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At least 19 recordsLinked to original sources
PubMed1998

FTY720, a novel immunosuppressant, induces sequestration of circulating mature lymphocytes by acceleration of lymphocyte homing in rats. I. FTY720 selectively decreases the number of circulating mature lymphocytes by acceleration of lymphocyte homing.

FTY720, given i.v. or orally at 0.03 mg/kg or more, significantly prolonged skin allograft survival in a dose-dependent manner and showed more potent immunosuppressive activity than cyclosporin A (CsA) or tacrolimus (FK506) in MHC-incompatible rat strains of WKAH donors and F344 recipients. However, unlike CsA or FK506, FTY720 up to 1000 nM did not affect IL-2 production in allogeneic MLC. Within 3 to 24 h after a single oral administration of FTY720 at 0.1 to 1 mg/kg, the number of lymphocytes in the rats was markedly decreased in the peripheral blood and thoracic duct lymph and partially in spleen. By contrast, the number of lymphocytes in peripheral lymph nodes (PLN), mesenteric lymph nodes (MLN), and Peyer's patches (PP) was significantly increased at the same time. Intravenous transfusion of calcein-labeled rat lymphocytes into rats revealed that FTY720 significantly accelerated lymphocyte homing to PLN, MLN, and PP, dose dependently. Since FTY720-induced lymphocyte homing was completely blocked by simultaneous treatment of the calcein-labeled lymphocytes with mAbs against CD62L, CD49d, and CD11a before the transfusion, the acceleration of lymphocyte homing by FTY720 appears to be mediated by lymphocyte-homing receptors. These findings indicate that FTY720 sequesters circulating mature lymphocytes into PLN, MLN, and PP by acceleration of lymphocyte homing and thereby decreases the number of lymphocytes in peripheral blood, thoracic duct lymph, and spleen. Based on these observations, sequestration of circulating mature-lymphocytes is presumed to be a main mechanism of the immunosuppressive activity of FTY720.

Animals↗
PubMed2004

Enterocolic lymphocytic phlebitis with lymphocytic colitis, lymphocytic appendicitis, and lymphocytic enteritis.

We describe a 53-year-old man with a history of diarrhea temporally related to the use of flutamide. He developed an acute abdomen, and presented with an ileocecal intussusception due to an edematous ischemic cecum. The ischemia was due to enterocolic lymphocytic phlebitis (ELP), with numerous associated thrombi. The phlebitis involved not only the ischemic area but also the grossly unaffected areas, including the entire right colon, terminal ileum, and appendix. All layers of the bowel wall were involved. Mesenteric veins were also prominently affected, but the arteries were spared. This rare form of vasculitis was associated with a marked lymphocytic infiltrate involving the epithelium of the entire right colon, ileum, and appendix. This is the first reported case of ELP occurring in conjunction with lymphocytic colitis, lymphocytic enteritis, and lymphocytic appendicitis. The temporal association of the patient's symptoms with flutamide use suggests that this peculiar form of lymphocytic inflammation of the veins and mucosa likely represents a drug reaction. We suggest that some cases of lymphocytic colitis may also be associated with ELP but are unlikely to be recognized unless affected submucosal vessels happen to be included in the biopsy.

Appendicitis↗
PubMedDate not supplied

Neonatal lymphocytes dominate against lymphocytes of their own mother but not against allogenic maternal or adult lymphocytes in bidirectional mixed lymphocyte cultures.

OBJECTIVE: Recent studies have shown a regular prenatal transfer of maternal immunocompetent cells into the fetal circulation. However, these cells engraft and proliferate only in a few exceptional cases if the fetus reaches an immunocompetent state. Thus the fetus has to have an immunologic defense mechanism against the engraftment of maternal cells. In the current study we investigated whether the fetus has such an immune defense and whether this defense mechanism specifically attacks cells of the mother. PATIENTS, MATERIAL AND METHODS: Blood samples were obtained from 15 mothers and 15 newborns directly after delivery. We compared individual vitality and spontaneous cytotoxicity between fetal and maternal lymphocytes in a cell ratio of 1:1 in nonstimulated bidirectional mixed lymphocyte cultures (MLC). The distribution of each cell population within the MLC was visualized by fluorescence in situ hybridization and X/Y-DNA probes. This was compared to MLCs between unrelated fetal and maternal as well as between unrelated adult lymphocytes. RESULTS: After 72 h, a significant cell shift was observed only in the MLC with neonatal lymphocytes mixed with cells of their own mother; there was a significantly higher number of neonatal cells (0.71 vs. 0.29) present. All other groups continued to have a cell distribution of 1:1. CONCLUSION: Our results show that neonatal lymphocytes specifically dominate against maternal but not allogenous maternal or adult lymphocytes in nonstimulated bidirectional MLCs.

