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I Goldschneider

Publications and source records attributed to I Goldschneider.

At least 37 records · Page 2Linked to original sources

Reproducible procedures for establishing mouse thymic stromal cell lines.

Mouse thymic epithelial cell lines (MTEC) were established from Day 14-18 fetal thymus by two novel protocols. The first protocol involved the selection of TEC by the formation of complexes with adult thymocytes after transformation with the helper-free Ad5.SVR4 recombinant virus. The second protocol involved the stimulation and selection of TEC in Ca(2+)-free medium by the formation of complexes with Day 14 fetal thymocytes. The resulting TECs formed several types of thymic epithelial clusters to which Day 14 fetal thymocytes could bind. Many of these fetal thymocytes could deeply infiltrate, colonize, and proliferate within the clusters of NCAM(high) LFA-1(low) TEC (MTSC-0420-1.4, MTSC-0420-1.5, and MTSC-0613-1.2 clusters), whereas very few could infiltrate the clusters of NCAM(low) LFA-1(high) TEC (MTSC-0531-5.1 and MTSC-0531-5.2) and none bound to or infiltrated an NCAM(neg) fibroblast cluster (MTSC-fibro.). Hence, it is possible that the NCAM-positive epithelial cell lines are derived from the thymus cortex, where they may play an important role in intrathymic migration and the clonal growth of pro-T cells in fetal thymus.

Adenoviridae↗

Relative susceptibility of SJL/J and B10.S mice to experimental allergic encephalomyelitis (EAE) is determined by the ability of prethymic cells in bone marrow to develop into EAE effector T cells.

SJL/J mice are highly susceptible to actively induced experimental allergic encephalomyelitis (EAE), whereas B10.S mice are resistant. However, both strains share the H-2s haplotype. We have previously shown that the relative susceptibility of SJL/J and B10.S mice to acute EAE correlates, respectively, with high and low responsiveness to myelin basic protein (MBP), as determined by cloning and limiting dilution analysis of in vitro T cell proliferation. Here, we have investigated the ability of SJL/J and B10.S mice to generate EAE-effector T cells in vivo. We have developed a new mouse strain, B10.S Thy 1.1, that differs at the Thy 1 locus from SJL/J and B10.S mice (both Thy 1.2) but has the same MHC and resistance pattern to EAE as do B10.S mice. Using radiation bone marrow chimeras formed between SJL/J and B10.S Thy 1.1 mice, we have shown that a population of radiosensitive prethymic cells in SJL/J bone marrow has an intrinsic potential to generate EAE-effector T cells, whereas that in B10.S Thy 1.1 bone marrow does not. This lack of detectable EAE effector cells in B10.S Thy 1.1 mice does not appear to be due to the generation of suppressor T cells or to a defect in antigen-presenting cells. Moreover, the potential of SJL/J bone marrow to generate EAE-effector T cells is not inhibited by the concomitant presence of B10.S Thy 1.1 bone marrow cells, thymocytes or dendritic cells in mixed chimeras. Hence, the relative susceptibility of SJL/J and B10.S mice to EAE appears to be directly related to the respective responder status of their T cells to MBP, as evidenced by their ability (or inability) to generate EAE-effector T cells. This high and low responder status appears in turn to be linked to non-MHC background genes, although this has not been established formally.

Animals↗

A selective culture system for generating terminal deoxynucleotidyl transferase-positive lymphoid cells in vitro. V. Detection of stage-specific pro-B-cell stimulating activity in medium conditioned by mouse bone marrow stromal cells.

