bluuebunny/crossref_metadata_2025_split huggingface dataset:
MATURATION OF B LYMPHOCYTES IN THE RAT
Authors: Strober Samuel , Dilley Jeanette 
Published: June 2004

The migration pattern, tissue distribution, and turnover rate of unprimed and primed B lymphocytes involved in the adoptive anti-DNP response was studied. The adoptive primary response restored by unprimed spleen or thoracic duct cells passaged through an intermediate host (intravenous injection and subsequent collection in the thoracic duct lymph) was markedly diminished as compared with that restored by unpassaged cells. On the other hand, the adoptive response restored by passaged spleen or thoracic duct cells from DNP-primed donors was greater than or the same as that restored with unpassaged cells, respectively. This suggests that unprimed B cells change from nonrecirculating to recirculating lymphocytes after exposure to antigen.
Studies of the adoptive anti-DNP response restored by unprimed or primed bone marrow cells showed little change in the time-course or amplitude of the response restored by either population of cells. The relative inability of marrow cells to carry immunological memory was related to the inability of recirculating memory cells to penetrate the marrow.
The turnover rate of unprimed and primed B cells was investigated by treating the cell donors with [3H]thymidine for 48 h before removal of thoracic duct or spleen cells. The adoptive anti-DNP response restored by unprimed or primed cells was not affected by [3H]thymidine treatment. This indicates that both populations of cells turn over slowly. However, our previous studies show that unprimed B cells involved in the adoptive antibody response to ferritin turn over rapidly. The different findings are discussed in the context of antigen-dependent B-cell maturation.
SURFACE MARKERS ON HUMAN B AND T LYMPHOCYTES
Authors: Jondal Mikael , Klein George 
Published: June 2004

Human peripheral lymphocytes were investigated for receptors binding Epstein-Barr virus (EBV) because of the regular association of this virus with infectious mononucleosis and Burkitt's lymphoma.
This was done by a cytoadherence technique where virus-producing cells, displaying fresh viral determinants in their cytoplasmatic membrane, were mixed with lymphocytes. Unfractionated lymphocytes were found to adhere to these cells in contrast to column-purified T lymphocytes. The specificity of the binding was confirmed by blocking experiments that showed that sera containing high titers of antibodies directed against the virus could partially inhibit the adherence in contrast to low-titer sera. It is concluded that B lymphocytes, in contrast to T lymphocytes, have receptors for EBV.
In a second line of experiments it was found that established human lymphoblastoid lines that carry the EBV genome had receptors characteristic for B lymphocytes and did not form T-lymphocyte rosettes. In contrast, a line of known T-lymphocyte origin that did not carry the EBV genome had receptors characteristic for T lymphocytes.
EBV-transformed simian lymphoblastoid lines had surface markers indicating a B-lymphocyte origin in contrast to HVS-transformed simian lines that lacked surface immunoglobulin but carried receptors for sheep red blood cells.
A CYCLICAL APPEARANCE OF ANTIBODY-PRODUCING CELLS AFTER A SINGLE INJECTION OF SERUM PROTEIN ANTIGEN
Authors: Romball Carole G. , Weigle William O. 
Published: June 2004

After a single intravenous injection of rabbits with aggregated HuIgG, IgM- and IgG-plaque-forming cells (PFC) in both the spleens and peripheral blood of rabbits peaked 5, 13, and 21 days after injection, while almost no PFC could be detected on days 8 and 16. The available data suggest that the secondary peaks of PFC (days 13 and 21) resulted from stimulation of memory cells by persisting antigen that was localized in the germinal centers in the spleen. No such persistence of antigen occurred in the lymph nodes, and these lymphoid tissues did not exhibit secondary peaks of PFC.
The identical kinetic patterns for IgM- and IgG-PFC indicate that the major portion of IgG-PFC did not result from IgM-secreting cells switching to IgG synthesis and secretion.
The present data suggest that the antibody produced and present at the site of interaction between committed cells and antigen is responsible for the regulation of antibody synthesis to persisting antigens. Possible cellular events involved in both the regulation and an apparent synchronous appearance of antibody producing cells in the spleens of rabbits were presented.
THYMUS INDEPENDENCE OF A COLLAGEN-LIKE SYNTHETIC POLYPEPTIDE AND OF COLLAGEN, AND THE NEED FOR THYMUS AND BONE MARROW-CELL COOPERATION IN THE IMMUNE RESPONSE TO GELATIN
Authors: Fuchs Sara , Mozes Edna , Maoz Arieh , Sela Michael 
Published: June 2004

