes from responding haplotype strains were incapable of removing MAS activity, and spleen cells devoid of Thy-1-positive cells retained their full absorbing capacity. The ability to effectively absorb MAS activity was abrogated by the pretreatment of spleen cells with anti-Ia antiserum and complement. Furthermore, the ability of spleen cells from responding haplotype strains to respond to MAS was blocked by the addition of anti-Ia serum to the cell cultures. Whereas the latter treatment resulted in an almost complete elimination of MAS responsiveness, the ability of similarly treated spleen cells to respond to the mitogens PHA and Con A was only minimally depressed. These results are consistent with our hypothesis that the mitogenic moiety of MAS actually binds to I-E/I-C-coded Ia antigens.
IgG induction in a human B cell line by red cell-mediated microinjection of the cytoplasm from T cell factor-stimulated B cells.
Authors: Kishimoto T , Miki Y , Kishi H , Muraguchi A , Kishimoto S , Yamamura Y 
Published: December 2022

Abstract
Generation of a cytoplasmic factor(s) that induced IgG secretion in nonstimulated cells was demonstrated in TRF-stimulated cells by using red cell-mediated microinjection. Injection of the cytoplasm from a TRF-stimulated B lymphoblastoid cell line (CESS) into nonstimulated cells induced an increase of IgG-producing cells. Injection of TRF itself did not induce an increase of IgG-producing cells. Active substance(s) in the cytoplasm were generated at 2 hr after TRF stimulation, and IgG-producing cells reached their maximum level at 40 hr after injection of the factor(s). DFP, but not actinomycin D, inhibited the generation of the cytoplasmic factor(s). The activity of the cytoplasmic factor(s) was not destroyed by RNase and not absorbed with anti-IgG. These results suggested that binding of TRF with its acceptors induced the generation of the cytoplasmic factor(s) involved in the transmission of TRF-mediated signals from membrane to nuclei.
Phenotypic characteristics of cell lines requiring interleukin 3 for growth.
Authors: Ihle J N , Keller J , Greenberger J S , Henderson L , Yetter R A , Morse H C 
Published: December 2022

Abstract
A number of cell lines have been derived from bone marrow cultures in the presence of WEHI-3 conditioned media (CM) that continue to require WEHI-3 CM for growth in vitro. Because the WEHI-3 cell line has been shown to constitutively produce a lymphokine (IL 3) that induces the expression of 20 alpha-hydroxysteroid dehydrogenase (20 alpha SDH) in cultures of splenic lymphocytes from athymic mice, we examined whether these cell lines were dependent upon IL 3 for growth. The results demonstrate that the factor required for growth of these cell lines copurifies with IL 3 activity on G-100, DEAE cellulose, and CM cellulose column chromatography as well as in preparative isoelectric focusing and on hydrophobic supports in reverse phase high pressure liquid chromatography. The biologic activity of peak fractions in each case was similar in both types of assays. These results strongly suggest that the WEHI-3 CM-dependent cell lines are dependent on IL 3 for growth in vitro. All the cell lines have readily detectable levels of 20 alpha SDH but have differing cell surface phenotypes. The C3HSFFV line is devoid of conventional lymphoid cell surface markers with the exception of Lyt-1, whereas the FDC-P1 expresses Thy-1, Ly-5, and H-11. Other cell lines have intermediate phenotypes.
Distribution of terminal deoxynucleotidyl transferase and purine degradative and synthetic enzymes in subpopulations of human thymocytes.
Authors: Ma D D , Sylwestrowicz T A , Granger S , Massaia M , Franks R , Janossy G , Hoffbrand A V 
Published: December 2022

