bluuebunny/crossref_metadata_2025_split huggingface dataset:
Human T cell antigens defined by monoclonal antibodies: the 65,000-dalton antigen of T cells (T65) is also found on chronic lymphocytic leukemia cells bearing surface immunoglobulin.
Authors: Royston I , Majda J A , Baird S M , Meserve B L , Griffiths J C 
Published: December 2022

Abstract
Peripheral blood lymphocytes from 15 patients with chronic lymphocytic leukemia (CLL), four patients with lymphosarcoma cell leukemia (LCL), four patients with hairy cell leukemia, and three patients with a monoclonal gammopathy (two with IgM, one with IgA) were tested for reactivity with the anti-T cell monoclonal antibody, T101. By immunofluorescent staining, all of the patients had circulating monoclonal surface Ig+ (sIg+) lymphocytes except for three CLL patients whose leukemia cells were sIg-. The leukemia cells of all of the sIg+ CLL cases were reactive with T101 antibody by indirect immunofluorescence; however, the abnormal cells in all of the remaining cases were unreactive. Reactivity of sIg+ CLL cells with T101 was confirmed by a radioactive binding assay, absorption analysis, and complement-dependent cytotoxicity. Moreover, a 65,000-dalton protein (T65), similar to that found on T cells, was precipitated by T101 antibody from the surface of sIg+ CLL cells. The fluorescent staining of sIg+ CLL cells by T101 antibody was weak as was the staining of the sIg. This was in contrast to the LCL cells, which had intense staining sIg and absence of staining with T101 antibody. These data demonstrate the existence of two major subtypes of CLL that have phenotypes sIg+ and T101+ and sIg-T101-. The implication of the finding of dual T and B markers on the major type of CLL, but not other B cell malignancies is discussed.
Influence of PGE on the immune response in melanoma-bearing mice.
Authors: Favalli C , Garaci E , Etheredge E , Santoro M G , Jaffe B M 
Published: December 2022

Abstract
This study was performed to correlate the role of exogenous and endogenous prostaglandins on humoral and cellular immune responses to and rate of growth of B-16 melanoma in vivo. B-16 melanomas synthesized 7 times as much PGE as did adjacent normal tissues, an effect that was abolished by indomethacin. In C57BL/6J mice bearing B-16 melanomas splenic plaque-forming cells, hemagglutinin titers, and delayed hypersensitivity (all to SRBC) were profoundly suppressed; these responses were significantly augmented by treating the mice with di-M-PGE2 (16, 16-dimethyl-PGE2-methyl ester), a long acting analogue of PGE2, and either further suppressed or unaffected by indomethacin, a potent inhibitor of endogenous PGE biosynthesis. Compared to control experiments, indomethacin hastened the rate of development of palpable subcutaneous B-16 tumors and facilitated the proliferation of these cells in solid tumors as well as in ascites. Pretreatment of mice with di-M-PGE2 (before inoculation with tumor cells) resulted in delay in the rate of appearance of tumors, decline in the growth rate, and increased survival. These data suggest that prostaglandins are involved in the control of in vivo tumor cell growth largely by virtue of their effects on the immune response.
Male determined accelerated autoimmune disease in BXSB mice: transfer by bone marrow and spleen cells.
Authors: Eisenberg R A , Izui S , McConahey P J , Hang L , Peters C J , Theofilopoulos A N , Dixon F J 
Published: December 2022

Abstract
Autoimmune disease in BXSB mice progresses more rapidly in male animals. We have investigated the cellular basis of this effect by transferring male and female bone marrow and spleen cells into male and female lethally irradiated BXSB recipients. The rate of development of disease was measured by the overall mortality rate, mortality from glomerulonephritis, and development of serologic abnormalities. We found that the pace of disease in the BXSB sex chimeras was determined entirely by the sex of the donor of the transferred cells. Lethally irradiated BXSB animals receiving male cells had rapidly progressive disease, whether the recipients were themselves male or female, whereas female-cell recipients of either sex had slowly progressive disease. The male-specific effect that accelerates autoimmune disease in the BXSB is thus not hormonally mediated, but rather is expressed in the hematopoietic stem cell populations.
The cellular basis for viral-induced immunodeficiency: analysis by monoclonal antibodies.
Authors: Reinherz E L , O'Brien C , Rosenthal P , Schlossman S F 
Published: December 2022