Several inbred mouse strains were screened for their ability to respond to the ordered periodic collagen-like polymer (Pro-Gly-Pro)n, to the random copolymer (Pro66, Gly34)n, to the protein conjugate Pro-Gly-Pro-ovalbumin, to rat tail tendon collagen, rat tail tendon gelatin, and to Ascaris cuticle collagen. Differences were obtained in the magnitude of the antibody titers towards the above immunogens among the strains tested. The level of the response to the ordered polymer (Pro-Gly-Pro)n was not similar to that towards the random (Pro66, Gly34)n, confirming differences in the antigenic determinants of the two immunogens.
The role of the thymus in the immune response to (Pro-Gly-Pro)n and (Pro66, Gly34)n as well as to two collagens and gelatin, was studied in order to find out a possible correlation with the structural features of the immunogens. Heavily irradiated recipients were injected with syngeneic thymocytes, marrow cells, or a mixture of both cell populations and were immunized with the above-mentioned antigens. An efficient immune response to the ordered collagen-like (Pro-Gly-Pro)n was obtained in the absence of transferred thymocytes. The thymus independence of (Pro-Gly-Pro)n was confirmed when thymectomized irradiated mice were used as recipients. In contrast with these results, cooperation between thymus and marrow cells was necessary in order to elicit an immune response to (Pro56, Gly34)n. Similarly, the immune response to the triple helical collagen was found to be independent of the thymus, whereas for an effective response to its denatured product, gelatin, thymus cells were required. These findings indicate that a unique three-dimensional structure of immunogens possessing repeating antigenic determinants plays an important role in determining the need for cell to cell interaction in order to elicit an antibody response.
IMMUNOCHEMICAL STUDIES ON MOUSE MYELOMA PROTEINS REACTIVE WITH DEXTRANS OR WITH FRUCTOSANS AND ON HUMAN ANTILEVANS
Authors: Cisar John , Kabat Elvin A. , Liao Jerry , Potter Michael 
Published: June 2004

Four BALB/c IgA mouse myeloma proteins (W3129, W3434, QUPC 52, and UPC 102) reactive with dextran, four myeloma proteins reactive with fructosans, three IgA (W3082, UPC 61, and Y5476), and one IgG2a (UPC 10), and two human antilevans were studied immunochemically. Quantitative precipitin and inhibition assays showed that W3129, W3434, and QUPC 52 had specificities for isomaltose oligosaccharides similar to those previously found with α(1 → 6)-specific human antidextrans. W3129 and W3434 were most complementary to IM5 but W3129 reacted equally with IM4 and IM3 while W3434 had a greater affinity for IM4 than IM3. QUPC 52 had a larger combining region and was most complementary to IM6. Protein UPC 102 (IgA), like MOPC 104E (IgM) (27), was most complementary to the α(1 → 3)-linked trisaccharide, nigerotriose, and thus differed from J558 (29), which was inhibited best by nigeropentaose. UPC 102 was similar to J558 but they differed from MOPC 104E in their reactions with non-α(1 → 3)-linked disaccharides.
The fructosan-specific myeloma proteins fell into two groups with different specificities. The first group, W3082 (IgA), UPC 61 (IgA), and the previously studied J606 (IgG3) (28, 29), reacted with inulin and W3082 and UPC 61 appeared to have identical specificities for ß(2 → 1)-linked fructofuranosyl residues with maximum complementarity for the tetrasaccharide ßDfructofuranosyl (2 → 1)ßDfructofuranosyl(2 → 1)ßDfructofuranosyl(2 → 6)Dglucose while protein J606 was inhibited best by the trisaccharide ßDfructofuranosyl(2 → 1)ßDfructofuranosyl(2 → 6)Dglucose. W3082 and UPC 61 also differed from J606 in their behavior toward sucrose and ßDfructofuranosyl(2 → 6)Dglucose as compared with αDglucosyl(1 → 3)Dfructose (turanose). The second group containing myeloma proteins UPC 10 (IgG2a) and Y5476 (IgA) behaved similarly to human antilevans in that neither reacted with inulin nor were they inhibited by the ß(2 → 1)-linked fructose oligosaccharides. Unlike the ß(2 → 1)-specific proteins, they reacted with perennial rye grass levan that contained over 90% ß(2 → 6)links. The differences in specificity and site size among homogeneous mouse myeloma proteins reactive with the same antigenic determinant are completely consistent with the concept that they represent products of homogeneous clones selected from the known heterogeneous population of antibody-forming cells.
THE ORIGIN OF CELL SURFACE IMMUNOGLOBULIN OF MARROW-DERIVED AND THYMUS-DERIVED LYMPHOCYTES OF THE RAT
Authors: Hunt Simon V. , Williams Alan F. 
Published: June 2004

