bluuebunny/crossref_metadata_2025_split huggingface dataset:
Suppression of interferon gamma production in mice treated with carrageenan
Authors: Suzuki Fujio , Maeda Hiroshi , Pollard Richard B. 
Published: February 2007

AbstractEffects of carrageenan (CAR) treatment on the response of interferon (IFN) production in vivo and in vitro after stimulation with an IFN‐γ inducer, staphylococcal enterotoxin A (SEA), was investigated. The IFN‐γ production in mice stimulated with SEA was impaired after i.v. administration of a 20 mg/kg dose of CAR. Spleen cells (SC) from CAR‐treated mice had decreased ability to produce IFN in vitro after stimulation with the same inducer. SC obtained from mice during the suppressive state inhibited IFN‐γ production when they were co‐cultured with mononuclear cells prepared from spleens of untreated control mice. This suppressor cell activity could be removed from SC by an adherence technique to plastic surface. The SC with suppressor activity were not inactivated by treatments with monoclonal anti‐Thy‐1.2 antibody, anti‐asialo GM1 antisera and anti‐mouse immunoglobulin antisera followed by complement. The suppressive activity was detected in cell‐free culture fluids of macrophage fractions containing suppressor cell activity. These results suggest that the decrease in IFN‐γ production in mice pretreated with CAR may associate with the presence of suppressor cells characterized to the monocytelmacrophage lineage.
Induction or prevention of immunopathological disease by cloned cytotoxic T cell lines specific for lymphocytic choriomeningitis virus
Authors: Baenziger Jürg , Hengartner Hans , Zinkernagel Rolf M. , Cole Gerald A. 
Published: February 2007

AbstractCloned lymphocytic choriomeningitis virus (LCMV)‐specific cytotoxic T lymphocyte (CTL) lines were prepared from spleens of 129/J (H‐2b) mice immunized 7‐9 months earlier with LCMV (UBC strain), or of C57BL/10J (H‐2b) mice immunized 4 to 5 weeks earlier with LCMV (Armstrong strain). One uncloned and 3 cloned cytotoxic T cell lines were assessed for their respective abilities to produce, or protect against, fatal disease upon transfer to appropriate recipients or to induce specific footpadswelling reaction. The effects of all lines were essentially identical. In recipient mice acutely infected with LCMV and immunosuppressed either by irradiation (750‐990 rds) or treatment with cyclophosphamide, cloned T cells administered intracerebrally (i.c.) caused a convulsive disease and death within 1‐4 days. No disease was produced when the same CTL were transferred to uninfected recipients or when they had been frozen and thawed prior to transfer to infected recipients. When admixed with 500 plaque‐forming units of LCMV and transferred i.c. to immunocompetent H‐2b mice, the T cell clones prevented overt disease. Allogeneic (H‐2k) recipients of this same admixture all developed typical LCM disease as did H‐2b recipients of the admixture after T cells had been frozen and thawed. Inoculation of cloned CTL into preinfected footpads induced a specific footpad‐swelling reaction, which reached maximum levels after about 36 h. Irradiated and infected recipients of cloned LCMV‐specific T cells showed the footpad‐swelling reaction only when they had been reconstituted with bone marrow cells. In contrast, cloned T cells induced LCM disease in i.c. infected and irradiated mice independent of bone marrow reconstitution. These findings indicate that both fatal LCMV‐induced neurologic disease and protection against it are mediated directly by virus‐specific CTL.
Rearrangements of T cell receptor loci can be found only rarely in B lymphoid cells
Authors: Traunecker André , Kiefer Michael , Dembić Zlatko , Steinmetz Michael , Karjalainen Klaus 
Published: February 2007

AbstractWe have studied the rearrangement status of the T cell receptor genes in 64 B lymphoid cell lines, and we found that, unlike the immunoglobulin heavy chain genes in T lymphocytes, T cell Receptor β and related γ chain genes are almost always in germ‐line configuration in B lymphoid cells. The only exception was a myeloma MOPC511 (IgA,x) which contained all T cell receptor genes, β1, β2, γ1, γ2, γ3, and α, in rearranged configuration in both homologous chromosomes. This exception supports the concept that all immunoglobulin and T cell receptor genes exploit the same recombinase to build their complete variable regions. Obviously, in MOPC511 cells the regulation, which confers the tissue specificity i.e. T vs. B lymphocytes, has failed.
Epithelial cell heterogeneity in the guinea pig thymus: Immunohistochemical characterization of four thymic epithelial subsets defined by monoclonal anti‐keratin antibodies
Authors: Nicolas Jean F. , Reano Alain , Kaiserlian Dominique , Thivolet Jean 
Published: February 2007

