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Results for “Lymphocytes”

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PubMed1991

Lymphocyte subset-specific and tissue-specific lymphocyte-endothelial cell recognition mechanisms independently direct the recirculation of lymphocytes from blood to lymph in sheep.

Tissue-specific and lymphocyte subset-specific lymphocyte recirculation patterns have been analysed simultaneously. Lymphocytes obtained from one lymph compartment were directly labelled with fluorochrome in vitro and returned to the blood of the same animal. Over the next 48-72 h, the recirculation of these cells into both the same lymph compartment and at least one different lymph compartment was monitored. The cells in all of these lymph collections, as well as an aliquot of the cells used for direct fluorescent labelling, were then phenotyped with monoclonal antibodies (mAb) which define the mutually exclusive small CD4+ and CD8+ T-lymphocyte subsets in sheep. All cell samples were analysed by flow cytometry and CD4/CD8 ratios were determined for the recirculated, fluorochrome-labelled population in each lymph collection. The mean CD4/CD8 ratio calculated for each lymph compartment was then compared with the CD4/CD8 ratio calculated for each lymph compartment was then compared with the CD4/CD8 ratio of the transfused, starting population. In one experiment employing efferent prescapular lymph cells, three experiments employing efferent intestinal lymph cells, and two experiments employing afferent intestinal lymph cells, tissue-specific recirculation was observed. In all of these experiments, the pattern of recirculation of small CD4+ and CD8+ T lymphocytes was non-random. Moreover, in each experiment, this non-randomness was completely unrelated to tissue-specific phenomena, since the mean CD4/CD8 ratio of the recirculated population was higher than the CD4/CD8 ratio of the transfused, starting population regardless of the lymph compartment examined. These data are therefore consistent with the hypothesis that tissue-specific and lymphocyte subset-specific lymphocyte-endothelial cell recognition mechanisms independently direct the recirculation of small lymphocytes from blood to lymph.

Animals↗

PubMed1978

The effect of sera from chronic lymphocytic leukemia patients on normal mitogen-stimulated lymphocytes. A possible correlation with the patients' T and B lymphocytes.

Serum from chronic lymphocytic leukemia (CLL) patients was examined for its effect on normal lymphocytes stimulated by phytohemagglutinin and pokeweed. Responses of the patients' lymphocytes were similarly examined. E and EAC rosettes were also tested. A significantly increased transformation response was found when normal lymphocytes were exposed to sera from those patients who had a reduced number of E-rosette-forming lymphocytes (mean 8%) as compared to the response to sera from patients with a higher number of E-rosette-forming cells. The results suggest that a factor is present in sera from some CLL patients which stimulates the transformation of mitogen-stimulated lymphocytes and which seems to be related to the number of the patient's T and B lymphocytes and perhaps with a T suppressor effect on B lymphocytes.

Aged↗

PubMed1986

A muscarinic receptor type in human lymphocytes: a comparison of 3H-QNB binding to intact lymphocytes and lysed lymphocyte membranes.

Human blood lymphocytes from normal blood donors exhibited specific binding of the muscarinic antagonist 3H-quinuclidinyl benzilate (3H-QNB). The 3H-QNB binding to intact viable lymphocytes as well as to lysed lymphocyte membranes "P2" was saturable and displaceable by both muscarinic agonists and antagonists. For the lysed lymphocyte membranes "P2" a single binding site with a Bmax of 109 pmol/g protein and a Kd of 15 nM was obtained. Intact viable lymphocytes also showed one binding site with a Kd of 24 nM and a Bmax of 1556 pmol/g protein. The higher Bmax value might be explained in terms of uptake of the ligand when using intact cells or through loss of binding sites when using lysed lymphocyte membranes "P2". IC50 values were lower by a factor of 10(2) for atropine and scopolamine and by 10(4) for pirenzepine when lysed lymphocyte membranes "P2" were used instead of intact viable lymphocytes.