Adult↗
PubMed1982

Effect of cyclosporin A on human lymphocyte responses in vitro. III. CsA inhibits the production of T lymphocyte growth factors in secondary mixed lymphocyte responses but does not inhibit the response of primed lymphocytes to TCGF.

The mechanism whereby Cyclosporin A (CsA) inhibits secondary mixed lymphocyte responses was assessed. CsA added to secondary MLR cultures inhibited proliferation and induction of cytolytic lymphocyte activity. This inhibition was found to be associated with the inhibition of T lymphocyte stimulating growth factor(s) (TCGF) production in the supernatants of secondary MLR cultures. As little as 1.0 micrograms/ml of CsA added to secondary MLR cultures resulted in no measurable TCGF activity. In contrast, moderate doses of CsA (1.0, 2.5 micrograms/ml), which completely inhibited the secondary MLR response to alloantigen, did not inhibit the proliferative and CML response of alloantigen-primed lymphocytes to these stimulating growth factors. Even at high doses of CsA (20 micrograms/ml), substantial levels of proliferation (50% of control response) and CML induction (60% of control response) were observed when the primed cells were exposed to secondary MLR supernatants containing TCGF activity. It was concluded that inhibition of secondary mixed lymphocyte responses by CsA may be due in part to the inhibition of TCGF production rather than the inhibition of the effect of TCGF on mature cytotoxic T lymphocytes.

Cyclosporins↗
PubMed1984

T-lymphocyte and B-lymphocyte dichotomy in anuran amphibians: III. Assessment and identification of inducible killer T-lymphocytes (IKTL) and spontaneous killer T-lymphocytes (SKTL).

We have established the existence of alloreactive inducible killer (IK) T-lymphocytes in Rana pipiens by injecting immunogenic concentrations of allogeneic frog erythrocytes (RBC). Assessment of specific IK activity was determined microscopically, observing effector-target conjugate formation, and spectrophotometrically as released hemoglobin (Hb) from lysed targets (RBC). The presence of spontaneous killer (SK) T-lymphocyte activity was also determined using unimmunized frogs and similar assay conditions. Assays using rabbit anti-frog Thy-1.1 antiserum inhibition, but not E-rosetted T-lymphocyte depletion, confirmed the T-lymphocyte category of both effector cell populations in Rana pipiens. For IK activity, we determined the 1) best priming doses, 2) best effector cell source (peripheral blood), 3) best priming route (intraperitoneal), 4) kinetics of immunity development, and 5) kinetics of lysis. Kinetics of lysis and organ distribution for spontaneous killer cells were also determined. Our results may assist 1) in establishing the evolutionary origin of cytotoxic T-lymphocytes (CTL) and natural killer (NK) cells, and 2) in predicting where the capacity of immuno-surveillance against modified-self appeared in phylogeny. The implications are important for understanding origins of mechanisms of resistance against neoplastic conditions.

Animals↗
PubMed1976

Recruitment of effector lymphocytes by initiator lymphocytes. Recruited lymphocytes are immunospecific and include graft-versus-host-reactive lymphocytes.

We have shown previously that initiator T lymphocytes (ITL), sensitized in vitro against fibroblast antigens, recruit effector T cells in vivo. After injection into hind footpads of syngeneic recipients, sensitized ITL migrated to the draining popliteal lymph nodes (PLN) and activated a trapping mechanism by which circulating lymphocytes were recruited in the PLN. This paper reports experiments designed to test the immunospecificity of these recruited T lymphocytes (RTL). We found that immunospecific RTL were depleted from other lymphoid organs during recruitment in the PLN. However, immunospecific ITL were not depleted from spleens during PLN recruitment. Thus ITL and RTL are functionally distinguishable. We show that specific GVH reactive lymphocytes were also lost from spleens and distal lymph nodes during trapping of RTL in the PLN. Thus, the trapping phase of the recruitment response is immunospecific, as are the sensitization and effector phases. The trapped RTL are antigen-specific, and include the pool of GVH-reactive-lymphocytes committed to the same alloantigen. Thus, it appears that GVH-reactive cells respond to syngeneic ITL sensitized against allogeneic fibroblasts.

