B and T lymphocytes

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Antigen heterogeneity of human B and T lymphocytes

Antigen heterogeneity of human B and T lymphocytes

lymphocytes. In an attempt to obtain a reagent specifically reactive with T (thymus-derived) lymphocytes, an antispleen antiserum was absorbed with cellf from five B- (bone marrow- derived) cell lines. After absorption, the antiserum killed 60-75% of peripheral blood lymphocytes and 40-50% of tonsil cells, so that there was a relationship between the percentage of killed cells and the proportion of T lymphocytes. However, when cells after cytotoxic treatment were assayed for rosette formation with sheep erythrocytes (a T-cell marker) 5-20% of viable rosette-forming lymphocytes were found. Therefore, this antiserum was cytotoxic for only 75-90% of T cells. From studies performed with antisera prepared against spleen and B-cell lines, we conclude that lymphoblastoid cells are antigenically different and deficient in comparison to normal B lymphocytes. In addition, cultured B-cell lines appear to be antigenically heterogenous, as shown by the cytotoxic activity remaining in antispleen and anti-B-cell lines sera after absorption with various numbers and types of lymphoid cell lines. After absorption with normal lymphocytes, an antiserum produced against chronic lymphatic leukemia cells had specific activity associated with 12 chronic lymphatic leukemia cells tested. Absorption of the same antiserum with leukemic cells […]
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Frequencies of circulating B- and T-lymphocytes  as indicators for stroke outcomes

Frequencies of circulating B- and T-lymphocytes as indicators for stroke outcomes

correlation between the infarct size or NIHSS and the percentage of lymphocytes. In particular, the frequency of T-lymphocytes on day 1 after stroke is negatively correlated with infarct volume and NIHSS. Interestingly, although the percentage of B-lymphocytes did not show significant difference as compared to healthy controls, a significantly negative correlation between B cell percentage and stroke outcomes was established. These results are in agreement with a previous study showing the lack of early reduction of B cell counts in stroke patients, but the infarct volume and B cell counts at baseline and day 4 after stroke were inversely correlated. 19 Dichotomizing stroke cohort based
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Quantification of newly produced B and T lymphocytes in untreated chronic lymphocytic leukemia patients

Quantification of newly produced B and T lymphocytes in untreated chronic lymphocytic leukemia patients

number of newly mobilized T cells from the thymus [4], it is not known whether this may also influence the release of new B cells from the bone marrow. To answer this question, we combined the method of kappa-delet- ing recombination excision circles (KRECs) detection, initially developed by van Zelm et al [5] and modified later by Fronkova et al [6], with the well established method of measuring T-cell receptor excision circles (TRECs) [7], thus obtaining a duplex Real-Time PCR assay allowing the simultaneous measure of newly pro- duced B and T cells. KRECs and TRECs are episomal DNA products generated during the lymphocyte devel- opment and differentiation process, when B- and T-cell receptor gene rearrangements occur and specific chro- mosomal sequences need to be excised [5-7]. These excision products cannot be replicated and, therefore, KRECs and TRECs are diluted when cells proliferate, and are lost when cells die. Since KRECs are randomly present in about 50% of B cells released from the bone marrow and TRECs in 70% of T cells leaving the thy- mus, their quantification is considered a reliable esti- mate of the amount of newly produced B and T lymphocytes [8,9]. Here, we applied the new assay, together with the flow cytometry, to quantify the num- ber of recently produced B and T cells and the periph- eral lymphocyte expansion in untreated CLL patients, who were at a very early stage of the disease.
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Role of B cells and cytotoxic T lymphocytes in clearance of and immunity to rotavirus infection in mice.

Role of B cells and cytotoxic T lymphocytes in clearance of and immunity to rotavirus infection in mice.

To understand these factors, we and others have used a mouse model of rotavirus infection (2, 10, 32). Previous studies with this model have produced conflicting results on the role of B cells and T cells in the resolution of primary infection and protection against rotavirus reinfection. It has been shown that mice with severe combined immunodeficiency (SCID mice) become chronically infected with murine rotaviruses (26). On the other hand, nude mice have been reported to clear rota- virus infection in the absence of a significant antibody response (8). The passive transfer of immune cytotoxic T lymphocytes (CTLs) has been shown both to protect against acute rotavirus- induced diarrhea in suckling mice (23) and to clear the chronic rotavirus infection from adult SCID mice (6). The rotavirus proteins recognized by the CD8 1 major histocompatibility complex-restricted T cells capable of mediating the clearance of chronic infection in SCID mice include both inner nonneu- tralizing and outer neutralizing proteins of the virus (5). Both clearance of primary infection and protection against reinfec- tion have been correlated with the presence of rotavirus-spe- cific intestinal immunoglobulin A (IgA) but not serum IgG (2,
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Perforin, granzyme B, and FasL expression by peripheral blood T lymphocytes in emphysema