Adult↗

PubMed1994

Lymphocyte subsets in relapsing-remitting multiple sclerosis: a longitudinal study of B lymphocytes and T lymphocytes.

Changes in lymphocyte subset populations may provide clues to the dysimmune mechanisms involved in relapsing remitting multiple sclerosis (RRMS). The lymphocyte subgroup CD4+ CD45RA+, thought to be responsible for the induction of suppression is decreased in some patients with MS compared to controls. A possible role for another lymphocyte subset, CD19+CD5+ lymphocytes, has been proposed in autoimmune diseases and multiple sclerosis (MS). To expand this we studied CD4+CD45RA+ (T) lymphocytes and CD19+CD5+ (B) lymphocytes in nine patients with relapsing-remitting MS (RRMS) and nine controls. The patients were examined monthly for an average of ten months and nine relapses were observed in seven patients. One patient underwent monthly gadolinium enhanced magnetic resonance imaging (MRI). Normal percentages CD4+CD45RA+ lymphocytes were found in patients with RRMS. No significant abnormalities in the CD19+CD5+ lymphocyte subpopulation were noted, although a tendency for higher percentages of this subset (approaching statistical significance, P = 0.056) was detected.

Analysis of Variance↗

PubMed2004

The imbalanced mixed lymphocyte reaction between maternal and fetal lymphocytes as well as between the lymphocytes of adult children and their parents is mediated by activated CD8+ T cells.

PROBLEM: The mixed lymphocyte reaction (MLR) between maternal and fetal lymphocytes as well as between adult children and their parents is imbalanced in bidirectional mixed lymphocyte cultures. The present investigation was aimed at examining which type of T cells has primary responsibility for this phenomenon. METHODS: Two-way mixed lymphocyte cultures between lymphocytes of five female and five male adults and five male and five female newborns against lymphocytes of their parents were performed. Unrelated adults served as the controls. Before and after 72 hr incubation the mixed leukocytes cultures (MLCs) were sorted by flow cytometry according to the surface markers CD4 and CD69 or CD8 and CD69. The single cell populations within the four resulting fractions were discriminated by fluoresence in situ hybridization (FiSH) using xy-DNA probes. RESULTS: Before incubation the share of CD8(+) CD69(+) cells in the MLCs between mothers and their newborn infants was significantly shifted toward the newborn cells (P < 0.01). After 72 hr incubation the CD8(+) CD69(+) ratio in the MLCs between mother and newborn cells and between adult children (male as well female) and their parents showed a significant shift of the CD8(+) CD69(+) cells toward the children's direction. All other MLCs showed a balanced cell population for all investigated cell types, both before and after incubation. CONCLUSION: The imbalanced MLR between maternal and fetal lymphocytes and lymphocytes of adult children against their parents is mediated by a specific imbalance of the activation of CD8(+) but not of CD4(+) T cells.

Adult↗

PubMed1976

Recruitment of effector lymphocytes by initiator lymphocytes. Circulating lymphocytes are trapped in the reacting lymph node.

In previous studies, we have shown that initiator T lymphocytes (ITL) sensitized in vitro recruit effector T lymphocytes in vivo. When ITL were sensitized against fibroblast antigens in vitro and injected into footpads of syngeneic recipients, they induced enlargement of the draining popliteal lymph node (PLN) and the development there of specific effector lymphocytes of recipient origin. To study the basis of this lymph node response in recruitment, we injected 51Cr-labeled spleen cells i.v. into recipients of sensitized ITL and found that the labeled circulating lymphocytes were trapped in the reacting PLN. The trapping depended on surface properties of the labeled circulating lymphocytes, as revealed by various enzymatic treatments. The trapping process was radiosensitive, both on the part of the trapped lymphocytes and the lymph node-trapping mechanism. Thus, sensitized ITL injected into the hind footpads migrate to the PLN and induce the trapping of circulating recruitable lymphocytes, which either differentiate into or regulate the differentiation of effector T lymphocytes.

