bluuebunny/crossref_metadata_2025_split huggingface dataset:
Thymus cell migration: analysis of thymus emigrants with markers that distinguish medullary thymocytes from peripheral T cells.
Authors: Scollay R , Wilson A , Shortman K 
Published: December 2022

Abstract
Peripheral T cells and cells from the thymic medulla have many phenotypic characteristics in common, and both populations are quite distinct from cortical thymocytes. The cells that migrate out of the thymus (thymus migrants) may be detected in the periphery as fluorescent cells shortly after intrathymic injection of fluorescein isothiocyanate. Our previous work has established that they resemble T cells and medullary thymocytes rather than cortical thymocytes, and are fully functional. In this report, we consider several phenotypic characteristics that differ between medullary thymocytes and peripheral T cells, namely size, buoyant density, and sensitivity to a new monoclonal antibody (B2A2) and complement. By these criteria, the fluorescence-labeled thymus migrants in spleen and lymph node tend to resemble medullary thymocytes and are distinct from the majority of T cells that surround them. This suggests, but does not prove, that migrants originate in the medulla. After adult thymectomy, the small population of medullary-thymocyte-like cells disappears from spleen and lymph node, further supporting the idea that cells leave the thymus with a medulla-like phenotype, and acquire normal peripheral T cell phenotype only after their arrival in the periphery. Thus, although thymus migrants appear to leave the thymus in an immunocompetent state and are phenotypically mature by most criteria, there are a few final maturation steps that occur after arrival in the periphery.
Cellular mechanism of primary anti-Thy-1 antibody responses in vitro induced by uniquely immunogenic thymocyte antigens.
Authors: Isobe K I , Nakashima I , Nagase F , Kato N , Mizoguchi K , Kawashima K , Lake P 
Published: December 2022

Abstract
Thy-1 antigens are the only cell membrane antigens known to be able to induce primary antibody responses in vitro. We have shown that antigens from the thymocytes of mice and rats were highly immunogenic in cultures of murine spleen cells for the induction of Thy-1.1-specific plaque-forming cell responses, whereas antigens from other tissues, including brains and bone marrow, were poorly immunogenic, if at all. The thymocyte-specific Thy-1 immunogenicity was carried by disrupted cell membranes, and the specific activity for inducing responses was closely linked to Thy-1. We then tried to determine the mechanism of anti-Thy-1 antibody responses in vitro that were induced by the uniquely immunogenic thymocyte antigens. The thymocyte Thy-1 antigens behaved as T cell-independent class 2 (TI-2) antigens: they induced responses in athymic nude mice but not in CBA/N mice with a B cell defect. The apparent TI-2 responses to thymocyte Thy-1 did, however, require Thy-1+ cells in the responder, similar to anti-DNP-Ficoll responses. The full development of the anti-Thy-1 responses required the participation of splenic adherent cells (SAC). Nevertheless, the mechanism of the SAC dependency of anti-Thy-1 responses did not involve antigen presentation to lymphocytes by antigen-pulsed SAC, which contrasted with the finding that the presentation of antigen by live SAC to lymphocytes was indispensable for responses to DNP-Ficoll. The poor Thy-1 responsiveness of SAC-depleted spleen cells was fully restored by the addition of soluble factors (IL 1-like molecules) released from SAC into the culture, which did not replace the SAC-requirement of responses to DNP-Ficoll. It was concluded from these results that Thy-1 or Thy-1-linked structures on thymocyte membranes have an intrinsic activity to directly signal either TI-2 B cells or immature T cells, or both, for activation in the presence of soluble factors released from adherent accessory cells. This conclusion is discussed in relation to a hypothetical view that the thymocyte Thy-1 would physiologically mediate cell-to-cell interactions among special subsets of lymphocytes under thymic influence.
Immunoregulation by monoclonal sheep erythrocyte-specific IgG antibodies: suppression is correlated to level of antigen binding and not to isotype.
Authors: Heyman B , Wigzell H 
Published: December 2022