Animals↗
PubMed1992

[Immunologic phenotype of lymphocytes in chronic B-cell lymphocytic leukemia. II. Studies of immunologic phenotype of peripheral blood and lymph node lymphocytes in patients with chronic lymphocytic leukemia or leukemic forms of lymphoplasmacytoid lymphoma].

UNLABELLED: In a group of 16 patients with chronic lymphocytic leukaemia and leukaemic forms of the lymphoma lymphoplasmocytoides immunophenotypes of peripheral blood and lymph node lymphocytes were studied. CONCLUSIONS: 1) immunophenotype heterogeneity observed in a minority of patients in lymph-nodes or peripheral blood seems to be connected with the co-existence of leukaemic and normal reactive B-cells, 2) SIgG+ cells seem to represent activated B lymphocytes producing and secreting autoantibodies, 3) circulating peripheral T lymphocytes do not reflect the distribution of T cell subpopulations in lymph-nodes.

Adult↗
PubMed1992

[Immunologic phenotype of lymphocytes in chronic B-cell lymphocytic leukemia. I. B- and T-lymphocytes in chronic lymphocytic leukemia].

This article contains the review and the critical discussion of studies of T and B lymphocytes in chronic B-cell lymphocytic leukaemia. It is not explicitly known now, which stage of differentiation of lympho-haemopoietic cells undergoes malignant transformation in CLL-B. Basing on VDJ recombination activity it is supposed that some cases derive from the stem cell, others--from B lineage cells.

Antigens, CD↗
PubMed1977

Distinctive functional properties of human blood L lymphocytes: a comparison with T lymphocytes, B lymphocytes, and monocytes.

Human blood lymphocytes with high affinity Fc receptors have been operationally named L lymphocytes because of membrane-labile IgG markers. L lymphocytes lack membrane-incorporated immunoglobulin and do not form rosettes with sheep red blood cells coated with IgM antibody and mouse complement. These lymphocytes are capable of binding IgG in normal human serum at 4 degrees C and will form rosettes with human lymphocytes coated with Ripley IgG. In this study, functional in vitro properties of isolated L lymphocytes were compared with T lymphocytes, B lymphocytes, and monocytes. To obtain these mononuclear populations, first, plastic adherent monocytes were harvested. T lymphocytes were then isolated by centrifugation of E rosette-forming cells, and other rosetting techniques were employed to isolate L and B lymphocytes by negative selection. The functional properties of L lumphocytes were completely unlike those of T cells, B cells, or monocytes. L lymphocytes did not proliferate in response to mitogens, soluble antigens, or cell surface antigens. Moreover, this population could not replace monocytes in helping T lymphocytes respond to concanavalin A and pokeweed mitogen. Once T cells were supplemented with monocytes, however, the addition of L lymphocytes to the culture greatly enhanced the T lymphocytes proliferative response to phytohemagglutinin, concanavalinA, purified protein derivative (PPD), and streptokinase/streptodornase. L lymphocytes were not a subset of B cells. They did not spontaneously develop surface Ig in culture, and pokeweek mitogen could not induce them to transform and generate cytoplasmic Ig detectable by immunofluorescence. Mixtures of B cells and T cells responded to pokeweed mitogen better than do T cells alone. In contrast, enhanced reactivity with L and T cell combinations was not observed. Another sharp difference between these two populations was the stimulator capacity of each in mixed lymphocyte culture. When B and L lymphocytes were carefully monocyte-depleted, only B cells were effective stimulators of autologous and allogeneic lymphocytes. In comparison with T cells, B cells, and monocytes, L lymphocytes were the only effective killers of human blood lymphocytes sensitized with IgG. L lymphocytes, then, have cytotoxic potential, but cannot proliferate in response to various stimulants or become antibody-producing cells. These findings suggest that L lymphocytes comprise a third lymphocyte population.

Antigen-Antibody Reactions↗
PubMed1994

Cytotoxic T-lymphocytes that kill autologous CD4+ lymphocytes are associated with CD4+ lymphocyte depletion in HIV-1 infection.