Perforin, granzyme B, and FasL expression by peripheral blood T lymphocytes in emphysema

tous smokers with evidence of systemic inflammation will show higher expression of cytotoxic and activation mark- ers such as perforin, granzyme B, and FasL than that of subjects with normal lung function. To test this hypothe- sis, we measured serum interleukine-6 (IL-6), tumor- necrosis factor (TNF), and C-reactive protein (CRP) in smokers with emphysema, smokers without emphysema, and in non smokers with normal lung function. Expres- sion of perforin, granzyme B, and FasL protein by systemic T lymphocytes and NK cells was compared between the three groups.

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B and T Lymphocytes in Primary Immunodeficiency Disease in Man

B and T Lymphocytes in Primary Immunodeficiency Disease in Man

B- and T-cell populations in 32 patients with different forms of primary immunodeficiency disease were studied. The B-cells in peripheral blood were investigated with respect to surface immunoglobulins by means of immunofluorescence. The T-cell function was studied utilizing quantitation of proliferative response to phytochemagglutinin (PHA) 1 and delayed allergy to various antigens. In 10 patients lymph node lymphocytes were also evaluated 11 male children with infantile x-linked agammaglobulinemia were divided into two subgroups. One did not show immunoglobulin spots on peripheral blood lymphocytes at all, the other contained a very low percentage of IgM- and occasionally IgA bearing
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Regulatory B and T lymphocytes in multiple sclerosis: friends or foes?

Regulatory B and T lymphocytes in multiple sclerosis: friends or foes?

Alemtuzumab Alemtuzumab is a humanized IgG1 mono- clonal antibody that targets the CD52 (Campath-1 antigen), a 12 amino acid glycoprotein anchored to glycosylphos- phatidylinositol, which is widely expressed on the cell sur- face of mature immune cells. Anti-CD52 induces a rapid and prolonged depletion of lymphocytes from the circula- tion, which results in a profound immunosuppression sta- tus followed by an immune reconstitution phase [160]. In EAE, anti-CD52 treatment abrogated B cell infiltration and disrupted existing B cell aggregates in the CNS [161]. Recently, it has been shown that it can also ameliorate coli- tis through suppressing Th1/17 mediated inflammation and promoting Tregs differentiation in IL-10 deficient mice [162]. Much of the research on alemtuzumab focuses on the lymphocyte repopulation progress and shows that CD4(+) CD25(+)CD127(low) Treg cells preferentially expand within the CD4(+) lymphocytes, reaching their peak within 1 month [163]. A recent study demonstrated that alemtu- zumab increased anti-inflammatory cytokines (such as IL-10 and TGF-β) while diminishing pro-inflammatory cytokines (such as IFN-γ, IL-17, IL-6 and TNF-α) within 6 months of treatment and increased Tregs percentage and function after 24 months post-treatment [164]. In addition, alemtuzumab seems to affect B cells, as it increased the per- centage of repopulated naïve/immature B cells [165, 166]. Alemtuzumab may thus be a promising therapy for MS [6]; however, it also causes loss of immune-tolerance leading to secondary autoimmunity such as Graves’ disease and marked anti-drug antibody responses [160, 167].
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Lymphocytic choriomeningitis virus-induced immunodepression: inherent defect of B and T lymphocytes.

Lymphocytic choriomeningitis virus-induced immunodepression: inherent defect of B and T lymphocytes.

Our results can be interpreted as showing that i unresponsiveness to mitogens of cells from LCMV-infected mice is not due to altered functions of the macrophages with respect to IL-1 pro[r]

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Herpesvirus sylvilagus infects both B and T lymphocytes in vivo.

Herpesvirus sylvilagus infects both B and T lymphocytes in vivo.

This indicated that unseparated spleen cells contained approximately two copies of circular viral DNA per cell lane 1, and in each of the purified cell populations lanes 2, 3, and 4 abou[r]

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Recognition of a B cell leukemia associated minor histocompatibility antigen by cytotoxic T lymphocytes.

Recognition of a B cell leukemia associated minor histocompatibility antigen by cytotoxic T lymphocytes.