The selective in vitro generation of rat, mouse, and human terminal deoxynucleotidyl transferase-positive (TdT+) lymphoid cells in our long-term xenogeneic bone marrow (BM) culture system is characterized by physical interaction between the developing lymphocytes and mouse BM-adherent stromal cells and macrophages. In the present study, experiments in which microporous membrane culture inserts were inoculated with rat BM cells demonstrated that although the generation of primitive B-lineage lymphoid cells requires the presence of a mouse BM feeder layer, cognitive recognition events are not necessary. Similarly, cell-free (and serum-free) medium conditioned with mouse BM (but not thymus or spleen) adherent cells and stromal-cell lines therefrom supported the proliferation of early rat lymphoid cells in a dose-dependent manner. Double immunofluorescence for incorporated bromo-deoxyuridine (BrdU) and early B-lineage markers of rat BM lymphoid cells maintained in culture inserts or conditioned medium (CM), and studies of their in vitro and in vivo developmental potentials, indicated that the lymphoproliferative response resulted from the selective stimulation of lymphoid stem and/or progenitor cells. The most primitive of these target cells had a HIS24+ HIS50- TdT- c mu- sIg-, pre-pro-B-cell phenotype. Whereas this subset normally constitutes less than 2% of B-lineage BM cells in vivo, it comprises more than 25% of total lymphoid cells in vitro. In addition, the number of TdT+ cells, predominantly of the early pro-B-cell phenotype (HIS24+ HIS50- c mu- sIg-), was increased approximately tenfold above input levels. Based on these and previous findings, a schematic model is proposed for the developmental pathway of early B-lineage cells in rat BM from the level of the committed (possibly common) lymphoid stem cell to that of the pre-B-cell.

Animals↗

A selective culture system for generating terminal deoxynucleotidyl transferase-positive lymphoid cells in vitro. III. Structure of the bone marrow microenvironment for early lymphopoiesis.

BACKGROUND: We have previously demonstrated the feasibility of generating terminal deoxynucleotidyl transferase-positive (TdT+) lymphoid precursor cells in vitro in the nonadherent compartment of a long-term xenogeneic culture system in which rat bone marrow (BM) cells are seeded onto established mouse BM adherent cell layers. We have also noted that the appearance of TdT+ cells in these cultures is preceded by the formation of clusters of lymphoblasts in close association with the mouse BM adherent cell layer. Inasmuch as the selective generation of such primitive lymphoid cells is not ordinarily observed in homogeneic (i.e., mouse: mouse, rat:rat) BM cultures, the nature of the microenvironment for the generation of committed lymphoid stem/progenitor cells has not yet been detailed. Consequently, the aim of this study was to define the cellular components in the adherent compartment of our xenogeneic culture system that are associated with the earliest stages of lymphopoiesis in vitro. EXPERIMENTAL DESIGN: The nature of the interactions between rat BM lymphoid precursor cells and mouse BM adherent microenvironmental cells was investigated by a combination of immunophenotyping and scanning and transmission electron microscopy of primary cultures. The kinetics of formation and composition of lymphoid clusters were also determined morphologically and phenotypically. Results were compared with those of other investigators who have studied lymphopoiesis in intact BM or in homogeneic cultures of pre-B cells. RESULTS: Two distinct microenvironmental regions are represented within the mouse BM adherent cell layer: (a) paucilayer (PL) regions, composed of two or three horizontally oriented layers of alkaline phosphatase-positive mouse stromal cells; and (b) multilayer (ML) regions, containing 4 to 8 layers of such stromal cells. In both regions, proliferating rat lymphoid cells, expressing the HIS24 (B220) and/or HIS50 (heat stable antigen) early B-lineage antigens, are "sandwiched" between adjacent layers of stromal cells and enveloped by cytoplasmic processes from interdigitating mouse macrophages (pseudoemperipolesis). More than 95% of the lymphoid cells are of rat origin, whereas more than 95% of the nonlymphoid cells are of mouse origin. Large clusters, containing up to 1,000 lymphoid cells, preferentially develop in the ML regions and are comprised primarily of TdT+ cells. Small clusters containing 5 to 50 lymphoid cells, preferentially develop in the PL regions and are comprised primarily of TdT- cells, that can generate TdT+ cells upon transfer onto fresh adherent cells layers. Formation of individual small clusters, which outnumber large clusters by approximately 10-fold, is initiated by as few as 25 unfractionated rat BM cells. This process is not preceded by a lag period, and is linear with respect to time and cell dose. Formation of large clusters requires approximately 30 times more input cells, and is linear with respect to time after a lag of 5 days. CONCLUSIONS: The number of small lymphoid clusters formed in vitro closely approximates the frequency of lymphoid stem/progenitor cells in the BM inoculum (3 to 5%). This suggests that, under ideal conditions, individual clusters are clonally derived and the seeding efficiency of the culture system approaches 100%. The results further suggest that large clusters are formed by the coalescence of numerous small clusters within ML regions of the adherent cell layer; and that the formation of ML regions may be supported by an underlying monolayer of macrophages. A novel aspect of this system appears to be the frequency of pseudoemperipolesis, rather than phagocytosis, of primitive lymphoid cells by macrophages, that has also been noted in vivo. Moreover, the ML regions themselves bear a close resemblance to the recently described pro-B cell-enriched, multicellular aggregate fraction of freshly harvested mouse BM. Hence, this system appears to structurally recreate in vitro the