Animals↗

PubMed1984

Soluble factor(s) released by Concanavalin A activated lymph node lymphocytes induce proliferation and maturation of chronic lymphocytic leukaemia (CLL) B lymphocytes.

An active supernatant (Ly Con A) was prepared by stimulating the normal human lymph node lymphocytes with Concanavalin A (Con A). Peripheral blood lymphocytes (PBL) from 3 healthy subjects and from 8 patients with chronic lymphocytic leukaemia (CLL) were cultured in the presence of Con A and Ly Con A. The latter induced a significant DNA synthesis both in normal and CLL lymphocytes. A proliferative response was still present in CLL after T lymphocytes depletion. The Con A and Ly Con A treatment also induced morphological changes in CLL lymphocytes consistent with plasma cell differentiation. In 3 cases the appearance of cytoplasmic light chains was detected by immunofluorescence. These findings suggest that peripheral blood B lymphocytes from CLL patients can be stimulated to maturation when helper factor(s) released by mitogen activated lymph node lymphocytes are provided.

Antibody-Producing Cells↗

PubMed1977

Human lymphocyte complement receptors. Quantitative requirements for C3 of normal and chronic lymphocyte leukemia lymphocytes.

Erythrocytes coated with varying amounts of human complement were used to detect lymphocytes with complement receptors from normal subjects and patients with chronic lymphocytic leukemia. The relationship between the percentage of lymphocytes rosetting and the quantity of C3 present on complement-coated erythrocytes were studied. Small quantities of C3 (less than 5 fg/erythrocyte) caused maximal rosetting of normal lymphocytes. Maximal rosetting with chronic lymphocytic leukemia lymphocytes was not reached until much greater amounts of C3 were used to coat the erythrocytes. This difference in sensitivity to erythrocyte-bound complement was not due to an increased fraction of complement receptor-bearing cells in the leukemic patients. This loss of sensitivity of the chronic lymphocytic leukemia lymphocyte for complement may play a role in the immune deficiency present in this disease.

Cell Membrane↗

PubMed1979

Regulatory functions of hapten-reactive helper and suppressor T lymphocytes. III. Amplification of a generation of tumor-specific killer T-lymphocyte activities by suppressor T-cell-depleted hapten-reactive T lymphocytes.

2,4.6-trinitrophenyl (TNP)-reactive T-cell activities were raised in mice by immunization with TNP-isologous mouse gamma globulin. After establishing that TNP-reactive T lymphocytes can serve as amplifier cells for induction of killer T lymphocytes in allogeneic system, we explored the possibility of this hapten-reactive T-cell system to amplify tumor-specific killer T-lymphocyte activity in the syngeneic system. We utlized relatively weak immunogenic syngeneic plasmacytoma X5563 in C3H/He mice. Analysis of the TNP-reactive T-cell activities revealed that such T lymphocytes express the biological functions of both major subtypes of regulatory T cells, namely suppressors and helpers, and that TNP-reactive suppressor and helper T lymphocytes, respectively, differ in their relative susceptibility to specific inactivation by TNP conjugates of the nonimmunogenic D-amino acid copolymer, D-glutamic acid, and D-lysine (D-GL). By taking advantage of the relative susceptibility-difference to TNP-D-GL, selective inactivation of TNP-reactive suppressor T cells was induced by appropriate treatment with TNP-D-GL, and the generation of TNP-reactive helper T-cell activity was amplified. The supplement of augmented TNP-reactive helper T-cell activity to the system at the immunization with syngeneic X5563 with TNP-haptenation, resulted in a striking augmentation of induction of tumor-specific killer T-lymphocyte activity, and a considerable number of hosts survived after the challenge with lethal dose of viable tumor cells. Thus, appropriate manipulations designed to induce potent hapten-reactive helper T-lymphocytes provided the potential for a very effective mode of immunoprophylaxis against tumor.

Animals↗

PubMed2006

Leptin receptor expression and signaling in lymphocytes: kinetics during lymphocyte activation, role in lymphocyte survival, and response to high fat diet in mice.