Abbreviations used in this paper: mHag, minor histocompatibility antigen; BMT, bone marrow transplantation; CVHD, graft-vs-host disease; GVL, grafl-vs- leukemia; B-ALL, B-[r]

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Immunohistochemical study on roe deer haemal nodes

Immunohistochemical study on roe deer haemal nodes

Ceccarelli et al. [4] have observed that most of the lymphoid cells in the haemal nodes and in the inter- follicular cords of the sheep and cows and the cells in the germinal centres of some secondary follicles could be identified as T-lymphocytes and most of the cells in the primary follicles and in the cortex of the secondary follicles could be identified as B-lymphocytes. Yoon et al. [18] have reported that B-lymphocytes were mainly located in lymphoid follicles of the haemal node, and that they were sparsely scattered in the sub capsular sinus. In the same study, it is mentioned that T-lymphocytes were sparsely scattered in the diffuse lymphatic tissues of the haemal node. Zidan and Pabst [19] reported that CD3-positive T lymphocytes were localised mainly at the margin of lymphoid follicles and in the medullary cords and that CD22-positive B lymphocytes were predominantly found in lymphoid follicles which are the typical localisation areas of these cells. Casteleyn et al. [3] reported that T cell lymphocytes marked with CD3 in the haemal node of bovine were mostly localised at the paracortex and the interfolic zone, and that medullary cords also con- tained CD3-positive cells, and that there were very few CD3-positive cells observed in the mantle zone of the follicles but almost no positive cells were ob- served in the germinal centre. They have determined that CD21-marked B-lymphocytes were confined to the follicles and had a predominant position in the germinal centres. Guerrero et al. [11] suggested that lymphatic tissue capable of forming into a cord-like shape in the cervical haemal nodes was composed of plasma cells, macrophages, B- and T-lymphocytes and demonstrated the anti-CD3 positive lymphocytes in the paracortex. Distribution of T-lymphocytes appears to be more compatible with the findings of Casteleyn et al. [3] in the haemal node of bovine even though it bears a resemblance to that of sheep, goat, cattle, camel and deer in general when data related to the distribution of T-lymphocytes in the literature are ex- amined. However, the existence of more T-lymphocyte
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Original Article Histopathological features of central nervous system in pediatric cases of fatal hand, foot and mouth disease

Original Article Histopathological features of central nervous system in pediatric cases of fatal hand, foot and mouth disease

lymphocytes and macrophages/microglia cells in the midbrain/pons, medulla oblongata and spinal cord of HFMD patients (P<0.05). In spinal cord, the ratio of CD4+ to CD8+ was remarkably higher in HFMD group (P<0.05). In HFMD group, the counting was noticeably higher of CD3+, CD4+, and CD8+T lymphocytes, B lymphocytes and macrophages/microglia cells in the midbrain/pons, medulla oblongata and spinal cord than in brain and cerebellum (P<0.05). In addition, the counting of CD3+T lymphocytes in the brain was significantly higher than that in cerebellum (P<0.05). Conclusions: Presence of lesions is mostly recorded in lower parts (midbrain/pons, medulla oblongata and spinal cord) than in upper parts (brain and cerebel- lum) in HFMD patients’ CNS. T lymphocytes-mediated immunity, B lymphocytes-mediated humoral immunity and macrophages/microglial cells-executed innate immunity may be involved in the local immune response of the CNS lesions of HFMD cases. Additionally, cellular immunity and innate immunity may play a more vital role in local im- mune response than humoral immunity. No CD57 + NK cells were found in any CNS tissue of HFMD patients. It was indicated that NK cells might not be involved in local immune response of advanced CNS lesions of HFMD patients.
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Distinctive distribution of lymphocytes in unruptured and previously untreated brain arteriovenous malformation

Distinctive distribution of lymphocytes in unruptured and previously untreated brain arteriovenous malformation

Iron deposition was assessed by hematoxylin and eosin and Prussian blue stains. Superficial temporal arteries (STA) were used as control. Results: Both Tlymphocytes and macrophages were present in unruptured, previously untreated bAVM specimens, whereas few B cells and plasma cells were detected. Iron deposition was detected in 8 specimens (42%; 95% confidence intervals = 20‑67%). The samples with iron deposition tended to have more macrophages than those without (666 ± 313 vs. 478 ± 174 cells/mm 2 ; P = 0.11).