Abstract
Viral infections are often associated with immunodeficiency states. Although T lymphocytes have been thought to suppress the host's response, the precise etiology remains unclear. Therefore, we characterized T lymphocytes from six patients during both acute and convalescent phases of infectious mononucleosis (IM) with monoclonal antibodies (titer, 10(-5) to 10(-7) to antigens restricted to the TH2- helper (T4) and TH2 suppressor (T5) T cell subsets as well as to a common T cell antigen (T3) and HLA-D related Ia antigens. It was found that during acute infectious mononucleosis, there is both activation and increase of suppressor T cells (T5+, Ia+ phenotype). Fuctionally, the acute IM lymphocytes suppress autologous T cell proliferation to antigens as well as pokeweed mitogen driven B cell immunoglobulin production. In contrast, convalescence is associated with a return to normal of T cell subsets and immune function. These results demonstrate that viral infections can preferentially activate a specific T cell subset and suppress the overall human immune response.
Genetic control of cytolytic T lymphocyte responses. III. The role of K and I region alleles on the specificity of the cytolytic T lymphocyte response to trinitrophenyl-modified syngeneic cells.
Authors: Burakoff S J , Riccio J , Billings P , Benacerraf B , Dorf M E 
Published: December 2022

Abstract
It has previously been demonstrated that genes in the H-2K and/or I-A region control the specificity of the cytolytic T lymphocyte (CTL) response to trinitrophenyl-(TNP) modified syngeneic cells. Strains of mice bearing the k allele in the K and/or IA region do not exhibit cross-reactive lysis of TNP-modified allogeneic targets after stimulation with TNP-modified syngeneic targets. In this report we present evidence for independent roles of genes in the H-2K and I-A regions on the control of CTL specificity. One gene, mapping in the H-2K region, is expressed on the stimulator cell population, whereas the other gene maps to the I region and is expressed in the population of responding cells and need not be expressed in the stimulator cell population. Thus, we suggest that Ir genes localized to the I region may influence the response for prekiller cells to H-2K/D gene products.
Regulatory role of IgE-binding factors from rat T lymphocytes. II. Glycoprotein nature and source of IgE-potentiating factor.
Authors: Yodoi J , Hirashima M , Ishizaka K 
Published: December 2022

Abstract
Previous experiments have shown that Fc epsilon receptor-bearing (Fc epsilon R(+)) T lymphocytes in mesenteric lymph nodes (MLN) of rats infected with Nippostrongylus brasiliensis (Nb) release a soluble factor that selectively potentiates the IgE response. The IgE-potentiating factor has affinity for IgE, and can be detected by the ability to inhibit rosette formation of Fc epsilon R(+) cells with IgE-coated erythrocytes. The factor was bound to IgE-coated Sepharose and was eluted from the beads at acid pH. It was also found that the IgE-potentiating factor binds to lentil lectin-Sepharose, indicating that the factor is a glycoprotein. The affinity of the factor for IgE was lost after treatment with trypsin but was maintained after treatment with neuraminidase. However, the ability of the factor to potentiate the IgE response was lost after neuraminidase treatment. The results suggested that the factor's binding site for IgE is associated with a protein (peptide) moiety but that its carbohydrate moiety is essential for its biologic activity. When MLN cells were incubated at 37 degrees C, a substantial amount of the IgE-potentiating factor was released into culture medium within 4 hr even in the presence of cycloheximide. Pretreatment of the cells with trypsin, which removed Fc epsilon R, markedly diminished the release of IgE-potentiating factor, suggesting that the factor is derived from Fc epsilon R on the cell surface.
Antigen recognition by T cells. II. Intravenous administration of native or denatured ovalbumin results in tolerance to both forms of the antigen.
Authors: Endres R O , Grey H M 
Published: December 2022