Abstract
Terminal deoxynucleotidyl transferase (TdT) and purine metabolic enzymes were examined in subsets of human infant thymocytes (defined by surface cell antigens) and normal peripheral T lymphocytes. Putative prothymocytes (RFB-1+, HTA-1+/- large blast-like cells), medium and high density cortical thymocytes (RFB-1+, HTA-1+), and medullary thymocytes (RFB-1-, HTA-1-, OKT3+) were isolated by density gradient centrifugation, monoclonal antibody and complement-mediated cytolysis, and cell-antibody affinity chromatography. Peripheral T lymphocytes were isolated from normal adult mononuclear cells using nylon fiber technique. Adenosine deaminase (ADA) and TdT were highest in prothymocytes 48.8 +/- 14.7 mumol/hr/10(8) cells (mean +/- SE) and 22.9 +/- 1.4 U/10(8) cells, respectively. Both enzymes decreased progressively down the maturation pathway. In peripheral T lymphocytes, ADA was 3.9 +/- 1.5 mumol/hr/10(8) cells, and TdT was undetectable. Purine nucleoside phosphorylase (PNP) and ecto-5'nucleotidase (5'NT) were lowest in cortical thymocytes (27.5 +/- 11.0 nmol/hr/10(6) cells and 2.8 +/- 1.3 nmol/hr/10(6) cells, respectively) and increased with T cell maturation. The PNP level was 124.9 +/- 17.2 nmol/hr/10(6) cells and 5'NT was 30.1 +/- 3.9 nmol/hr/10(6) cells in peripheral T lymphocytes. The deoxynucleoside kinases (deoxyguanosine, deoxyadenosine, and deoxycytidine kinases) paralleled the changes in ADA and TdT activity among the different T subsets. The proliferative activity (labeling index) was highest in the prothymocyte fraction and lowest in peripheral T cells. Variation in the distribution of these enzymes in T cell subsets may explain their different sensitivities to deoxyadenosine and deoxyguanosine toxicity and the different effects on T cell development of ADA or PNP deficiency.
Corticosteroid alteration of human monocyte to macrophage differentiation.
Authors: Rinehart J J , Wuest D , Ackerman G A 
Published: December 2022

Abstract
Human monocyte to macrophage differentiation in vitro is associated morphologically with an increased cell size, an increased number of lysosomes, and rough endoplasmic reticulum. Functional changes associated with monocyte to macrophage differentiation include increased tumoricidal activity and increased cell protein, acid phosphatase, and 5'-nucleotidase. Hydrocortisone succinate (HCS) at 2.5 microM markedly altered monocyte to macrophage differentiation: HCS inhibited the development of tumoricidal activity and the increased levels of cell protein, acid phosphatase, and 5'-nucleotidase. By transmission electron microscopy, macrophages incubated with HCS failed to develop an increased complement of lysosomes and developed an increased number of membrane-bound electron lucent vacuoles. Dexamethasone inhibited the development of tumoricidal activity at a 10-fold lower concentration than HCS. HCS also markedly inhibited monocyte 3H-uridine incorporation. Mechanisms of HCS alteration of monocyte differentiation are discussed. These data suggest that corticosteroid alteration of monocyte differentiation may be a mechanism of HCS immunosuppression in vivo.
Two monoclonal anti-human T lymphocyte antibodies have similar biologic effects and recognize the same cell surface antigen.
Authors: Burns G F , Boyd A W , Beverley P C 
Published: December 2022

Abstract
Two independently produced monoclonal antibodies, UCHT1, an IgG1 antibody, and OKT3, an IgG2 antibody, which specifically identify all human peripheral T lymphocytes, were shown to possess similar functional properties. Both were highly mitogenic to peripheral blood T lymphocytes, and UCHT1 blocked specific T lymphocyte killing of autologous B lymphoblasts when present during either the induction or the cytotoxic phase of the reaction; this, too, is a property reported for OKT3 in an analogous situation. Both antibodies also inhibited the 6-day proliferative response to soluble antigens and mixed lymphocyte culture, although this may be attributable to their strong mitogenicity earlier in culture. These properties were not found with other monoclonal antibodies directed against human T lymphocytes, and suggested that UCHT1 and OKT3 recognize important functional structure(s) on the T cell surface. The identity of the antigen recognized by these two antibodies was demonstrated by 2-directional co-capping, by cold antibody inhibition of binding of radiolabeled antibody, and by immunoprecipitation and two-dimensional gel analysis of labeled T cell surface proteins. Both UCHT1 and OKT3 bound with similar affinities (Ka approximately 2 X 10(9) M-1) to the same number of binding sites (2.8 X 10(4) sites/activated T cell), and both precipitated the same glycoprotein complex with a m.w. of approximately 19,000 in the presence of reducing agent.
Monoclonal antibodies to streptococcal group A carbohydrate. I. A dominant idiotypic determinant is located on Vk.
Authors: Nahm M H , Clevinger B L , Davie J M 
Published: December 2022