Animals↗

Thymocytopoiesis is maintained by blood-borne precursors throughout postnatal life. A study in parabiotic mice.

This study was designed to resolve the long standing controversy as to whether hematogenous precursors or resident intrathymic precursors maintain thymocytopoiesis in postnatal life. The kinetics of thymic chimerism was examined over a 21-wk period in 105 pairs of nonirradiated, Thy-1-alloantigen-disparate, parabiotic B10.S mice. Thymic chimerism reached reached maximum levels of 25% in the Thy-1b and 16% in the Thy-1a partners (mean 20.5% and 9.8%, respectively) 6 to 7 wk after parabiotic union. Most of the donor-origin thymocytes were located in the thymus cortex and expressed high levels of Thy-1 Ag and terminal deoxynucleotidyl transferase. Thymic chimerism did not reach 50% because circulating prothymocytes, unlike peripheral T cells, do not distribute randomly in the blood of parabiotic partners. This was shown in irradiated pairs of Thy-1-alloantigen-identical parabiotic mice, one member of which was injected i.v. with Thy-1-alloantigen-disparate bone marrow cells. Only 10% of the total donor-origin prothymocyte activity was detected in the opposite parabiont 72 h later. Similarly, the level of thymic chimerism in nonirradiated, Thy-1-alloantigen-disparate parabionts closely corresponded to the donor: host ratio of prothymocytes in the blood (i.e., between 10 and 20%), as determined directly by an intrathymic adoptive transfer assay. The continued dependence of thymic chimerism on blood-borne precursors was formally demonstrated by surgically separating mice 9 wk after parabiosis. Twelve weeks later, thymic chimerism was 50 to 80% lower in the separated parabionts than in sham-operated controls. The possible role of "stress" in initiating or maintaining thymic chimerism during parabiosis appeared to be excluded by the existence of similar kinetics of thymocytopoiesis (including the onset of thymic involution) in parabiotic and nonparabiotic mice; and by the occurrence of similar levels of thymic chimerism in adrenalectomized and nonadrenalectomized parabiotic mice. Thus these experiments demonstrate that the maintenance of thymocytopoiesis in postnatal life, as in prenatal life, is primarily dependent upon blood-borne prothymocytes, and that intrathymic precursors are replaced at an average rate of 2 to 3%/day.

Adrenalectomy↗

Relative susceptibility of SJL/J and B10.S mice to experimental allergic encephalomyelitis is correlated with high and low responsiveness to myelin basic protein.