The origin of immunoglobulin on the surface of TDL in the rat has been studied by comparing the binding of purified alloantibodies recognizing the Ig-1a allotype of rat light chain, with that of rabbit antirat Fab antibodies. Both reagents labeled all TDL from rats of the DA strain (Ig-1a) with two categories of cells being detected; one binding 100–2,000 molecules of antibody, the other 10,000–100,000 molecules. These categories were likely to be synonomous with T and B cells, respectively. The [125I]antiallotype antibodies did not bind to TDL from rats of the PVG/c strain (Ig-1b).
When the binding to TDL from (PVG/c x DA)F1 animals was studied it was found that allelic exclusion occurred in the heavily labeled cells, but not in the lightly labeled ones. Furthermore, when lymphocytes of one allotype were transferred to irradiated recipients of the opposite allotype and recovered from the TDL or spleen of the recipient 20–30 h later, the immunoglobulin on heavily labeled cells was of the donor type, while that of lightly labeled ones bore the recipient marker. Thus heavily labeled cells (B lymphocytes) had synthesized their own immunoglobulin while lightly labeled cells (T lymphocytes) had acquired theirs passively by adsorption. The class of immunoglobulin on lightly labeled cells was also studied and it was found that [125I]anti-IgM antibodies bound to an extent approaching the [125I]anti-Fab binding, while [125I]anti-IgG2a+2b antibodies gave much less binding.
MECHANISMS OF GENETIC RESISTANCE TO FRIEND VIRUS LEUKEMIA IN MICE
Authors: Kumar Vinay , Bennett Michael , Eckner Robert J. 
Published: June 2004

Resistance to malignant erythropoiesis induced by Friend spleen focus-forming virus and resistance to marrow stem cell allografts are under genetic control. Strains of mice, e.g., C57BL/6 and B10.D2, which are homozygous for resistance at the Fv-2 locus, are also good rejectors of most bone marrow allografts. 89Sr, a bone-seeking isotope, irradiates marrow but not other lymphoid organs and abrogates resistance to marrow allografts without suppressing T- or B-cell functions. Thus, marrow-dependent effector cells (M cells) seem to resist allogeneic stem cells. To test if the genetic resistance to Friend virus (FV) is also mediated by M cells, B6 mice were treated with 89Sr using a dosage schedule known to abrogate resistance to allogeneic marrow cells. 9 days after FV infection of such mice, the spleens showed malignant erythroblastosis which could not be suppressed by prior hypertransfusion, a procedure which suppresses physiologic erythropoiesis. Such 89Sr-treated B6 mice also supported extensive virus replication, while control mice did not. FV markedly suppressed the ability of 89Sr-treated B6 mice to produce antisheep red blood cell (SRBC) antibodies, a feature seen normally only in genetically susceptible mice. Thus, 89Sr-treated B6 mice behaved in these respects as if they were susceptible to FV. When increasing doses of 89Sr were administered to B6 mice, a dose-related loss of resistance to FV was seen. Therefore, it appears that 89Sr-sensitive M cells mediate the genetic resistance to FV.
The results of experiments with 89Sr indicated that genetically resistant mice would be expected to possess target cells which are susceptible to transformation by FV. To verify this corollary, bone marrow cells from B10.D2 (Fv-2rr) mice were transplanted into previously infected and lethally irradiated DBA/2 (Fv-2ss) recipients which share the same H-2d alleles. 5–15 days later, the spleens of DBA/2 primary recipients yielded transformed cells which were capable of producing splenic tumor colonies upon transplantation into adult, unirradiated B10.D2 secondary recipients. Various control experiments clearly indicated that the tumor colonies so induced were of B10.D2 marrow origin. This indicated that B10.D2 stem cells could be transformed when allowed to interact with FV in the spleens of susceptible DBA/2 mice. However, 30 days after transplantation of B10.D2 bone marrow cells into DBA/2 recipients, no transformed cells were detected. Apparently, in the 30-day interval precursors in the B10.D2 marrow gave rise to mature M cells which resisted the leukemic process. Since M cells recognize hybrid or hemopoietic histocompatability antigens expressed on primitive normal and transformed hematopoietic cells, we suggest that M cells may exert surveillance by rejecting leukemic cells. Thus, marrow transplantation from genetically resistant donors may provide a new mode of treatment for leukemia, by providing precursors of M cells and other immunocompetent cell types.
ANTIGENIC DIFFERENCES BETWEEN HEMOPOIETIC STEM CELLS AND MYELOID PROGENITORS
Authors: Van den Engh Gerrit J. , Golub Edward S. 
Published: June 2004