Abstract
Six different monoclonal IgG antibodies with specificities for sheep erythrocytes (SRBC) were tested for immunosuppressive ability. Four of them, one IgG3, two IgG2a, and one IgG1, could yield suppression of more than 90% of the anti-SRBC response. The remaining two antibodies, which were both IgG2a, were found to have no significant effect. The degree of suppression correlated well with the amount of antibodies used that could bind to SRBC, as measured by an ELISA assay. High avidity for SRBC was also a factor making the monoclonal antibody more efficient as an immunosuppressor. The response against antigenic determinants on the SRBC other than those for which the monoclonals were specific, was suppressed to an equal degree. This was established by immunizing mice with SRBC using monoclonal anti-SRBC antibodies that did or did not bind to goat RBC (GRBC). The PFC responses against both SRBC and GRBC were then measured. The anti-SRBC and GRBC responses were suppressed in parallel regardless of whether or not the monoclonal reacted with GRBC. None of the tested antibodies displayed any significant ability to enhance the anti-SRBC response. Thus, IgG1 is not the only murine isotype that can efficiently suppress the immune response against SRBC, but IgG2a and IgG3 can also exert this capacity. The mechanism of IgG-mediated suppression is not one of merely blocking single epitopes but involves the immunogenicity of the entire SRBC.
Mechanisms of the failure of resting B cells to present tetanus toxoid antigen to T cells.
Authors: Brozek C , Umetsu D , Schneeberger E , Geha R S 
Published: December 2022

Abstract
The present study examines the failure of resting B cells to present tetanus toxoid (TT) antigen to T cells. A hybrid antibody directed against TT and against human IgM was prepared from immunosorbent-purified rabbit anti-TT and rabbit anti-human IgM. Peripheral blood B cells were prepared by double rosetting with sheep red cells and were depleted of monocytes by double adherence over plastic plates and by passage over a Sephadex G-10 column followed by treatment with OKM1 and complement. B cells were preincubated with medium or with hybrid antibody (60 micrograms/ml) for 1 hr at 4 degrees C, washed, irradiated (2500 R), and tested for their capacity to present TT to an autologous TT-specific T cell clone. B cells coated with the hybrid antibody took up equivalent amounts of 125I-TT as monocytes or EBV-B cells and they internalized fluorescein-labeled TT. In contrast, in the absence of hybrid antibody B cells took up negligible amounts of TT antigen. However, B cells preincubated with the hybrid antibody failed to induce proliferation of autologous TT-specific T cell clones in response to TT. This was not corrected by the addition of partially purified human interleukin I. EBV-B cells sequentially pulsed with hybrid antibody and then with TT for 1 hr at 4 degrees C were equivalent in their capacity to induce T cell proliferation to EBV-B cells presenting soluble TT to the T cells. In contrast EBV-B cells pulsed with TT alone at 4 degrees C failed to take up and present TT. Thus the failure of hybrid antibody-coated resting B cells to present TT reflects an intrinsic inability of the resting B cells to present antigen. Monolayers of hybrid antibody-coated B cells pulsed with TT were prepared on anti-human Fab-coated dishes and were compared with monolayers of TT-pulsed monocytes for their capacity to adsorb TT-specific autologous T cells. In contrast to TT-pulsed monocytes, TT-pulsed hybrid antibody-coated B cells completely failed to bind TT-specific T cells. These results suggest that in addition to their poor antigen uptake resting B cells are incapable of processing antigen and generating the immunogenic moiety recognized by the T cells.
Human antigen-specific IgA responses in blood and secondary lymphoid tissue: an analysis of help and suppression.
Authors: McCaughan G W , Adams E , Basten A 
Published: December 2022

Abstract
Antigen-specific IgA responses to influenza virus were obtained from lymphocytes derived from human secondary lymphoid tissue but not from the circulating pool (blood). T helper cells for IgA were present in both the circulating pool and secondary lymphoid tissue, were of the Leu-3A+ subset, and were relatively radioresistant. In addition, T alpha cells were shown to be important, but not crucial, for IgA helper responses. T cell-dependent suppression of IgA responses was demonstrated with T cells from both mucosal and systemic lymphoid tissue and was mediated by a radiosensitive Leu-2a+ cell. In contrast to T cells, functional B cell precursors for antigen-specific IgA responses were found only in secondary lymphoid tissue and not in the circulating pool.
Identification of HBsAg determinants in immune complexes from hepatitis B virus-associated vasculitis.
Authors: Gupta R C , Kohler P F 
Published: December 2022