Abstract
In an effort to better define the antibody repertoire to streptococcal group A carbohydrate (GAC), somatic cell hybrids were prepared from A/J mice immunized with streptococcal vaccine. Most antibodies were IgG3K and IgMK, while 2 of 26 antibodies were lambda type. Each of the IgG3 antibodies had a distinct isoelectric point consistent with previous estimates of clonal repertoires of approximately 200. IEF analysis of the L chains, however, showed that about half of the antibodies produce a common L chain, called VK1GAC, previously identified in A/J anti-GAC serum antibodies. Additional support for the structural similarity of these L chains was gained by developing an idiotype antiserum to VK1GAC. All proteins with the common L chain spectrotype react strongly with anti-VK1GAC. Thus, it appears that anti-GAC antibodies are composed of H chains bearing a few VH regions pairing with a few L chains.
Prostaglandin D2 generation after activation of rat and human mast cells with anti-IgE.
Authors: Lewis R A , Soter N A , Diamond P T , Austen K F , Oates J A , Roberts L J 
Published: December 2022

Abstract
Anti-IgE-dependent activation of rat and human mast cells resulted in the preferential generation of the cyclooxygenase products prostaglandin D2 (PGD2) and prostaglandin I2 (PGI2) in the rat and PGD2 in the human. The average net generation of PGD2, determined by gas chromatography-mass spectrometry, was 13.1 ng/10(6) purified rat mast cells and 39.5 ng/10(6) dispersed, enriched human mast cells. After IgE-dependent activation, there was a linear relationship between the net quantities of PGD2 generated and of histamine secreted from dispersed human pulmonary cells when the number of mast cells was varied but the total number of cells was held constant, indicating that it is the number of mast cells participating in IgE-dependent activation, rather than total mast cell number, that determines PGD2 generation. A linear relationship was also shown between PGD2 generation, determined by radioimmunoassay, and the release of the granule marker beta-hexosaminidase from purified rat mast cells on the dose-response portion of the plot of their response to anti-IgE challenge. With higher concentrations of anti-IgE, PGD2 generation from rat mast cells plateaued, whereas net percent beta-hexosaminidase release increased further. In kinetic studies of rat mast cells activated with anti-IgE, the onset (1 to 2 min) and time of maximum generation (5 to 10 min) for PGD2 were delayed relative to the onset (15 to 30 sec) and completion (1 to 2 min) of beta-hexosaminidase release. Thus, the extracellular appearance of PGD2 during IgE-dependent mast cell activation represents a response additional to the secretion of granule-associated mediators.
Identification of T cell subsets and B lymphocytes in mouse brain experimental allergic encephalitis lesions.
Authors: Sriram S , Solomon D , Rouse R V , Steinman L 
Published: December 2022

Abstract
Tissue section immunoperoxidase staining, employing monoclonal antibodies specific for T cell antigens (Lyt-1, Lyt-2) and B cells (B220), was used to study the brains of mice with experimental allergic encephalitis. Cells bearing phenotypes characteristic of both helper (Lyt-1+2-) and cytotoxic/suppressor (or precursor) (Lyt-2+) T cells, as well as B cells, are present in the perivascular cuffs in brains of EAE mice during active disease and the recovery phase. Lyt-1+ cells comprise 49% of the inflammatory cell population, and Lyt-2+ and B220+ cells are found at frequencies of 10% and 12%, respectively.
The immune response to homologous lens crystallin. I. Antibody production after lens injury.
Authors: Goldschmidt L , Goldbaum M , Walker S M , Weigle W O 
Published: December 2022