Abstract
In the accompanying report, suppressor T cells were demonstrated that did not recognize cross-reactivity between native and denatured ovalbumin (N-OVA and D-OVA). Here we show that the T cell tolerance induced by i.v. injections of antigen does detect cross-reactivity between N-OVA and D-OVA. Mice that had been immunized with either N-OVA or D-OVA in adjuvant could be rendered profoundly unresponsive if either N-OVA or D-OVA, but not an unrelated protein, were injected i.v. Cross-tolerance was observed in assays of antigen-induced T cell proliferation and helper T cell activity. Tolerance was distinguished from suppressor T cell activity by three criteria: 1) specificity for N-OVA and D-OVA, 2) sensitivity to abrogation by cyclophosphamide, 3) duration of effectiveness. These results confirm observations made by others that suggest that tolerance is mediated by an additional mechanism(s) other than suppressor T cells. Based on a hypothesis that cross-reactivity between native and denatured antigen is related to macrophage processing of antigen, these data also suggest a critical role for processed antigen in the induction of tolerance when antigen is administered i.v.
A comparative analysis of the cell surface properties of activated vs endogenous mouse natural killer cells.
Authors: Kiessling R , Eriksson E , Hallenbeck L A , Welsh R M 
Published: December 2022

Abstract
Mouse natural killer (NK) cells can be activated by interferon and by interferon inducers, such as viruses. In the present report we compared the cell surface properties of the nonactivated "endogenous" NK cells from normal mice with NK cells activated in vivo by acute infection with lymphocytic choriomeningitis virus (LCMV) or in vitro by interferon. Several striking differences were found: 1) in vivo LCMV-activated as well as in vitro interferon-activated NK cells were more adherent to nylon wool columns than the endogenous NK cells; 2) activated NK cells were more EA-monolayer adherent than endogenous NK cells; this adherence could be blocked by streptococcal A protein, indicating that activated NK cells expressed greater Fc receptor mediated adherence; 3) LCMV-activated NK cells that passed through nylon wool columns expressed relatively low EA adherence properties; 4) the sensitivity of NK cells to anti-theta serum + complement treatment was increased in spleen cells late after LCMV infection (day 6 to 7) but not in spleen cells early after infection (day 2 to 3); 5) as shown by centrifugal elutriation, LCMV-activated spleens contained a population of large NK cells that were not present among endogenous spleen cells. In contrast to previous reports, these findings show that there are several distinct changes as a result of both long-term in vivo activation or of short-term in vitro activation of NK cells. These changes might functionally be involved in the increased lytic ability of activated NK cells.
Immunologic abnormalities in HRS/J mice. I. Specific deficit in T lymphocyte helper function in a mutant mouse.
Authors: Morrissey P J , Parkinson D R , Schwartz R S , Waksal S D 
Published: December 2022

Abstract
An immunologic analysis of mutants HRS/J mice was done comparing hr/hr homozygotes to hr/+ heterozygotes. It was shown that hr/hr spleen but not lymph node cells show a defect specific for functions associated with T helper cells as compared to hr/+ littermates. This defect, which is expressed by depressed proliferative responses to alloantigens, does not affect the ability of hr/hr spleen cells to respond normally to T cell mitogens nor does it affect their ability to generate normal cytotoxic effector cells in vitro. It is further suggested that this defect is due to an abnormality in thymus epithelium, which is also related to the high grade expression of xenotropic virus in old hr/hr thymocytes and subsequent development of leukemia.
Monoclonal antibodies to murine cell surface antigens. I. Lyt-1.1.
Authors: Hogarth P M , Potter T A , Cornell F N , McLachlan R , McKenzie I F 
Published: December 2022

Abstract
The production and properties of a monoclonal anti-Lyt-1.1 antibody are described. The monoclonal antibody is of the IgG2a subclass, is cytotoxic, and reacts with Staphylococcal protein A. The tissue culture supernatant has the same activity (titer on thymus &gt; 1/1000) as an anti-Lyt-1.1 produced by a standard immunization procedure, and after in vivo passage of the hybridoma cell line, the serum titer was &gt; 1:10(6). The monoclonal antibody has the same strain and tissue distribution as the conventional antibody, including reactions on Lyt-1 congenic strains, and it precipitates a cell surface molecule of m.w. approximately 67,000. In nonprimed mice, there were similar numbers of Thy-1+ and Lyt-1+ cells in spleen, lymph node, and thymus. By using the monoclonal reagent, T-helper and T-killer cells in an allogenic system were shown to be Lyt-1.1.
Delayed hypersensitivity to crude and partially purified murine tumor-specific transplantation antigens and alloantigens utilizing the footpad swelling assay.
Authors: Macek C M , Kahan B D , Pellis N R 
Published: December 2022