SJL/J mice are highly susceptible to actively induced experimental allergic encephalomyelitis (EAE), whereas B10.S mice are not. Yet both strains share the H-2s major histocompatibility complex (MHC) haplotype. In order to help determine the cellular basis for the disparate susceptibility to EAE, the antigen-specific in vitro proliferative responses of lymph node (LN) T cells from SJL/J and B10.S mice primed with porcine myelin basic protein (MBP) were assessed. The results indicated that SJL/J mice were high responders and B10.S mice were low responders to both porcine and murine MBP, as demonstrated by limiting dilution analyses and cloning efficiency analysis of MBP-reactive T cells. The low response of B10.S mice to MBP was not due to elevated suppressor cell activity or to a discernible defect in antigen-presenting cell activity. Rather, it appeared to be due to a paucity (or defect in function) of high affinity MBP-reactive T cells in B10.S as compared to SJL/J mice. This difference in MBP responsiveness must, by necessity, be linked to non-MHC background genes. Therefore, assuming that the relative number of MBP-reactive T cells parallels that of EAE-effector T cells in SJL/J and B10.S mice (as separate in vivo studies indicate), the present results suggest that differences in the T cell repertoire for the encephalitogenic determinants of MBP may contribute significantly to the observed differences in antigen reactivity, and may relate to differences in susceptibility to EAE.

Animals↗

Evidence that cyclosporine treatment causes the appearance in rat lymph node of T cells having the antigenic phenotypes of cortical thymocytes.

The antigenic phenotypes and relative size distributions of thymocytes and LN cells from young adult M520 strain rats, injected s.c. with cyclosporine (15 mgm/kg) for 10 consecutive days, were determined by FACS analysis and fluorescence microscopy. In addition, the prothymocyte activity in BM from these CsA-treated rats was assayed by i.v. adoptive transfer into sublethally irradiated, but non-CsA-treated, BUF strain recipients. The results showed that short-term CsA treatment causes a selective and almost complete depletion of both the CD4+8- and CD4-8+ subsets of medullary thymocytes, but that this effect is unrelated to any apparent influence of CsA on the proliferative or developmental potential of prothymocytes in the BM of the treated animals. The results also demonstrated that, early in the course of CsA treatment, there is a marked accumulation of LN T cells that display the antigenic phenotypes and size distribution of cortical thymocytes. Approximately 67% of these T cells had a CD4+8+ TdT+ Thy 1+ phenotype; 17% had a CD4-8+ TdT+ Thy 1+ phenotype. These "immature" lymph node T cells expressed the RT7 pan-T cell alloantigen, but lacked the RT6 postthymic T cell subset alloantigen. All were sIg-. In aggregate they were approximately 30% of the total CsA-LN T cells, as compared with fewer than 3% in controls.

Animals↗

Characterization of RT6-bearing rat lymphocytes. II. Developmental relationships of RT6- and RT6+ T cells.

The derivation of RT6+ T cells from postthymic RT6- T cells in weanling rats was formally demonstrated by the intravenous transfer ("parking") of highly purified populations of RT6- lymph node T cells into thymectomized, irradiated, and bone-marrow-reconstituted (TXBM) RT6 and RT7 alloantigen-disparate recipients. Parallel experiments in irradiated and bone-marrow-reconstituted rats, and in rats whose RT6+ T cells had been depleted by injection of DS4.23 anti-RT6.1 mAb, suggested that the transit time between the pre-RT6+ and the RT6+ T-cell compartments approximated 4-5 days. A more precise estimate of the transit time was made by linear regression analysis of the generation of RT6+ T cells in rats that were treated with DS4.23 mAb at timed intervals after thymectomy. This study indicated that 50% of the pre-RT6+ T cells differentiated into RT6+ cells within 4 days, 75% within 8 days, and more than 90% within 16 days. Despite the apparent absence of pre-RT6- T cells 3 weeks after thymectomy, numerous RT6- T cells persisted for at least 10 weeks in thymectomized rats, even after treatment with DS4.23 mAb. Moreover, these RT6+ T cells failed to generate RT6+ T cells after transfer into adoptive hosts. Quantitative and phenotypic analyses indicated that this population of "true" RT6- T cells: (1) constitutes approximately 50% of the total RT6- T cells normally found in control rats; (2) contains CD4+ and CD8+ subsets; (3) expresses both the CD5 pan-T-cell antigen (which is absent from NK cells) and the R73 alpha/beta TCR constant-region determinant; and (4) lacks sIgM. Hence, the present results indicate that the "true" RT6- and the RT6+ T-cell subsets have stable antigenic phenotypes and represent developmentally discrete populations of postthymic cells in normal rats. This is supported by associated phenotypic and functional studies that suggest that the "true" RT6- T-cell subset contains antigenically naive and/or autoreactive clonotypes, whereas the RT6+ T-cell subset contains memory and/or regulatory cells. It remains to be determined whether the "true" RT6- and the RT6+ subsets represent separate lineages of T cells or a single lineage at different stages of activation or maturation.