Abstract
Using a sensitive radioimmunoassay to homologous mouse alpha-crystallin, it was established that autoantibodies are produced to this self constituent in mice after rupture of the lens capsule by needling. Antibody to lens crystallin was detected within 4 days of lens rupture and persisted for 24 days, suggesting that these mice are not tolerant to alpha-crystallin at the B cell level. However, T cells from mice immunized with homologous crystallin cannot be stimulated to proliferate by either homologous or heterologous crystallin. On the other hand, lymphocytes from mice immunized with bovine alpha-crystallin can be stimulated to proliferate to bovine crystallin, but not to either unfractionated mouse crystallin (MC) or purified mouse alpha-crystallin. At the level of detection, therefore, T cells appear to be tolerant to homologous alpha-crystallin, but not to heterologous alpha-crystallin. LPS resulting from bacterial contamination after needling was ruled out as a necessity for antibody production because antibody to mouse alpha-crystallin was produced after sterile lens rupture with a laser. However, LPS and poly A:U did enhance the antibody response to alpha-crystallin. These data suggest that T cells, but not B cells, are tolerant to homologous crystallin and that antibody results from circumvention of specific helper T cell requirements for antibody synthesis. The implications of these findings for tolerance and autoimmune uveitis are discussed.
Enhanced resistance to Nocardia brasiliensis infection in mice depleted of antigen-specific B cells.
Authors: Rico G , Ochoa R , Oliva A , Gonzalez-Mendoza A , Walker S M , Ortiz-Ortiz L 
Published: December 2022

Abstract
This study deals with the roles of T and B cells in Nocardia brasiliensis infection in mice. Nocardia injected into the animals' footpads caused inflammatory responses and mycetomas in situ, resulting in granulomatous lesions of subcutaneous tissues and eventual bone destruction. These clinical features resemble those of humans infected with Nocardia. The effect, if any, of antibody was studied by passively transferring anti-Nocardia serum into either immunologically normal or T-deficient infected mice. Such transfers had no protective function in either group. To the contrary, the antibody seemed to favor infection and worsen bone disease compared to that in mice not given antibody. Furthermore, passive transfer of the antibody along with injection of Nocardia coated with the antibody magnified the severity of subsequent symptoms. Although these experiments ruled out any role for antibody in protection from Nocardia, they did not directly prove T cell participation in such resistance. Therefore, the role of T cells during Nocardia infection was examined further by transferring spleen cells depleted of B lymphocytes bearing receptors for a Nocardia extract (NE). Lethally irradiated mice reconstituted with a population depleted of NE-specific B cells totally lacked the ability to form antibodies to NE; however, they mounted effective delayed-type hypersensitivity reactions and completely controlled their Nocardia infection, establishing the importance of cell-mediated immunity in halting this disease process.
Cloned lines of human cytotoxic T lymphocytes with specificity for influenza virus.
Authors: Fleischer B 
Published: December 2022

Abstract
The generation of human cytotoxic T cell clones with specificity for influenza virus and some of their characteristics are described. The clones were generated by limiting dilution of peripheral blood lymphocytes after two in vitro stimulations with autologous influenza A/USSR virus-infected cells and were grown in T cell growth factor. The majority of the virus-specific clones showed cross-reactivity for different influenza A virus subtypes but did not recognize influenza B virus-infected cells. The HLA specificity of two clones was further analyzed. One clone, LL33, was specific for HLA-Bw60, the other, clone WH5, for HLA-A1. Clone WH5 also seemed to recognize the serologically related HLA-A26 as restriction element for the recognition of the viral antigen. Whereas the virus-specific CTL clones had the OKT3+,4-,8+ phenotype, another clone, WH 49, exhibiting natural killer-like activity, was found to have the OKT3+,4+,8- phenotype.
Depressed T cell proliferative responses in Hodgkin's disease: role of monocyte-mediated suppression via prostaglandins and hydrogen peroxide.
Authors: Fisher R I , Bostick-Bruton F 
Published: December 2022