Leptin has direct effects not only on neuroendocrine function and metabolism, but also on T cell-mediated immunity. We report in this study that leptin receptor (ObR) is expressed on resting normal mouse CD4(+), CD8(+), B cells, and monocyte/macrophages. ObR expression is up-regulated following cell activation, but with different kinetics, in different lymphocyte subsets. Leptin binding to ObR results in increased STAT-3 activation in T cells, with a different activation pattern in resting vs anti-CD3 Ab stimulated T cells. Leptin also promotes lymphocyte survival in vitro by suppressing Fas-mediated apoptosis. B lymphocytes appear to be more susceptible to the antiapoptotic effects of leptin, and they show higher surface expression of ObR, compared with T cells. Moreover, CD4(+) T cells isolated from ObR-deficient mice displayed a reduced proliferative response, compared with normal controls. Furthermore, ObR/STAT-3-mediated signaling in T lymphocytes is decreased in the diet-induced obese mouse model of obesity and leptin resistance. In summary, our findings show that the ObR is expressed on normal mouse lymphocyte subsets, that leptin plays a role in lymphocyte survival, and that leptin alters the ObR/STAT-3-mediated signaling in T cells. Taken together, our data further support the notion that nutritional status acting via leptin-dependent mechanisms may alter the nature and vigor of the immune response.

Animals↗

PubMed1981

The parallel, time-dependent, bimodal change in lymphocyte cholinergic binding activity and cholinergic influence upon lymphocyte-mediated cytotoxicity after lymphocyte activation.

The potent muscarinic cholinergic antagonist 3-quinuclidinyl benzilate has been used to detect muscarinic acetylcholine receptors on rodent and human lymphocytes. Binding to B lymphocytes was minimal and was not saturable or ligand specific. Half-maximal binding of (3H)-quinuclidinyl benzilate to T lymphocytes occurred at concentrations comparable to those described in other systems, and was displaceable at physiologic concentrations by muscarinic but not nicotinic agonists and antagonists. Binding to T lymphocytes was both saturable and specific, and was found to rapidly increase significantly after mitogen activation. Activation of T lymphocytes or the Lyt 1+ subset produces an early increase and later fall in muscarinic binding, and the ability od cholinergic agonists to augment the effector function of cytotoxic T lymphocytes harvested from alloimmune rat spleen is directly related to the magnitude of muscarinic binding.

Animals↗

PubMed1980

Individual cell-by-cell quantitation of lymphocyte surface membrane Ig in normal and CLL lymphocyte and during ontogeny of mouse B lymphocytes by immunoperoxidase assay.

A new quantitative immunoperoxidase method is presented for determining absolute amounts of peroxidase and, consequently, surface antigen densities of individual cells in B lymphocytes from normal individuals, from subjects with CLL and prolymphocytic leukemia, and during ontogeny of B lympocytes in the mouse. The following results were observed: (1) The density of B antigenic sites were lower on CLL than on normal B lymphocytes. (2) The B antigens density of leukemic lymphocytes varied less from cell to cell, forming a homogeneous peak on histograms. (3) In a very rare case of CLL, the antigen density was measured at the time of initial diagnosis (22,500 sites or 647 U) and during the development of a blastic crisis (135,000 sites or 2576 U). The cell by cell distribution changed from a homogeneous peak with a low number of antigenic sites per cell to a heterogeneous peak with a high number of antigenic sites per cell. (4) In prolymphocytic leukemia, the density of B antigenic sites was greater than on normal B lymphocytes and much more heterogeneous than on CLL lymphocytes. (5) During ontogeny of B lymphocytes in the mouse, maturation is associated with the appearance of a population of cells of intermediate to high Smig density. The finding of a decrease in, and altered distribution of, surface markers in CLL is compared with these ontologic findings in the mouse, and the concept that a monoclonal B lymphocyte in CLL may be arrested at a particular stage in its differentiation is discussed.