AbstractKeratins are a family of related polypeptides constitutive of the cytoskeleton of epithelial cells and are never found in nonepithelial tissues. Thymic epithelial cells (TEC), known to induce T cell differentiation, are the keratin‐containing cells within the thymus. Using four monoclonal anti‐keratin antibodies (KL1, KL4, AE2, AE3) directed against keratins of different molecular weight, we have investigated the guinea pig thymic epithelium. The immunohistochemical analysis of thymic cryostatic sections revealed that the keratin expression of TEC varied according to their location in the thymic lobula; the thymic cortex was specifically stained by AE3 whereas the thymic medulla and the subcapsular cortex were recognized by KL4. In addition, KL1 and AE2 exclusively labeled Hassall's corpuscles. The biochemical analysis of keratins extracted from the thymus showed that each TEC subset was characterized by an unique pattern of keratin polypeptides. This study extends the concept of thymic epithelium heterogeneity and suggests that anti‐keratin antibodies which allow the typing of TEC subsets may be valuable tools for studying the differentiation of thymic epithelium and its in vitro function on T lymphocytes.
Selective reversal of H‐2‐linked genetic unresponsiveness to lysozymes: II. Alteration in the T helper/T suppressor balance, owing to gene(s) linked to Ir‐2, leads to responsiveness in BALB.B
Authors: Sadegh‐Nasseri Scheherazade , Dessi Vitalia , Sercarz Eli E. 
Published: February 2007

AbstractImmune responsiveness to lysozyme in H‐2b mice is under the control of H‐2‐linked Ir genes, with T suppressor (Ts) cells playing a dominant role in strains such as C57BL/6 (B6), C57BL/10 and A.BY. However, non‐H‐2‐genes were found to be capable of specific reversal of the effect of the H‐2‐linked genes in responsiveness to chicken lysozyme (HEL), but not to human lysozyme (HUL).Therefore, studies were performed to identify any lesion in the suppressor circuit in BALB.B. It was known that HUL‐induced suppressor cells could cross‐suppress the anti‐HEL response in B10.Q mice, which are responsive to HEL but nonresponsive to HUL. Similarly, BALB.B Ts cells were able to suppress the anti‐HEL response, using as T helper (Th) source a T cell line (BB‐l), derived from HEL‐primed BALB.B periaortic and inguinal lymph node cells. A protocol designed to examine the in vivo suppression by the use of HUL‐induced suppressor cells also demonstrated a significant suppression to the anti‐HEL response.Since the suppressive circuitry seemed intact in the BALB.B, the possibility was examined that a step in T‐B cell collaboration was more efficient in this strain than in the B6 nonresponder. With a B6‐derived HEL‐specific T cell line, BO1H, the B cell and antigen‐presenting (B/APC) populations from B6 required addition of concanavalin A supernatant for anti‐HEL antibody formation, whereas BALB.B B/APC were capable of responding to HEL in culture without the addition of concanavalin A supernatant. In agreement with this finding, when B/APC cell populations from BALB.B and B6 were compared for their extent of anti‐HEL responsiveness, as measured with BB‐1 Th cells, BALB.B B/APC populations responded significantly higher than B6 populations when the responses were activated by picogram/nanogram amounts of HEL. The response level of (BALB.B × B6)F1 B/APC measured in the same assay resembled that of B6. However, when HEL was used at the microgram level, both B6 and BALB.B strains responded equivalently.The above data are consistent with the expression of the reversing non‐H‐2 Ir gene(s) resulting from the balance of antigen presentation to Th and Ts cells in the H‐2b mouse. In the B6, processing and handling of antigen may be inefficient in activating response‐enhancing Th, and more effective in triggering Ts cells, while the reverse may be true for the BALB.B.
In vivo induction of H‐2K/D antigens by recombinant interferon‐γ
Authors: Momburg Frank , Koch Norbert , Möller Peter , Moldenhauer Gerhard , Hämmerling Günter J. 
Published: February 2007