Human immunodeficiency virus type 1 (HIV-1)-infected individuals, but not HIV-seronegative controls, have non-HLA-restricted T-cell receptor alpha beta+ CD8+ cytotoxic T-lymphocytes (CTL) that kill activated uninfected CD4+ lymphocytes. In vitro stimulation of peripheral blood mononuclear cells from HIV-1-infected individuals with concanavalin A (Con A) or by coculture with phytohemagglutinin-activated autologous lymphoblasts induced CTL that killed autologous and heterologous CD4+ lymphocytes, but not Con A-activated CD8+ lymphocytes or Epstein-Barr virus (EBV)-transformed B lymphocytes. EBV did not stimulate such CTL in two subjects tested, although stimulation with Con A or autologous lymphoblasts induced CTL activity against CD4+ lymphocytes in both subjects. CTL activity against autologous CD4+ lymphocytes varied over time; killing of heterologous CD4+ lymphocytes was often higher than that of autologous CD4+ lymphocytes. HIV-infected individuals with Con A-inducible CTL against autologous CD4+ lymphocytes lost more CD4+ lymphocytes within 6 months of testing than HIV-infected individuals with no such CTL (p < .01). The mean (+/- SD) decrease in CD4+ lymphocyte counts in a group of HIV-infected individuals with CTL activity against autologous CD4+ lymphocytes was 121 +/- 84, or 36%, of total CD4+ lymphocytes over 6 months. In contrast, there was no significant change in mean CD4+ lymphocyte count over 6 months in a group of HIV-infected individuals without CTL activity against autologous CD4+ lymphocytes. In some HIV-infected individuals, CTL activity against autologous CD4+ lymphocytes fell coincident with a drop in CD4+ lymphocyte number in vivo.(ABSTRACT TRUNCATED AT 250 WORDS)

CD4-Positive T-Lymphocytes↗
PubMed1989

The role of dendritic cells as stimulators of minor lymphocyte-stimulating locus-specific T cell responses in the mouse. I. Differential capacity of dendritic cells to stimulate minor lymphocyte-stimulating locus-reactive T cell hybridomas and the primary anti-minor lymphocyte-stimulating locus mixed lymphocyte reaction.

The response of T cells to minor lymphocyte-stimulating locus (Mls) determinants remains poorly understood with respect to the antigenic determinants responsible for T cell stimulation and the types of APC capable of stimulating the response. In this report, we demonstrate that highly purified dendritic cells (DC) as well as B cells have the capacity to stimulate Mls-specific responses. Unseparated spleen cells, purified DC, resting B cells, and activated B cells were compared for their capacity to stimulate several Mls-reactive T cell hybridomas. Whereas the entire panel of Mls-reactive T cell hybridomas was stimulated strongly by unseparated spleen cells and activated B cells, the hybridomas responded only weakly to purified DC or resting B cells. Activation of resting B cells with either B cell stimulatory factor-1 (1 day pre-treatment) or LPS/dextran (2 or 3 day pre-treatment) greatly augmented their Mls-stimulatory capacity. In contrast, the Mls-stimulatory capacity of DC was not augmented by a 1-day pre-treatment with either B cell stimulatory factor-1 or supernatant from the DC-induced primary anti-Mls-MLR. In the primary anti-Mls-MLR, both purified DC and LPS/dextran-stimulated B blasts were found to elicit vigorous T cell proliferative responses. Much weaker responses were elicited by unseparated spleen cells. The stimulation of the primary anti-Mls-MLR by purified DC was further confirmed by producing Mls-specific T cell clones which were preferentially stimulated by DC. Autologous (Mlsb) DC were found to markedly enhance the primary anti-Mls-MLR response to small numbers of Mlsa B blasts. Thus, DC possess other "accessory cell" properties that augment the primary anti-Mls-MLR despite the predicted low level of Mls determinant expression on DC based on the results obtained with Mls-reactive hybridomas. Possible accessory cell properties of DC relevant to this phenomenon are discussed.

Animals↗
PubMed1975

Separation of T lymphocytes from normal individuals and patients with B lymphocyte chronic lymphocytic leukaemia.