Abstract
Antigen preparations extracted from C3H/HeJ methylcholanthrene-induced fibrosarcomas by the 3M KCl extraction procedure were assessed for tumor-specific and allospecific antigenicity. Specificity of crude tumor antigen preparations and of fractions from preparative isoelectric focusing was investigated by evocation of footpad swelling (FPS) in syngeneic mice immunized with irradiated fibrosarcoma cells. Tumor immune mice displayed delayed hypersensitivity as positive FPS responses to challenge with 3M KCl extract and with fraction (Fr) 15 (pH 5.7 to 6.0) from preparative isoelectrically focused 3M KCl extract. Crude extracts and Fr 15 exhibited immunoprotective activity in vivo. Immune mice demonstrated a specific FPS response only to crude antigen preparations of Fr 15 from immunizing tumors, not to materials from a noncross-reactive neoplasm. DBA/2J mice immunized with C3H/HeJ spleen cells displayed FPS to challenge with crude antigen preparations, but not with the tumor-specific Fr 15. Alloantigen activity, however, was detected by a positive FPS response in C3H-immune DBA mice in fractions from the pH range 5.1 to 5.5. These experiments demonstrated that the FPS assay provides the setting for detection of specific delayed hypersensitivity responses to crude and fractionated tumor antigen preparations and for delineation of tumor-specific and histocompatibility antigen activities in fractions from crude extracts.
Macrophage accumulation in murine ascites tumors. I. Cytoxan-induced dominance of macrophages over tumor cells and the anti-tumor effect of endotoxin.
Authors: Dye E S , North R J 
Published: December 2022

Abstract
The host cellular response to i.p. growth of the SA-1 spindle cell sarcoma was studied in semisyngeneic AB6F1 hybrid mice. At progressive stages of tumor growth mice were sacrificed, their ascites were collected, and changes in the numbers of tumor cells, macrophages, lymphocytes, and granulocytes were determined. It was found that macrophages were the predominant host cell that accumulated locally in response to tumor growth. Cytoxan treatment caused a 90% reduction in tumor cells without affecting the accumulation of macrophages. Six days after treatment with cytoxan, macrophages exceeded all other cell types present in the peritoneal cavity and outnumbered tumor cells by 20:1. However, in spite of this macrophage dominance, the tumor cells ultimately regrew to kill the host. Ascites tumors could be completely regressed, however, by following cytoxan treatment ith an appropriately timed intratumor injecton of endotoxin. The relatively long delay before endotoxin caused the tumor to regress suggests that endotoxin acted by stimulating the generation of anti-tumor immunity, rather than by directly augmenting the tumoricidal activity of macrophages.
Alterations in cyclic nucleotides and cyclase-specific activities in T lymphocytes of aging normal humans and patients with Down's syndrome.
Authors: Tam C F , Walford R L 
Published: December 2022

Abstract
The levels of cyclic adenosine 3'5'-monophosphate (cAMP) in unstimulated (resting) peripheral blood thymus-derived lymphocytes (T cells) from normal old humans and young-adult Down's syndrome (DS) patients were markedly decreased when compared with those of young normal humans. By contrast, the cyclic guanosine 3'5'-monophosphate (cGMP) in resting T cells from normal old and young-adult DS patients were greatly increased. The cAMP/cGMP ratios for unstimulated T cells therefore declined in normal aged and DS subjects. The specific activity of adenylate cyclase (ATP pyrophosphate-lyase[cycling]E.C.4.6.1.1) was elevated in T cells from the aged and DS groups, whereas that of guanylate cyclase (GTP pyrophosphate-lyase[cycling]E.C.4.6.1.2) decreased with age and in DS. These results denote the existence of substantial age-related biochemical changes in peripheral T cells. An imbalance in resting cyclic nucleotide levels and their generating enzymes in T cells of normal aging and DS subjects might contribute to the immune dysfunction occurring both with aging and in DS.
Development of B lymphocytes in the mouse; studies of the frequency and distribution of surface IgM and IgD in normal and immune-defective CBA/N F1 mice.
Authors: Scher I , Berning A K , Kessler S , Finkelman F D 
Published: December 2022