Bone marrow contains pluripotent stem cells which give rise to colonies when injected into irradiated syngenic hosts as well as more differentiated progenitor cells of the myeloid cell which are able to form colonies in vitro. Antisera against brain is known to contain antistem cell antibody. The present experiments were designed to determine if the myeloid progenitor cell still expresses the stem cell antigen.
Bone marrow cells were treated with antibrain antiserum plus complement and then survival of stem cells was determined by injection into irradiated hosts. Survival of myeloid progenitor cells was determined by culturing the cells in vitro. It was found that stem cells were eliminated by the antiserum but that myeloid progenitors were not. Inefficient in vitro lysis was ruled out as the reason for this difference since in vitro colonies were not reduced when the cells were treated with anti-immunoglobulin or after passage through an irradiated host. In the differentiation from stem cell to myeloid progenitor there is an associated surface antigen change.
THE IMMUNOLOGY OF EXPERIMENTAL CHAGAS' DISEASE
Authors: Santos-Buch Charles A. , Teixeira Antonio R. L. 
Published: June 2004

Experiments that consisted of incubation of Trypanosoma cruzi-sensitized lymphocytes derived from chronically infected rabbits and from rabbits repeatedly immunized with a small particle or membrane fraction derived from homogenates of T. cruzi forms, showed destruction of allogeneic, parasitized and nonparasitized heart cells in vitro. Mononuclear cells collected from peripheral blood were incubated for 1 h at 37°C to isolate the lymphocytes. Following incubation, over 99% of the cells in the supernate were lymphocytes, which were utilized in these experiments. At the start of these experiments, 70–80% of the sensitized lymphocytes were unattached, small and round, with sparse filipodia. In the ensuing hours, marked heart cell destruction, similar to that seen in an active lesion when lymphocytes invade heart tissue, were observed. After 18 h incubation, about 65–70% of the lymphocytes were attached, larger, and rough surfaced.
Inhibition of monocyte migration tests, each in the presence of the antigens of subcellular fractions of T. cruzi organisms and of allogeneic heart myofibers, indicated the presence of a cross-reacting antigen common to both the parasite and the heart in the small particle or membrane fractions. The particulate antigens of the 30,000 g, 35-min fraction of heart muscle gave rise to inhibition of monocyte migration as did the counterpart fraction derived from T. cruzi organisms.
The destruction of nonparasitized target heart cells by T. cruzi-sensitized lymphocytes is an in vitro model of the chronic myocarditis of Chagas' disease, and the recognition of cross-reactive antigens of the host cell by T. cruzi-sensitized lymphocytes is believed to be the pathogenic basis for subsequent tissue injury in the chronic phase of this disease.
ROLE OF EXTRAPULMONARY CONVERSION IN MEDIATING THE SYSTEMIC PRESSOR ACTIVITY OF ANGIOTENSIN I
Authors: Oates Helen F. , Stokes Gordon S. 
Published: June 2004

The effect of antibodies against angiotensin II (AII) on systemic pressor responses to intravenously injected AII and angiotensin I (AI) was studied in a group of bioassay rats. AII antibody was only 29% as effective in neutralizing AI given intravenously as it was in neutralizing AII injected by the same route. Control plasma caused no change in the relative potencies of AI and AII.
In a further series of experiments, AII antibody was significantly less effective in blocking intra-arterial AI than in blocking intravenous AI. The potency of intra-arterial AI, initially less than that of intravenous AI, became nearly twice that of intravenous AI after antibody administration, a result which could not occur if AI were inactive before lung transit. Thus, AI can elicit systemic pressor activity independently of pulmonary conversion to AII. However, since the intra-arterial AI responses were abolished by an inhibitor of angiotensin-converting enzyme, the activity would appear to be mediated by peripheral conversion to AII rather than by an intrinsic action of the decapeptide.
Both series of experiments suggest that the efficacy of AII antibody in abolishing the systemic pressor activity of AI is highly dependent on the site of conversion of the AI to AII. The occurrence of localized intramural conversion of AI to AII near arteriolar receptors in vivo may so minimize exposure of the liberated AII to circulating antibody as to render AII immunization an inefficient means of blocking endogenous pressor activity of the renin-angiotensin system.
CHARACTERISTICS OF IMMUNOLOGICAL MEMORY IN MICE
Authors: Black S. J. , Inchley C. J. 
Published: June 2004