Abstract
Circulating immune complexes were characterized from 25 sera obtained from five patients with polyarteritis nodosa and three with cutaneous venulitis associated with hepatitis B virus infection. Complexes were isolated by polyethylene glycol and conglutinin-anticonglutinin precipitation methods and were analyzed for HBsAg and anti-HBsAg. Low pH was used to dissociate the complexes, and components were separated into antigen and antibody fractions by using immobilized protein A. In this study, three observations were significant: 1) complexes were frequent and quantitatively more in cutaneous venulitis than in polyarteritis; 2) the levels of HBsAg in the antigen fractions of polyarteritis were greater and correlated with the clinical improvement of the disease; the serum levels of HbsAg remained the same throughout the course of the disease; and 3) complexes from polyarteritis were not completely dissociable at pH 2.6 compared with those from patients with cutaneous venulitis and chronic active hepatitis. The antigen fractions electrophoresed in polyacrylamide gel with SDS demonstrated 6 to 10 protein bands with m.w. ranging between 17,000 and 120,000 daltons. To precisely define the polypeptide antigen moiety involved in the immune complex formation, a transfer blotting technique was used employing human anti-HBsAg globulin as probe. Polypeptides with m.w. 97,000, 49,000, and 23,000 were found to form complexes in both groups of patients.
Monocyte antibody-dependent cellular cytotoxicity in splenectomized subjects.
Authors: Gill P G , De Young N J , Kiroff G K , Leppard P I , McLennan G 
Published: December 2022

Abstract
Monocyte antibody-dependent cellular cytotoxicity (ADCC) was determined in normal subjects by using human A1 erythrocytes and immune human anti-A1 antiserum. The experimental data were fitted to a mathematical model and the values for maximal cytotoxicity and monocyte numbers required to produce 15% specific cytotoxicity (MD15) were subsequently computed and compared with the values for these two parameters estimated from the dose response curves. The values for both were significantly associated, and the mathematical model permitted precise quantitation of cytotoxicity in instances where this was impossible by standard methods. Maximal monocyte ADCC was significantly reduced in a group of splenectomized subjects, whereas the MD15 was increased. These findings emphasize the possible influences of the method of quantitation of ADCC and provide one explanation for the apparent conflict of published data.
Interferons as modulators of human monocyte-macrophage differentiation. I. Interferon-gamma increases HLA-DR expression and inhibits phagocytosis of zymosan.
Authors: Becker S 
Published: December 2022

Abstract
The development of HLA-DR (Ia) expression in the presence and absence of interferon-gamma was monitored in monocyte-macrophage cultures. Overnight incubation with doses as low as 5 U/ml gave elevated values for Ia expression and the maximum increase was obtained with 200 U/ml. In contrast interferon-alpha had only a slight effect on the expression of Ia at doses as high as 2000 U/ml. The increase seen at 24 hr was maintained during the first 2 days of culture. The interferon-gamma-treated cells expressed four to five times more Ia than fresh monocytes. During the same time, monocytes cultured in the absence of interferon expressed approximately two times the amount of fresh monocytes. When the surface density of Ia was calculated, the interferon-gamma-treated monocytes expressed twice that of the untreated cells. Major changes in morphology and size occurred between days 3 and 4 of monocyte to macrophage development. Consequently a rapid increase in Ia expression took place; however, when the surface density was calculated this value increased only slightly when the monocytes matured to macrophages. The interferon-gamma-treated cells continued to express more total Ia as well as having increased surface density of this antigen. Interferon-gamma was also added to monocyte-macrophages several days after culture initiation (days 3, 4, and 5). Despite being in different stages of maturation, the cells responded to the interferon with increased Ia expression and surface density. The phagocytic activity of opsonized zymosans was also monitored. In contrast to Ia expression, this activity was downregulated by interferon-gamma, and the lower levels of phagocytosis were maintained through the 7 days of observation. Thus, interferon-gamma appears to change the differentiation pathway of the monocyte. The signal stimulates an increased level of Ia that may assist in the initiation of immune responses, and at the same time downregulates the scavenger role of removing opsonized particles. Once the monocyte has received this specific signal it continues to develop in a pathway different from that of the nontreated monocytes.
Influence of Y and X chromosomes on B cell responses in autoimmune prone mice.
Authors: Rosenberg Y J , Steinberg A D 
Published: December 2022