ADP Ribose Transferases↗

Rat immunoglobulin genes have comparable patterns of JH rearrangement in normal peripheral B cells and in pre-B and cultured TdT+ cells from bone marrow.

Pre-B cells from normal rat bone marrow were isolated by first rosette-depleting granulocytes, T cells and stem cells with W3/13 mAb and mature B cells with anti-Ig mAb, and then in some samples enriching by FACS-sorting HIS24+ cells. Presumptive precursors of these pre-B cells possessing terminal deoxy-nucleotidyl transferase were prepared by culture of normal marrow. The extent of rearrangement of kappa and heavy chain genes was estimated on both these types of cells and on mature peripheral B cells by measuring the disappearance of the germ-line restriction fragments encoding J segments (other than JH1) relative to a non-rearranging CK fragment. Pre-B cells and B cells showed similar degrees of rearrangement of their kappa genes, leaving roughly half in germ-line form; the TdT+-enriched cells showed approximately similar heavy chain rearrangement as the peripheral B cells. Some non-germ-line restriction fragments hybridising with JH in sufficient amount to register as discrete bands on Southern blots were found in common between these different cell populations taken from different individual donors. These may represent preferred D-JH or perhaps V-D-JH rearrangement arising repetitively in independent clones, or may be due to dominance by a few preferred clones.

Animals↗

Characterization of RT6 bearing rat lymphocytes. I. Ontogeny of the RT6+ subset.

The RT6 alloantigen is present on approximately 70% of peripheral T cells in the rat, but is absent from thymocytes and bone marrow lymphocytes. The results of further phenotypic analysis in the present study demonstrated that the RT6 alloantigen is expressed on approximately 45% of the helper/inducer (CD4; W3/25+) and 80% of the cytotoxic/suppressor (CD8; OX8+) peripheral T-cell subsets. Ontogenetic and thymus ablation studies indicated that the RT6+ T-cell subset is thymus-dependent and normally develops after the appearance of RT6-T cells in neonatal rats, and that the expression of RT6 is a post-thymic maturational event. Furthermore, intrathymic adoptive transfer of bone marrow cells demonstrated that RT6+ T cells are thymus-derived cells. These results show that most if not all RT6+ T cells are the progeny of RT6- T cells. However, they do not exclude the possibility that a separate lineage of RT6- T cells exists, which also has OX8+ and W3/25+ subsets. The possible developmental and functional relationships of RT6- and RT6+ T cells in the rat are discussed.

Aging↗

Defective lymphopoiesis in the bone marrow of motheaten (me/me) and viable motheaten (mev/mev) mutant mice. III. Normal mouse bone marrow cells enable mev/mev prothymocytes to generate thymocytes after intravenous transfer.

Bone marrow prothymocytes from me/me and mev/mev mutant mice fail to generate thymocytes in irradiated (600 rad) +/+ wild-type recipients after intravenous injection. However, these same prothymocytes readily generate thymocytes after intrathymic injection. The results of the present study demonstrate that this apparent defect in the thymus-homing capacity of mev/mev prothymocytes can be corrected by mixing irradiated wild-type bone marrow cells with mev/mev bone marrow cells before intravenous injection. However, this defect is not corrected by passage of mev/mev bone marrow cells through the bone marrow of irradiated wild-type recipients. One interpretation of these results is that the maturation of prothymocytes is reversibly arrested in mev/mev mice by a defect in the radiosensitive compartment of the bone marrow microenvironment.