Animals↗

PubMed1991

[Chronic lymphocytic leukemia with peripheral T lymphocytes expressing CD 2+, CD 3+, CD 4-, CD 8-, CD 16+, and CD 56+ and lymph-node lymphocytes expressing CD 2+, CD 3-, CD 4-, CD 8-, CD 16+, CD 38+, and CD 56+].

A 33-year-old man was hospitalized because of thrombocytopenia and severe splenomegaly. On admission 78% of peripheral lymphoid cells were abnormally large, with pale cytoplasm. Flow cytometry of the abnormal lymphocytes showed that they expressed CD 2, CD 3, CD 11, CD 16, and CD 56, but not CD 4 nor CD 8, so they were T-cell large granular lymphocytes (T-LGL). Abnormal lymphocytes obtained from a lymph node expressed CD 2, CD 16, CD 38, and CD 56, but not CD 3, CD 4, and CD 8, so they were natural killer(NK) cells. Splenectomy was performed and the operative specimen showed diffuse infiltration of pleomorphic lymphocytes, probably chronic lymphocytic leukemia cells. After splenectomy, the platelet count returned to normal but the lymphocytosis continued. Two years after discharge, chemotherapy was done because of thrombocytopenia and hepatomegaly. The patient died of disseminated intravascular coagulation arising from sepsis. The differences and similarities between peripheral and lymph-node lymphocytes suggest that LGL and NK cells may be differentiated from the same kind of cell, somewhat differentiated from stem cells.

ADP-ribosyl Cyclase↗

PubMed1990

Comparison of some lymphocyte markers in B-cell chronic lymphocytic leukaemia and systemic lupus erythematosus (the B lymphocyte subset).

Spontaneous mouse red-cell rosette formation (M-rosette), Leu 1 (CD 5) monoclonal antibody binding, ecto-nucleotidase enzyme reactions and mitogen responses of peripheral blood lymphocytes in 10 patients with B-cell chronic lymphocytic leukaemia (CLL), in 8 with systemic lupus erythematosus (SLE) and in 10 controls were studied. The numbers of Leu 1 (CD 5) positive B lymphocytes in CLL and SLE were higher than in controls. These are called "autoregulatory" B lymphocytes, which are thought to be independent of T-cell regulatory effects. A significant increase of mouse rosette forming cells (MRFCs) was found in CLL, while in SLE and in controls their number was low. Compared to the B lymphocytes of SLE patients and controls, those of CLL patients showed diminished responses to pokeweed mitogen stimulation parallel to their decreased level of 5'-nucleotidase. Correlations between these markers and the features of isolated M-rosette positive CLL B lymphocytes are discussed.

5'-Nucleotidase↗

PubMed1978

Effect of released lymphocyte proteins on human lymphocytes in vitro. II. Protein synthesis of nylon-wool separated cells in the presence of proteins derived from lymphocytes.

Protein synthesis of nylon-wool adherent (B) and non-adherent (T) human tonsillar lymphocytes was examined in the presence of three protein fractions precipitated with ammonium sulfate from the medium of the above lymphocytes incubated in vitro for 4 hours. One fraction precipitated with ammonium sulfate at 0--30% saturation was found to inhibit amino acid incorporation into proteins mainly in unseparated cells while the fraction precipitated at 30--70% saturation decreased the rate of protein synthesis in B cells. The fraction precipitated at 70--100% saturation inhibited protein synthesis slightly in T lymphocytes. Protein synthesis in B and T as well as in unseparated cells was also examined in the presence of proteins obtained from the medium of B and T lymphocytes. It is assumed that proteins released by lymphocytes without mitogenic activation in vitro are involved in the mediation of lymphocyte interactions and may be related to lymphokines synthesized and released by activated cells.

B-Lymphocytes↗

PubMed1978

Pulmonary processes of mature-appearing lymphocytes: pseudolymphoma, well-differentiated lymphocytic lymphoma, and lymphocytic interstitial pneumonitis.