Abstract
BXSB mice, unlike other autoimmune strains, carry a Y chromosome-linked gene for accelerated autoimmunity, reflected by early onset disease in male but not female animals. To investigate whether the Y chromosome factor acts through other autosomal genes or is in itself sufficient for early disease, partially inbred congenic NZB.BXSB and NZW.BXSB mice were developed and studied for levels of Ig-secreting cells (IgFC) as a measure of their autoimmune state. In such mice, the BXSB contributed only the male chromosome and 3% of the autosomal genes. The results indicate that for full expression of autoimmunity, both the Y chromosome and one or more BXSB autosomal genes are required. In addition, the presence of the CBA/N xid gene results in a total reversal of any Y-linked effects.
Natural release of covalently bound C3b from cell surfaces and the study of this phenomenon in the fluid-phase system.
Authors: Venkatesh Y P , Minich T M , Law S K , Levine R P 
Published: December 2022

Abstract
Covalently bound C3b is released from cell surfaces (EAC1423 and zymosan-C3b) on incubation under physiologic conditions. The release of C3b from cell surfaces occurs by the cleavage of the covalent bond. Sodium dodecyl sulfate (SDS) abolishes the release, thereby indicating the requirement of the native structure of C3b in this process. The phenomenon of release of C3b from cell surfaces has also been observed in the fluid-phase system by using C3b-[3H]glycerol. The kinetics of the release of [3H]glycerol from C3b-[3H]glycerol were studied at 37 degrees C in 0.15 M phosphate buffer, pH 7.4. The first-order rate constant was found to be 0.028 +/- 0.003 hr-1. The release does not take place in either 8 M urea or 6 M guanidine hydrochloride, at pH 7.4. Under alkaline conditions, the rate of release is unaffected in the presence of SDS, indicating that the release in this pH range is not dependent on the native structure of the protein. From the Arrhenius plot in the temperature range 18 to 37 degrees C, an apparent activation energy for the hydrolysis reaction of 21.2 kcal/mol was calculated. The release phenomenon is exclusive for ester-linked complexes, as inferred by the absence of release of [3H]threonine from C3b-[3H]threonine, wherein the linkage is of the amide type. The presence or absence of the C3a portion of the molecule has no effect on the rate of release. The modification of the -SH group of C3i-/C3b-[3H]glycerol alters the rate of hydrolysis of the ester bond between C3i/C3b and [3H]glycerol. Protease inhibitors (PMSF, benzamidine HCl, and DFP) do not alter the rate of release, indicating that the hydrolysis reaction is not due to trace amounts of contaminating proteases. Thus, it appears that some chemical group(s) of C3i/C3b is (are) involved in the intramolecular hydrolysis of the ester bond between C3i/C3b and small molecules. This phenomenon may play an important role in the release of C3b from receptive surfaces once the biologic functions that require covalently bound C3b have been mediated.
Development of respiratory mucosal tolerance during Haemophilus influenzae type B infection in infancy.
Authors: Rosales S V , Lascolea L J , Ogra P L 
Published: December 2022

Abstract
Groups of patients with different forms of infection with Haemophilus influenzae type B (Hib), namely meningitis, epiglottitis, arthritis, and periorbital cellulitis, were evaluated for the appearance of serum IgG, IgA, IgM, and nasopharyngeal secretory (NPS) IgA (SIgA) antibody response to Hib capsular antigen at various intervals after the onset of clinical illness, by using an indirect enzyme-linked immunosorbent assay. The serum immune response was characterized by its predictable absence in infants under 23 mo of age, and in those with meningitis who, regardless of age, had high levels of circulating antigen. On the other hand, antibody response was frequently detected in the serum of older infants. Significantly, however, the appearance of SIgA antibody was demonstrated in virtually all patients with Hib infections under 23 mo of age. In addition, a positive correlation was observed between the concentration of antigen NPS, the level of SIgA activity in the NPS, and the absence of antibody response in the serum. These observations are strikingly similar to the development of systemic hyporesponsiveness (oral tolerance) observed after oral administration of certain infectious or nonreplicating antigens in experimental animals. It is suggested that similar mechanisms may underlie the immunologic abnormalities observed in the serum antibody response in infants with Hib meningitis.
Characterization of T lymphocyte colony-forming cells in the mouse. The colony-forming cell is confined to Lyt-1,2,3+ cell subsets in the thymus and the lymph nodes.
Authors: Röpke C 
Published: December 2022