Animals↗

Defective lymphopoiesis in the bone marrow of motheaten (me/me) and viable motheaten (mev/mev) mutant mice. II. Description of a microenvironmental defect for the generation of terminal deoxynucleotidyltransferase-positive bone marrow cells in vitro.

We have presented evidence in a previous paper that the development of prothymocytes, pre-B cells, and TdT+ lymphoid precursor cells in the bone marrow of motheaten (me/me) and viable motheaten (mev/mev) mice is defective. In the present study, we have used a selective culture system that supports the generation of rat- and mouse-origin TdT+ bone marrow lymphoid cells in vitro to further investigate the early stages of lymphopoiesis in me/me and mev/mev mice. The results demonstrate that bone marrow stromal cell feeder layers derived from me/me and mev/mev mice do not support the growth of rat TdT+ cells in vitro, whereas stromal cell feeder layers from heterozygous (+/-) littermates and wild type (+/+) control mice do. Moreover, composite feeder layers formed by mixing as few as one part me/me and mev/mev bone marrow cells with 7 to 9 parts +/- littermate bone marrow cells also fail to effectively support the generation of TdT+ cells in vitro. In contrast to me/me and mev/mev mice, other mutant mouse models of autoimmune (NZB, NZB/W), immunodeficient (nu/nu), and hemopoietic (W/Wv, Sl/Sld) disorders form feeder layers that support normal to elevated levels of TdT+ cell growth in vitro. Thus, to date, only the me/me and mev/mev mutant mice have been found to lack the appropriate microenvironment for the generation of TdT+ bone marrow cells. Histologic analysis of the stromal cell feeder layers that are formed in our culture system shows that multilayered cellular patches, which normally are the most active sites of TdT+ cell development in vitro, are absent in feeder layers of me/me and mev/mev cells. Moreover, feeder layers from mev/mev mice contain a population of MAC 1+, basophilic, nonvacuolated, macrophage-like cells; whereas feeder layers from control mice contain MAC 1+, eosinophilic, vacuolated macrophage-like cells. Stromal cell feeder layers formed by mixtures of me/me or mev/mev and control mouse bone marrow cells contain numerous multilayered cellular patches and vacuolated mononuclear cells, but also contain large numbers of basophilic mononuclear cells. These composite feeder layers have a disproportionately reduced capacity to support the generation of TdT+ cells in vitro. Although the stromal microenvironment of me/me and mev/mev bone marrow does not support the growth of TdT+ cells in vivo or in vitro, the bone marrow from these mutant mice contains detectable numbers of pre-TdT+ cells. Thus, when cultured on normal mouse feeder layers, mutant mouse bone marrow rapidly generates TdT+ cells in vitro, albeit at significantly reduced levels as compared to +/- littermate controls.(ABSTRACT TRUNCATED AT 400 WORDS)

Acid Phosphatase↗

Monoclonal antibodies to RT7 and LCA antigens in the rat: cell distribution and segregation analysis.

Fluorescein-conjugated monoclonal antibodies (mAb) have been used to examine the cellular distribution and genetic relationship of the RT7 and the leukocyte common antigen (L-CA) in the rat. We demonstrate here that the RT7.1 alloantigen, recognized by the mAb BC84, is present on B lymphocytes as well as T lymphocytes, although at markedly different apparent concentrations; T cells binding approximately 4 times more BC84 than do B cells. In contrast, the polymorphic L-CA recognized by the NDS58 mAb and the non-polymorphic L-CA recognized by the OX1 mAb appear to be expressed in equal concentrations on T and B cells and differ in their tissue distribution from the RT7.1 alloantigen. We have also tested a new mAb termed 8G6.1, that is reactive with RT7b rat strains and has a cell, tissue and strain distribution profile resembling that of a polymorphic L-CA. Segregation analysis of the RT7 and polymorphic L-CA antigenic systems using a single backcross model demonstrate that the alloantigens recognized by BC84 and NDS58 cosegregate and that both are allelic with respect to 8G6.1. The L-CA antigenic determinant defined by OX1 was non-polymorphic and thus was not allelic with any of the antigenic systems tested. These results suggest that there is a close genetic relationship between the expression of RT7 and L-CA in the rat.