Previous studies have shown that lymphocytes from patients with chronic lymphocytic leukaemia have a diminished response to mitogens which stimulate T cells. Chronic lymphocytic leukaemia is most often a disease of accumulating B cells so that T lymphocytes are diluted by large numbers of leukaemic cells. Direct comparison with the responses of normal lymphocytes to mitogenic stimulation is therefore suspect. To circumvent this difficulty, a method of isolating T cells from normal individuals and patients with chronic lymphocytic leukaemia was developed. Lymphocytes containing an average of 16.1 per cent B cells from normal individuals were applied to IgG-anti-IgG-coated Degalan bead columns and held at 4 degrees for 2 hours. The eluted cells contained less than 2 per cent B cells. When chronic lymphocytic leukaemic lymphocytes, containing an average of 68.6 per cent B cells, were applied to IgG-anti-IgG columns, the eluted cells contained 36.4 per cent B cells. To improve the purification of T lymphocytes, columns of uncoated Degalan beads were used to remove non-specifically adherent cells. Eluted lymphocytes were then applied to IgG-anti-IgG columns. This resulted in the recovery of purified populations of T cells with less than 2 per cent contamination with B cells. Patients with chronic lymphocytic leukaemia were found to have lymphocytes with either a normal density or a low density of surface immunoglobulins. B cells were successfully removed from lymphocyte suspensions in all cases of chronic lymphocytic leukaemia with a normal density of lymphocyte surface immunoglobulins. In the three cases of chronic lymphocytic leukaemia with low density surface immunoglobulins, separation by this method was unsuccessful. However, an enriched T-cell population was obtained when leukaemic lymphocytes which had lost all detectable surface immunoglobulins were passed through a column coated with heat-aggregated IgG.

Animals↗
PubMed1976

Lymphocyte transformation induced by autologous cells. IV. Human T-lymphocyte proliferation induced by autologous or allogeneic non-T lymphocytes.

An autologous mixed lymphocyte reaction was demonstrated between T and non-T lymphocytes. Sheep erythrocyte rosetting was used to separate human lymphocytes into T and non-T lymphoid preparations. Non-T lymphocytes stimulated the proliferation of autologous T lymphocytes. The cell in this preparation that was most stimulatory had the characteristics of a K lymphocyte. The allogeneic mixed lymphocyte reaction was also shown to reflect the proliferation of T lymphocytes stimulated by allogeneic non-T lymphocytes. Proliferation of T lymphocytes in the allogeneic mixed lymphocyte culture probably reflects a response to both foreign histocompatibility determinants and determinants present on non-T lymphocytes. It is suggested that the proliferative response of T lymphocytes to autologous non-T lymphocytes may be a step in the process by which T lymphocytes regulate immunity.

Blood↗
PubMed1984

T lymphocyte-dependent B lymphocyte proliferative response to antigen. II. Induction of polyclonal B lymphocyte activation of normal B cells and of Lyb-5- B cells from xid mice via recognition of self-IA antigens.

We extended our investigations into the genetic requirements and antigen dependence for the induction of polyclonal B lymphocyte proliferation by primed T lymphocytes. By using recombinant inbred mouse strains and antigen-specific T lymphocyte clones that lack alloreactivity, the genetic requirement was mapped to the IA subregion of the MHC. Furthermore, approaches that prevented or limited the accessibility of antigens to the B lymphocyte surface demonstrated that antigen binding onto the B lymphocyte surface was probably not necessary for induction of B lymphocyte proliferation. These experiments suggest strongly that T lymphocyte recognition of B lymphocyte Ia molecules in the absence of sIg cross-linking or in the absence of antigen bound nonspecifically to B lymphocytes can cause cellular activation. Similar T lymphocyte-dependent B lymphocyte activation was seen when Lyb-5- cells from CBA/N mice with the xid defect were cultured. Increases in the number of cells secreting immunoglobulins could be detected in the proliferating B lymphocyte cultures, suggesting that the culture conditions had fulfilled the requirements for B lymphocyte differentiation into antibody-producing cells. Although anti-Ig did not interfere with the B lymphocyte proliferative responses, it did diminish the number of cells secreting immunoglobulins. The implications of these experiments in extending our understanding of the activation pathway of Lyb-5- and Lyb-5+ B lymphocytes are discussed.

Animals↗
PubMed1992

Antigen presentation by B lymphocytes to CD4+ T lymphocytes in vivo: importance for B lymphocyte and T lymphocyte activation.

B lymphocytes, like macrophages and dendritic cells, can present antigen to CD4+ T cells. Antigen presentation by B cells is essential for the generation of an in vivo T cell dependent antibody response, and repeated antigen presentation by B cells to T cells is necessary to induce B cell clonal expansion. Presentation of antigen by resting B cells to unprimed T cells tolerizes T cells, while anti-IgD antibody activates B cells and allows B cell antigen presentation that productively activates T cells. However, activation is not all that is required for B cells to productively present antigen to T cells.