AbstractB10.BR mice received i.v. increasing doses of recombinant interferon‐γ (rIFN‐γ) on three consecutive days. Using an immunoperoxidase technique the distribution of H‐2K/D antigens was studied in frozen tissue sections of thirteen organs (kidney, liver, pancreas, esophagus, stomach, small intestine, colon, lungs, heart, brain, thymus, lymph node and spleen). Class I antigens were shown to be induced or enhanced in almost every organ after exposure to IFN‐γ. This effect was particularly conspicuous for renal tubular cells, hepatocytes, bronchiolar epithelial cells, gastric mucous cells, thymic cortical lymphocytes and capillary endothelial cells in heart and kidney. Neurons, glial cells, gastric chief and parietal cells, and pancreas cells were not inducible. The findings show that i.v. application of IFN‐γ leads to strong induction or enhancement of major histocompatibility complex class I antigens in a wide variety of tissues.
Anti‐interleukin 2 receptor monoclonal antibodies. Respective role of epitope mapping and monoclonal antibody‐receptor interactions in their antagonist effects on interleukin 2‐dependent T cell growth
Authors: Olive Daniel , Raymond Jérǒme , Dubreuil Patrice , Charmot Dominique , Jacques Yannick , Mawas Claude 
Published: February 2007

AbstractFunctional studies, using mainly interleukin 2 (IL 2)‐dependent growth of human T cell lines or clones but also mixed lymphocyte cultures and mitogen T cell activation, allowed a collection of locally produced anti‐IL2 receptor monoclonal antibodies (mAb) to be classified. They fell into two groups: one with strong to moderate inhibition of IL2, the other without any detectable functional activity in in vitro assays. Direct and sequential immunoprecipitation as well as peptide mapping confirm that all the mAb recognize the same surface molecule. The parameters responsible for such functional dichotomy were characterized: the main parameter was found to be linked to the epitopic cluster recognized on the molecule by the mAb. All functional mAb pertained to a given epitopic cluster and all the nonfunctional ones to an alternative cluster. Studies on mAb receptor and IL2 receptor interactions confirmed these findings and strongly suggest that functional mAb interact with a region on the IL2 receptor identical or very close to the site of ligand‐receptor interaction. These data could facilitate the choice of mAb to be used in therapeutical approaches in vivo when ethical objections could be overcome by appropriate committees.
Analysis of the role of interferon‐gamma, interleukin 2 and a third factor distinct from interferon‐gamma and interleukin 2 on human B cell proliferation. Evidence that they act at different times after B cell activation
Authors: Romagnani Sergio , Giudizi Grazia M. , Almerigogna Fabio , Biagiotti Roberta , Alessi Anna , Mingari Cristina , Liang Chi‐Ming , Moretta Lorenzo , Ricci Mario 
Published: February 2007

AbstractRecombinant interferon‐gamma (rIFN‐γ) was able to induce proliferation of human tonsillar B cells activated with suboptimal concentrations of anti‐μ antibody. The B cell growth factor (BCGF) activity of rIFN‐γ was not due to substances contaminating the IFN‐γ preparation, nor was it mediated by factors released by T cells or large granular lymphocytes following activation by rIFN‐γ. The response of B cells to rIFN‐γ peaked on day 3 of culture and rapidly declined thereafter, whereas the response of parallel anti‐μ‐activated B cell cultures to recombinant interleukin 2 (rIL2) appeared on day 3, but continued at least until day 5. In addition, B cells responsive to rIFN‐γ could be at least in part separated from those responsive to rIL2, the former being primarily contained in B cell fractions enriched for high‐density small B lymphocytes. Finally, the addition to anti‐μ‐stimulated B cell cultures of very low concentrations of rIFN‐γ potentiated the B cell proliferation promoted by rIL2.The simultaneous addition of monoclonal antibodies against IFN‐γ and T cell activation antigen to anti‐μ‐stimulated B cell cultures strongly reduced the B cell proliferative response promoted by three different crude BCGF preparations obtained by polyclonal T cell activation in mixed lymphocyte culture. However, the supernatant from a T cell clone (DP5/11) apparently free of IL2, which manifested a BCGF activity similar to that of rIFN‐γ, still maintained its ability to promote proliferation of anti‐μ‐activated B cells after complete removal of IFN‐γ.Taken together, our data indicate that although some T cell clones are able to produce a BCGF distinct from both IFN‐γ and IL2, these lymphokines account for most of the BCGF activity of supernatants obtained from polyclonal T cell populations. They also suggest that IFN‐γ and the BCGF distinct from IFN‐γ and IL 2 act primarily in the earlier phases of B cell activation and potentiate the proliferative response of activated B cells to IL2.
Virgin B cell recruitment and the lifespan of memory clones during antibody responses to 2,4‐dinitrophenyl‐hemocyanin
Authors: Gray David , Maclennan Ian C. M. , Lane Peter J. L. 
Published: February 2007