Abstract
Affinity-purified anti-mouse mu and delta antibodies and flow microfluorometric techniques were utilized to study the frequency and distribution of sIgM and sIgD on adult and neonatal B lymphocytes of immunologically normal mice and mice with the immune-defect characteristic of the CBA/N strain. Neonatal normal B lymphocytes can be distinguished from their adult counterparts by the presence of increased amounts of sIgM on sIgM+ cells and by the increased number of sIgM+IgD- cells. The most primitive B lymphocytes of immunologically normal mice appear to reside in the bone marrow of 1- to 2-wk-old mice and are distinguished from splenic B lymphocytes at this time by their relatively low amounts of sIgM. However, in the adult, splenic and bone marrow B lymphocytes are indistinguishable with regard to the quantities of their sIgM or sIgD. Adult immune-defective mice have increased amounts of sIgM on their B lymphocytes, although the number of sIgM+ IgD- cells in these mice is not increased. During development, however, larger than normal numbers of sIgM+ IgD- cells are found in the spleen and bone marrow of these mice; and the low frequency of such cells seen in normal adults is not achieved in immune defectives until after the 56th day of life. Thereafter, immune-defective mice have low frequencies of B lymphocytes with high relative amounts of sIgM, even after 1 yr or age.
Cell-mediated immunity in interstitial nephritis. III. T lymphocyte-mediated fibroblast proliferation and collagen synthesis: an immune mechanism for renal fibrogenesis.
Authors: Neilson E G , Jimenez S A , Phillips S M 
Published: December 2022

Abstract
Fibroblast proliferation and collagen synthesis play an important role in the progression of intersititial nephritis. To evaluate the involvement of immune mechanisms in this process, we induced intersititial nephritis in guinea pigs utilizing injections of tubular antigens. Over a 3-week period, injected animals developed a nephritis characterized by mononuclear infiltrates and expanding areas of fibrotic scar formation. Involved kidneys contained increased collagen as compared to controls. To identify mediators of the observed fibrogenesis, T lymphocytes from nephritic and control animals were stimulated with soluble tubular antigens. Dialyzed supernatants from control lymphocyte cultures contained an inhibitor of both fibroblast proliferation and collagen synthesis. In contrast, supernatants from nephritic animals demonstrated absence of inhibition and a progressively increasing titer of a factor that enhanced both kidney fibroblast proliferation and collagen synthesis. As the disease progressed, however, nephritic lymphocytes also began secreting an inhibitor of proliferation that could be detected in low levels. These studies suggest, therefore, that immune mechanisms and altered lymphocyte function may play an important role in the development, progression, and regulation of renal fibrogenesis in intersititial nephritis.
Developmental profile of chicken splenic lymphocyte responsiveness to Con A and PHA and studies on chicken splenic and bone marrow cells capable of inhibiting mitogen-stimulated blastogenic responses of adult splenic lymphocytes.
Authors: Kline K , Sanders B G 
Published: December 2022

Abstract
Embryonic and newly hatched chicken splenic lymphocytes were analyzed for their ability to respond to 2 mitogens, Con A and PHA. Acquisitions of the ability to respond to both mitogens began at hatch and responses to both mitogens reached normal adult blastogenic response levels by 11 days post-hatch. Splenic lymphocytes in the developing embryo and newly hatched chicken were found to be capable of inhibiting the Con A- and PHA-mediated blastogenic responses of both syngeneic and allogeneic adult splenic lymphocytes. The ability to suppress adult responses was first observed on E12, reached a maximum of suppressive ability on E18, and the suppressive ability was gradually lost with development such that no suppressive ability was exhibited after H11. Ability to suppress adult splenic lymphocyte proliferation to mitogens was found to not be a unique property of splenic lymphocytes but was also exhibited by bone marrow cells. The ability of bone marrow cells to suppress adult splenic lymphocyte proliferation to Con A and PHA gradually decreased with chicken aging but the suppressive ability was never lost and adult bone marrow cells were found to exhibit significant degrees of suppressive ability. The mechanism of suppression by the 1-day-hatched splenic lymphocytes was found to be cell-to-cell contact mediated and did not require any newly synthesized H1 splenic products, since x-ray killed cells were able to suppress as well as live cells.