Abstract
When cell populations from the thymus were studied with FACS, it was found consistently that the brightly labeled Thy-1.2+ populations contained very few T colony-forming cells (CFC), while these latter cells were numerous in the cell populations showing lower Thy-1.2 antigen density. This was paralleled by findings after peanut agglutinin (PNA) separation that showed enrichment of CFC in the PNA-negative medullary population, and by sorting based on TL, T-200, and H-2 determinants or light scatter properties of the cells. By FACS sorting of Lyt-labeled thymic cells, it was also shown that CFC were predominantly present in cell populations that were brightly Lyt-1+, and exclusively in populations that were Lyt-2+ and Lyt-3+. After FACS sorting of lymph node cells, no major differences in colony formation were found between dully- and brightly-labeled Thy-1.2+ or Lyt-1+ populations, or between lymphoid cells showing different light scatter characteristics. In addition, it was shown that CFC--like thymic CFC--were of the Lyt-1,2,3+ phenotype. It is concluded that the CFC may be present in several differentiation steps of Lyt-1,2,3+ cell lines, and that the frequency of these cells increases from the thymic cortex via the medulla and to peripheral lymphoid tissues.
The immune response to bacterial dextrans. IV. Antibody idiotypes.
Authors: Ivars F , Holmberg D , Cazenave P A , Coutinho A 
Published: December 2022

Abstract
Anti-idiotypic antisera (a-Id) were prepared in SJL mice against the dextran B512 (Dex)-specific hybridoma antibody D.16.6 (mu, kappa) of C57BL/6 origin. Such a-Id were specific for the D.16.6 antibody, but the idiotypic determinants recognized were not hapten modifiable. The a-Id were used in radioimmunoassays (RIA) to study the genetic control of the expression of the D.16.6 idiotype (Id) in a variety of mouse strains. It was found that all mouse strains tested expressed this Id as a component of the normal background immunoglobulin (Ig) in their sera. Only in mice of the IgCHb haplotype, however, was the Id found in association with Dex-specific antibodies. Furthermore, even in IgCHb mouse strains, not all individuals expressed Id-positive anti-Dex antibodies. Because the D.16.6 Id is a "recurrent" natural Id, but a "non-dominant" Id in the Dex response of IgCHb mouse strains, these observations contradict our previous suggestions on the selection of "dominant" Id from the pool of "naturally" produced Ig.
mIgM:mIgD ratios on B cells: mean mIgD expression exceeds mIgM by 10-fold on most splenic B cells.
Authors: Havran W L , DiGiusto D L , Cambier J C 
Published: December 2022

Abstract
The relative frequency of mIgM and mIgD molecules on B cell surfaces is important in determining, in large part, the isotype involvement in antigen binding and signal transduction. Although it is generally assumed that on most mature B cells, mIgM and mIgD occur in roughly equal quantities, no formal analysis of this question has been reported. In this report, we describe such an analysis based on the quantitation of anti-Fab or anti-kappa specific immunofluorescence of splenic B cells before or after capping with rabbit anti-IgD or anti-IgM antibodies or both. The results indicate that, whereas mean expression of IgD exceeds IgM on splenocytes by threefold, members of the major B cell subpopulation (60 to 70% of cells) express 10-fold more IgD than IgM.
A genetically restricted suppressor factor that requires interaction with two distinct targets.
Authors: Aoki I , Usui M , Minami M , Dorf M E 
Published: December 2022

Abstract
We have previously described a genetically restricted suppressor factor (TsF3) that suppresses the terminal phases of the contact sensitivity response. The activity of TsF3 is restricted by genes in the H-2 (I-J) and Igh complexes. This report analyzes the mechanisms responsible for these genetic restrictions. One cellular target of TsF3 is an I-J-bearing antigen-presenting cell population that is sensitive to low doses of cyclophosphamide. To elicit suppression I-J homology is required between this antigen-presenting cell population and the TsF3 donor. In contrast, the Igh-linked genetic restriction exists between TsF3 and an unprimed cell population present in the recipient. These findings suggest that under these experimental conditions TsF3 acts by bridging the APC with cells of the host. Finally, we demonstrated that nonspecific bystander or cognate suppression can be mediated by TsF3, provided specific antigen is present in the site of the ongoing T cell response.