Animals↗
PubMed1985

Plasminogen-dependent fibrinolytic activity in normal human lymphocytes: diminished lymphocyte plasminogen activator in chronic lymphocytic leukemia.

Discrepancies in correlations between fibrinolytic activity and metastatic potential of malignant cells has resulted in speculation on the putative role of plasminogen activators (PA) in cancer. In this report we have compared lymphocyte PA from 40 patients with chronic lymphocytic leukemia (CLL) to normal human B- and T-lymphocytes. Lymphocytes were isolated from peripheral blood by Ficoll-Hypaque centrifugation. The B- and T-cells were further separated on nylon wool columns. Cell PA activity and cell membrane PA were determined using 3H-fibrin-coated plates with added human plasminogen. Lymphocytes did not lyse 3H-fibrin in the absence of plasminogen. Plasminogen-dependent fibrinolytic activities of normal B- and T-lymphocytes were comparable. The addition of protease inhibitors with trypsin or plasmin specificity to lymphocytes significantly inhibited normal PA, thus substantiating the serine protease spectrum of lymphocyte PA. Examination of lymphocytes from greater than 95% of patients with chronic lymphocytic leukemia revealed a marked decrease in lymphocyte and cell membrane PA as compared to normals. No correlation between Stage of CLL and lymphocyte PA was observed. Likewise, an inhibitor of PA in CLL lymphocytes was not detected. The function of PA in normal B-lymphocyte physiology and the potential pathogenetic role of diminished PA in CLL lymphocytes remain to be explored.

Fibrinolysis↗
PubMed1988

The role of lymphocyte function-associated antigen 1 (LFA-1) in the adherence of T lymphocytes to B lymphocytes.

The functional role of the LFA-1 molecule in the interaction between helper T lymphocytes and B lymphocytes was investigated using lymphocytes from patients with leukocyte adhesion deficiency, an inherited immunodeficiency characterized by a defective leukocyte expression of the LFA-1, Mac-1 (CR3) and p150,95 molecules. The ability of LFA-1- T lymphocytes to provide antigen-specific help for HLA-identical LFA-1+ B lymphocytes was reduced while their antigen-specific activation was normal. Antigen-independent conjugate formation between resting, nonactivated LFA-1- T lymphocytes and LFA-1+ B lymphocytes was impaired while LFA-1- B lymphocytes bound LFA-1+ T lymphocytes normally. Conjugate formation of activated LFA-1- T lymphocytes was mostly mediated by the CD2-LFA-3 adhesion pathway while the ICAM-1 molecule, a ligand of LFA-1, had no function. These results demonstrate that LFA-1 plays a major role in the cognate interaction between helper T lymphocytes and B lymphocytes that cannot be mediated instead by CD2 or other molecules on resting T lymphocytes.

Antibodies, Viral↗
PubMed1983

Regulation of lymphocyte production in the bone marrow. I. Turnover of small lymphocytes in mice depleted of B lymphocytes by treatment with anti-IgM antibodies.

To examine the concept that the genesis of lymphocytes in the bone marrow may be regulated by homeostatic feedback signals from peripheral B lymphocytes or their products, lymphocyte production was measured in mice selectively depleted of B lymphocytes by repeated administration of anti-IgM antibodies from birth. The turnover of small lymphocytes was quantitated radioautographically after DNA labeling by continuous infusion of 3H-thymidine. In the femoral marrow of anti-IgM-treated mice, the number of small lymphocytes was reduced and their turnover time was shorter than in control mice, presumably reflecting the premature elimination from the marrow of maturing cells about to express surface IgM. The absolute number of small lymphocytes being produced per femur in unit time, however, was identical in anti-IgM-treated and control mice. Lymphocyte production in the thymus was also unaffected by anti-IgM suppression whereas in the spleen the turnover of small lymphocytes was reduced due to the lack of young immigrant B lymphocytes from the bone marrow. The results demonstrate that the normal large-scale production of lymphocytes in mouse bone marrow is independent of the magnitude of the peripheral pool of B lymphocytes or the level of circulating immunoglobulins, suggesting the process is not subject to feedback control. Some implications for the genesis and diversity of primary B lymphocytes are discussed.

Animals↗