Patients with pseudolymphoma, well-differentiated lymphocytic lymphoma, and lymphocytic interstitial pneumonitis were studied. Diagnoses were confirmed by recently developed immunochemical staining techniques. Radiographic findings in pseudolymphoma were different from those in well-differentiated lymphocytic lymphoma, and clinical findings in lymphocytic interstitial pneumonitis were different from those in the other two types of lesions. The interstitial infiltrate of lymphocytic interstitial pneumonitis had two patterns: basilar with an alveolar component and diffuse with associated honeycombing. Pseudolymphoma and lymphocytic interstitial pneumonitis are being polyclonal inflammatory processes without malignant potential. Well-differentiated lymphocytic lymphoma, a monoclonal neoplasm, often has an indolent course.

Humans↗

PubMed1988

Virus-lymphocyte interactions. II. Expression of viral sequences during the course of persistent lymphocytic choriomeningitis virus infection and their localization to the L3T4 lymphocyte subset.

Viruses that cause in vivo persistent infections need to selectively compromise the host's immunologic surveillance machinery in order to survive. To understand the molecular basis of how this is accomplished we have analyzed persistent virus infection by lymphocytic choriomeningitis in its normal host, the mouse. Earlier we noted by infectious center analysis that five in 10(4) lymphocytes carried by persistently infected mice contained infectious materials throughout the course of infection. A previous publication extended these results, in BALB mice by showing that the L3T4+ lymphocyte subset in lymph nodes and spleens was predominantly involved. Using cDNA labeled probes to the viral genome and in situ hybridization we report that 1 to 2% of circulating lymphocytes from several mouse strains contain viral RNA sequences for the three viral structural genes. By FACS analysis, the Thy-1.2+, L3T4+ subset primarily harbors virus while viral sequences are usually not detected in the Lyt-2+ subset as early as 6 days after initiating infection in newborns and throughout the course of the persistence. These findings suggest that incomplete, presumably defective, virus is generated in a subset of Th lymphocytes during persistent infection and that during this time infection of cytotoxic T cell subsets is minimal.

Animals↗

PubMed1988

Studies on cytotoxicity generated in human mixed lymphocyte culture. IV. Interleukin 2 alone or from mixed lymphocyte culture yields natural killer-like cytotoxic cells distinct from allospecific cytotoxic T lymphocytes.

High levels of cytotoxic activity against the natural killer (NK) cell-sensitive target K562 and the NK-resistant target UCLA-SO-M14 (M14) can be generated in vitro either by mixed lymphocyte culture (MLC) or by culture of lymphocytes in interleukin 2 (IL2) (lymphokine activated killer (LAK) cells). The purpose of this study was to identify similarities and differences between MLC-LAK and IL2-LAK cells and allospecific cytotoxic T cells. Induction of cytotoxicity against K562 and M14 in both culture systems was inhibited by antibodies specific either for IL2 or the Tac IL2 receptor. Like NK effector cells, the precursors for the MLC-LAK cells were low density large lymphocytes. However these precursors differed from the large granular lymphocytes that mediated NK cytolysis in sensitivity to the toxic lysosomotropic agent L-leucine methyl ester (LME). The resistance of the MLC-LAK precursors to LME indicated that the precursors included large agranular lymphocytes. Although interferon-gamma (IFN-gamma) is produced in MLC and in IL2 containing cultures, it is not required for induction of either type of cytotoxic activity. Neutralization of IFN-gamma in MLC- and IL2-containing cultures with specific antibodies had no effect on the induction of cytotoxic activities. Both allospecific cytotoxic T lymphocyte (CTL) and LAK activities were enhanced by IL2 and IFN-gamma at the effector cell stage. However, the mechanism of cytolysis was different in the two systems. NK- and MLC-induced LAK activities were independent of CD3-T cell receptor complex while CTL activity was blocked by monoclonal antibodies specific for the CD3 antigen. These results suggest that NK and the in vitro induced LAK cytotoxicities are a family of related functions that differ from CTL. Furthermore, MLC-induced and IL2-induced cytotoxicities against K562 and M14 appear to be identical.

Antibodies, Monoclonal↗