Alleles↗

Defective lymphopoiesis in bone marrow of motheaten (me/me) and viable motheaten (mev/mev) mutant mice. I. Analysis of development of prothymocytes, early B lineage cells, and terminal deoxynucleotidyl transferase-positive cells.

This study identifies defects in the early stages of lymphopoiesis that may contribute to the abnormalities in the development and/or function of peripheral T and B lymphocytes in mice homozygous for the motheaten (me/me) and viable motheaten (mev/mev) mutations. The results indicate that in me/me and mev/mev mice prothymocytes in bone marrow are present in essentially normal numbers, as determined by intrathymic injection, but apparently lack the ability to home effectively to the thymus, as determined by intravenous transfer; early B lineage cells in bone marrow, identified by the B220 antigen, are markedly depleted, including immature B cells (sIg+), pre-B cells (cIg+, sIg-), and pro-B cells (B220+, cIg-, sIg-); TdT+ bone marrow cells, especially a subset that expresses the B220 B lineage antigen, are markedly depleted by two weeks of age; normal numbers of TdT+ thymocytes are present during the first 3 wk of postnatal life, but rapidly decrease thereafter. The results further indicate that neither the defective thymus homing capacity of prothymocytes nor the deficiency of TdT+ bone marrow cells is due to autoantibodies. The possible relationship of the defective development of lymphoid precursor cells to the premature onset of thymic involution and to the abnormalities of peripheral T and B lymphocytes in me/me and mev/mev mice is discussed; as are the results of in vitro studies (presented in a companion paper), which suggest that a primary defect in the stromal microenvironment of the bone marrow is responsible for the abnormal development of the lymphoid precursor cells.

Animals↗

T cell lines derived from the spinal cords of mice with experimental allergic encephalomyelitis are self reactive.

Experimental allergic encephalomyelitis (EAE) is an animal model of T cell-mediated, central nervous system neuropathology that may be a relevant animal model for multiple sclerosis. EAE is usually induced by sensitization of animals with a xenogeneic myelin basic protein (MBP). Recently, MBP-reactive T cell lines and clones derived from lymphoid tissue of animals with EAE have proved very useful in elucidating certain aspects of the pathogenesis in EAE. However, questions relating to how T cells actually mediate the pathologic changes seen in EAE remain unresolved. We now report for the first time the derivation of long-term, interleukin 2-dependent T cell lines and sublines from a site of pathology in murine EAE--the spinal cord. All of the spinal cord-derived T cell lines and sublines were found to be "autoreactive" in that they responded to self (murine) MBP as well as to the xenogeneic immunogen, porcine MBP. The ability to derive T cell lines and sublines from the spinal cords of mice with EAE should now aid in the elucidation of pathogenetic mechanisms in EAE by allowing for a characterization of those T cells found at the site of pathology.

Animals↗

Production and characterization of a monoclonal antibody (A1-3) that binds selectively to activated monocytes and inhibits monocyte procoagulant activity.

We describe the generation and characterization of a new monoclonal antibody, A1-3, which possesses two unique properties. First, A1-3 binds selectively to stimulated human monocytes. Secondly, A1-3 inhibits the procoagulant activity expressed by stimulated monocytes and by human brain tissue factor. Unstimulated human peripheral blood cells (granulocytes, lymphocytes, monocytes, red blood cells, and platelets), prepared in the absence of detectable endotoxin, express no procoagulant activity and fail to bind A1-3. Stimulation of peripheral blood monocytes. alveolar macrophages, or the monocyte-like cell line U937, however, results in the expression of procoagulant activity and the binding of A1-3. The surface antigen recognized by A1-3 was recovered from endotoxin-stimulated human monocyte vesicles by immune precipitation and demonstrated an apparent m.w. of approximately 52,000. It is proposed that the monoclonal antibody A1-3 detects a differentiation antigen on human monocytes that is expressed in response to stimuli for monocyte activation.

Animals↗