AbstractThe extent to which B cells newly formed in the bone marrow contribute to primary and secondary B cell responses was investigated. This was assessed by constructing chimeras between congenic strains of rats differing in their kappa light chain allotype. Recipient animals received 800 cGy whole body irradiation with hind limb shieldin to protect a proportion of their hemopoietic capacity. These rats then received 3 × 108 kappa allotype‐marked thoracic duct lymphocytes from donors previously immunized twice with either dinitrophenylated spider crab (Maia squinada) hemocyanin (DNP‐MSH) or MSH alone. The chimeras were immunized with DNP‐MSH and the production of anti‐DNP antibody of both donor and host origin was measured. In the period immediately after immunization both newly formed host virgin B cells and donor memory B cells gave rise to substantial proportions of the anti‐DNP antibody. After this initial period, antibody production became sustained by activation of memory B cells only. The chimeras were reimmunized with DNP‐MSH at 32 days after their first immunization. There was again evidence of a brief period of both virgin and memory B cell activation followed by memory B cell activation only. Donor B cell clones remained dominant in the established response throughout the 5 months each chimera was studied. The data are interpreted as indicating two phases of B cell activation. It is suggested that the first phase where both virgin and memory B cells are activated may be associated with antigen presentation on dendritic or interdigitating cells outside follicles. It is argued that the second phase where only memory B cells are activated is more likely to be associated with antigen on follicular dendritic cells.
Effect of liposomes on lymphocytes: Induction of proliferation of B lymphocytes and potentiation of the cytotoxic response of T lymphocytes to alloantigens
Authors: Grover Amita , Sundharadas G. 
Published: February 2007

AbstractLiposomes of certain lipid composition prepared by the detergent removal method (Brunner, J. et al., Biochim. Biophys. Acta 1976. 455: 322) induced the proliferation of spleen cells from different mouse strains. Spleen cell populations enriched in B lymphocytes and those obtained from nude mice were induced to proliferate, whereas spleen cell fractions enriched in T lymphocytes and thymocytes were not. The mitogenic effect of liposomes resembled that of lipopolysaccharide (LPS) and it depended upon their lipid composition. Liposomes prepared from dimyristoyl lecithin (DML), 2:1 dimyristoyl lecithin:cholesterol (DML:C), 2:1 dioleoyl lecithin: cholesterol (DOL:C), and 2:1 egg yolk lecithin:cholesterol (EYL:C) were mitogenic, whereas liposomes prepared from egg yolk lecithin (EYL) alone were not mitogenic for spleen cells. The mitogenic effects of these liposome preparations were in the decreasing order DML > DOL: C ⩾ EYL: C > DML: C > EYL. The results suggest a correlation between the membrane fluidity of liposomes and their mitogenic effect.Although no proliferative response was induced on T lymphocytes, two of these liposomes, DML and EYL: C, had the ability to potentiate the cytotoxic response of T lymphocytes to alloantigens in mixed leukocyte culture. In responder‐stimulator combinations which differed for the H‐2K, H‐2D or the entire H‐2 region, these liposomes potentiated the cytotoxic response significantly. The results suggest that liposomes have an ability to modulate T lymphocyte response.
Autonomous activation of B and T cells in antigen‐free mice
Authors: Pereira Pablo , Forni Luciana , Larsson Eva‐Lotta , Cooper Max , Heusser Christoph , Coutinho Antonio 
Published: February 2007