The kinetics of the generation of primed IgM and IgG antibody-forming cell precursors, and of helper T-cell populations, were analyzed in mice whose primary responses to high and low doses of SRBC were arrested at intervals by the immunosuppressive agents cyclophosphamide monohydrate and specific antibody. The extent to which immunological memory was established in these animals before blockade of the primary response was assessed by the hemolytic plaque assay following challenge 12 wk after priming. The presence of IgG B-memory cells and T-memory cells in suppressed mice was further investigated by the transfer into these animals of syngeneic SRBC-stimulated thymocytes or anti-θ-treated spleen cells.
It was found that the progenitors of secondary IgM-synthesizing cells were primed almost immediately after injection of antigen, and that early blockade of the primary response resulted in a raised IgM response after challenge. On the other hand, priming for a secondary IgG response took at least 4 days, and was dose-dependent, although helper T populations for a secondary IgG response appeared 3 days after antigen injection. It appeared that both IgM and IgG memory cells may be considered as Y cells in terms of the X-Y-Z scheme of lymphocyte activation, but that the two populations are generated at different times after exposure to antigen. The size of either Y-cell population at any given time is dependent upon the amount of antigen available to provoke differentiation to antibody-forming Z cells, and the IgM Y-cell population in particular is likely to be depleted during the course of a normal 1° response. When IgM Y cells were maintained for long periods as a result of immunosuppression, their secondary antibody response was independent of the primed T cells necessary for a secondary IgG response.
EARLY AND DISCRETE CHANGES IN PERMEABILITY OF ESCHERICHIA COLI AND CERTAIN OTHER GRAM-NEGATIVE BACTERIA DURING KILLING BY GRANULOCYTES
Authors: Beckerdite Susan , Mooney Carolyn , Weiss J. , Franson R. , Elsbach Peter 
Published: June 2004

Rapid killing of Escherichia coli by intact or disrupted rabbit granulocytes or by granulocyte fractions was found to be accompanied by an equally rapid increase in permeability of the E.coli envelope. This increase in permeability was detected by determining entry of substances that normally do not cross E.coli's permeability barrier, namely actinomycin D and o-nitrophenyl-ß-D-galactopyranoside (ONPG), a substrate for cytoplasmic ß-galactosidase.
Because E.coli continue to incorporate radioactively labeled precursors into bacterial RNA and protein for at least 1 h, despite rapid killing by granulocytes, entry of actinomycin D could be measured by its inhibitory effect on macromolecular synthesis. Entry was evident within minutes after exposure to granulocytes or granulocyte fractions and is independent of pH over a range of 6.5–9.0.
The effect of disrupted granulocytes or partially purified fractions on susceptibility of E.coli to actinomycin D and entry of ONPG is dose dependent. That the entry of actinomycin D and ONPG was not caused by gross destruction of the envelope is indicated by two sets of observations: (a) net influx of 42K was maintained for at least 15 min, even though efflux of potassium was immediately accelerated upon addition of bactericidal concentrations of granulocyte fractions; (b) ß-galactosidase did not leak out of E.coli under conditions that produce maximal inhibition by actinomycin D.
Different species of gram-negative bacteria exhibited different susceptibilities to the bactericidal and permeability effects of granulocyte fractions. Thus, three strains of E.coli and one strain of Salmonella typhimurium were highly susceptible to both the bactericidal and the permeability enhancing effects of granulocyte fractions, whereas two strains of Serratia marcescens and one strain of Pseudomonas aeruginosa were resistant to both effects. Another strain of P. aeruginosa was rendered susceptible to actinomycin D without being killed and two strains of S. typhimurium remained insensitive to actinomycin D while being killed by granulocytes.
IMMUNOLOGICAL FUNCTIONS OF HUMAN T-LYMPHOID CELL LINE (MOLT)
Authors: Takada Akikazu , Takada Yumiko , Minowada Jun 
Published: June 2004

A short term incubation of the mixture of established human T-lymphoid cells (MOLT) and sheep red blood cells (SRBC) resulted in the release of factors which nonspecifically suppressed the response of mouse spleen cells against heterologous erythrocytes in vitro. Neither human B-cell line (RPMI 1788), nor the supernate of MOLT cell suspension in the absence of SRBC had such suppressive effects.
The supernate of the mixture of MOLT cells with chicken red blood cells (CRBC) did not suppress either anti-CRBC or anti-SRBC responses of mouse spleen cells. Since CRBC did not form rosettes with MOLT cells, it is suspected that the origin of the production of these factors might be MOLT cells forming SRBC rosettes. Some of these factors are dialysable.