Abstract
We studied the contribution and mechanisms of monocyte-mediated suppression in the depressed T cell proliferative responses observed in patients with Hodgkin's disease. Mononuclear leukocytes from 22 untreated patients had significantly lower proliferation after stimulation with suboptimal doses of phytohemagglutinin than normals controls (p less than 0.001). When indomethacin was added to the cultures, the mean percent increase in patient proliferation exceeded that of normals (160 +/- 19% vs 81 +/- 9%; p less than 0.008), yet patient proliferation remained only 36% of normal. Catalase alone caused a minimal increase in proliferation in all cultures. When catalase plus indomethacin were added to either normal or patient cultures, however, a synergistic increase was observed. The mean percent increase in patient proliferation was 300 +/- 80%, although once again the absolute proliferative response of the patients remained subnormal (p less than 0.003). Removal of adherent monocytes from patient cultures produced increases in proliferation comparable to that observed with the addition of indomethacin. Long-term disease-free survivors of Hodgkin's disease had depressed T cell proliferation but no significant increase after the addition of indomethacin. We conclude: 1) although untreated patients with Hodgkin's disease have increased monocyte suppressor activity that is mediated by increased prostaglandin production, this is not the major cause of the depressed T cell proliferative responses observed in Hodgkin's disease; 2) depressed proliferative responses in cured Hodgkin's disease are not mediated by prostaglandins; 3) hydrogen peroxide suppresses T cell proliferation in both normals and untreated patients; and 4) other factors, probably inherent in the T cell itself, are the major cause of depressed T cell responses in Hodgkin's disease.
Characterization of the cytolytic reaction mechanism of the human natural killer (NK) lymphocyte: resolution into binding, programming, and killer cell-independent steps.
Authors: Hiserodt J C , Britvan L J , Targan S R 
Published: December 2022

Abstract
Various parameters of the cytolytic reaction mechanisms of the human natural killer (NK) lymphocyte were studied to characterize the lytic cycle. NK cytolysis was determined to occur in three definable steps. 1) Binding of PBL to the NK-sensitive targets Molt-4 or K562 was rapid (less than 1 min), occurred at temperatures below 37 degrees C, was Mg++3-dependent, Ca++3-independent, and was prevented by dispersion of the cells into 10% dextran. 2) Subsequent to binding, programming for lysis as determined by a Ca++ pulse method was more protracted, requiring up to 2 hr to occur and was strictly dependent on Ca++ for cytolysis to proceed. In standard cytotoxicity assays, however, programming for lysis was more rapid occurring in 10 to 30 min. Programming was inhibited by EDTA, EGTA/Mg++ and by temperatures below 37 degrees C. Furthermore, after binding but in the absence of initiation of programming for lysis, the frequency of target binding cells did not change and the NK cell did not lose its lytic potential. 3) Killer cell-independent cytolysis (KCIL) was determined by the addition of EDTA to "programmed" targets and dispersion of these cells into dextran-containing medium, which resulted in virtually 100% dissociation of conjugated cells. KCIL was Ca++ and Mg++-independent and was blocked at reduced temperatures only if the dextran was prechilled to 4 degrees C before addition. The kinetics of 51Cr release during KCIL was rapid and complete 30 min after dispersion. Interferon-activated NK cells expressed an increased rate of cytolysis in Ca++ pulse experiments. This was due to an increased rate of the Ca++-dependent step(s) during the programming events. The rate of the Ca++-independent steps, however, were similar with control and IFN-activated cells.
Abnormalities induced by the mutant gene Ipr: expansion of a unique lymphocyte subset.
Authors: Morse H C , Davidson W F , Yetter R A , Murphy E D , Roths J B , Coffman R L 
Published: December 2022

Abstract
Mice carrying the Ipr mutation develop massive lymphoadenopathy and severe autoimmune disease. The characteristics of the cell population that proliferates in lymphoid tissues were evaluated by the use of a) monoclonal antibodies and FMF, and b) molecular genetic studies of Ig heavy chain genes. The lymph node cells of different strains of mice homozygous for the Ipr mutation were shown to be almost uniformly Thy-1+, Ly-1+, Ly-2-, H-11+, Ly-5+, sIg-, ThB-, 2C2+, I-A-, 6B2+, and therefore to have surface characteristics of both T and B cells. Molecular genetic studies of the arrangements of Ig heavy chain genes showed that they were not rearranged as in pre-B and B cells. These results suggest that an abnormal proliferating population of T cells in Ipr/Ipr mice aberrantly express B cell surface markers.