AbstractThe spleen of adult antigen‐free mice contains a sizable proportion (5‐15%) of activated cells in all lymphocyte sets, as marked by the membrane expression of immunoglobulins, L3T4 and Lyt‐2 antigens. The frequency of activated cells is very high in early post‐natal life, and reaches adult levels by 6 weeks of age when it is comparable to that observed in healthy unmanipulated mice raised in conventional conditions. The effector B cell compartment is quantitatively similar in antigen‐free mice and specific pathogen‐free mice, but the former is deficient in isotype diversification, since IgG‐ and IgA‐secreting cells are drastically reduced. The effector T cell compartment is slightly reduced in number, but is equally competent in providing help or suppression of syngeneic B cells. The results indicate the existence of a compartment of the immune system displaying autonomous self‐determined activity which is predominant early in life. This compartment, physically localized to the spleen, appears to be distinct from an antigen‐dependent compartment which is essential for the development of peripheral lymphoid organs draining sites of “natural” environmental immunization.
Age‐ and strain‐dependent polymorphism in IgE antibody against the phosphorylcholine hapten
Authors: Gerber Verena , Ponnappan Usha , Heusser Christoph H. , Blaser Kurt , Cinader Bernhard 
Published: February 2007

AbstractThe magnitude of the IgE antibody response against the phosphorylcholine (PC) hapten and the rate of age‐related change of IgE formation is polymorphic in the three long‐lived and six relatively short‐lived strains of mice studied. Long‐lived mice showed an early increase, followed by a decline in the levels of anti‐PC IgE antibody. The rate of increase and decrease was strain dependent. Among short‐lived strains, MRW/Mp‐lpr and MRL/Mp‐+ mice showed an early decline in IgE antibody. The extent and rate of decline with age was more rapid in MRL/Mp‐lpr animals than in MRL/Mp‐+ mice. In contrast, there was an early increase of IgE antibody in female SJL, NZB/BIN, BXSB/Mp and male BXSB/Mp. Thus, opposite age‐related changes in IgE antibody production can occur in animals with a tendency to develop autoimmune disease. In hybrids of (SJL × BALB/c)F1 and (BALB/c × MRL/Mp‐lpr)F1, the levels of IgE antibodies were higher than those observed in either parental strain, and declined steeply with advancing age. We suggest that this could be attributed to recessive inheritance.
Peptides related to the antigenic determinant block T cell recognition of the native protein as processed by antigen‐presenting cells
Authors: Lakey Ellen K. , Margoliash Emanuel , Flouret George , Pierce Susan K. 
Published: February 2007

AbstractA mouse T cell hybrid specific for pigeon cytochrome c in the context of I‐Ekresponds by secreting interleukin 2 when co‐cultured with the native antigen and the B cell lymphoma, LK‐35.2, or naive splenic B cells as antigen‐presenting cells (APC). Cytochromes c and their corresponding C‐terminal fragments which are not capable of stimulating the TPc9.1 cells, including the autologous mouse cytochrome c, block the T cells' response to pigeon cytochrome c. In contrast, nonstimulatory N‐terminal peptides of cytochrome c, which share no homology with the antigenic peptide, do not block. Blocking is observed when the nonstimulatory cytochromes c or peptides are present in culture with the live APC and nonsaturating concentrations of pigeon cytochrome c. it can be overcome with supraoptimal concentrations of pigeon cytochrome c. With tobacco hornworm moth cytochrome c as antigen, a protein for which the T cell has a higher functional affinity, the response of TPc9.1 cannot be blocked by the nonstimulatory cytochromes c or by peptides, even when limiting concentrations of the tobacco hornworm moth cytochrome c are used. When paraformal‐dehyde‐fixed APC are employed, no native cytochrome c can stimulate the T cells, including the tobacco hornworm moth protein which with the live APC is effective at 50 to 100‐fold lower concentrations than pigeon cytochrome c. However, with fixed APC the T cells are stimulated by the C‐terminal fragments containing residues 81‐ 104 of the pigeon protein or residues 81‐103 of the tobacco hornworm moth protein as readily and with the same relative efficiencies as the native protein, presented by live APC. The nonstimulatory peptides, but not the native cytochromes c, block T cell activation by pigeon cytochrome c pulsed‐fixed APC, indicating that the nonstimulatory peptides compete with the stimulatory pigeon cytochrome c peptides produced by the APC. This competition appears to be due to nonstimulatory peptides which associate at the APC surface and not to those acting from solution because the APC which have been incubated with pigeon cytochrome c and nonstimulatory peptides and washed free of excess antigen and peptides are not stimulatory to the T cell hybrid. It was concluded that the activation of a pigeon cytochrome c‐specific T cell, which recognizes a peptide fragment of the native protein on the surface of an APC, can be blocked by an excess of nonstimulatory homologous peptides when these are also associated on the surface of the APC. The ability to block T cell activation does not appear to be competition for processing of the native molecule but may represent a competition for specific peptide binding sites on the APC or on the T cell receptor.