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Comparison of Lymphocyte Number and Their Subsets in Patients with Diabetes Mellitus Type II,Tuberculosis and Concomitant TB and Diabetes

Comparison of Lymphocyte Number and Their Subsets in Patients with Diabetes Mellitus Type II,Tuberculosis and Concomitant TB and Diabetes

Materials and Methods: This study was performed in NRITLD between August 1999 and August 2001 to elucidate the quantitative status of cellular immunity. We measured the number of B lymphocytes, T lymphocytes, Natural Killer (NK) cells, and their sub-units in three groups of patients with diabetes mellitus (DM), pulmonary tuberculosis (TB) and pulmonary tuberculosis associated with DM (TB+ DM); and compared their results with age - matched healthy controls.

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Human Decidual Cells Activity in Women with Spontaneous Abortions of Probable CMV Aetiology During the First Trimester of Gestation. An Immunohistochemical Study with CMV-Associated Antigen

Human Decidual Cells Activity in Women with Spontaneous Abortions of Probable CMV Aetiology During the First Trimester of Gestation. An Immunohistochemical Study with CMV-Associated Antigen

week of gestation respectively, and in which CMV reactivation was ruled out from serological evaluation of the pregnant women at admission, versus equal controls after voluntary abortion following well-documented maternal viral recurrence. In addition, a panel of monoclonal antibodies for the identification of leukocytes (CD45/LCA), B-lymphocytes (CD20/L-26), and T-lymphocytes (CD45RO/UCHL1), was performed. All women received hormonal medication to support gestation, in the cases of spontaneous abortions. Results: Immunohistochemical examination using a specific antibody against cyto- megalovirus showed large multinucleated infected cells with intranuclear inclusions, located primarily in the decidual stroma within a lymphoplasmacytic infiltrate in the cases of spontaneous abortions. No evidence of infection was observed in the chorionic villi. In the cases of voluntary abortions same findings were observed in the relevant areas, and a strong evidence of infection was observed in the chorionic villi. Conclusion: This study demonstrates 1) that the decidual endometrial stro- mal cells can express the CMV-associated antigen prior to serological manifestation of the viral replication, 2) the expres- sion of the antigen is higher in cases of hormonal administration to support gestation. In these cases a mild mononuclear infiltrate of UCHL1 (T marker) positive cells, accompanies the CMV-associated antigen positive cells.
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Glucocorticoids Administered In Vivo Inhibit Human Suppressor T Lymphocyte Function and Diminish B Lymphocyte Responsiveness in In Vitro Immunoglobulin Synthesis

Glucocorticoids Administered In Vivo Inhibit Human Suppressor T Lymphocyte Function and Diminish B Lymphocyte Responsiveness in In Vitro Immunoglobulin Synthesis

The effects of corticosteroid given in vivo on human lymphocyte subpopulation function were investigated using an in vitro system of pokeweek mitogen-stimulated immunoglobulin production. Peripheral blood lymphocytes were obtained from normal volunteers before and 4 h after the intravenous administration of methylprednisolone. Unfractioned peripheral blood lymphocytes showed a consistent decrease (mean @ 50%) in immunoglobulin and total protein synthesis after steroid administration. Utilizing separated thymus-derived (T) and bone marrow-derived (B) lymphocyte fractions, the pathophysiology of this alteration in immunoglobulin production was elucidated. B lymphocytes obtained after steroid treatment showed a markedly diminished immunoglobulin response (20% of normal) to normal T lymphocytes and to normal T cells that had been irradiated to remove suppressor T
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Pure Choriocarcinoma of Testis with Tumor Infiltrating Lymphocytes and Granulomas

Pure Choriocarcinoma of Testis with Tumor Infiltrating Lymphocytes and Granulomas

the connective tissue between tumor nodules and within tumor nests (Fig. 2A). These cells were mostly CD3-positive T-lymphocytes and CD68- positive histiocytes. Many plasma cells were also admixed. Most of the T-cells were CD8-positive cytotoxic cells (Fig. 2C), which also expressed granzyme-B and TIA-1 (Fig. 2D). Occasionally, loose aggregates of epithelioid histiocytes forming granulomas were noted (Fig. 2B). The immuno- stainings of Fas and FasL showed that the tumor cells were diffusely positive for FasL (Fig. 1D), but negative for Fas. In contrast, infiltrating lympho- cytes were strongly positive for both Fas and FasL.
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Memory CD4+ T-Lymphocyte Loss and Dysfunction during Primary Simian Immunodeficiency Virus Infection

Memory CD4+ T-Lymphocyte Loss and Dysfunction during Primary Simian Immunodeficiency Virus Infection

To evaluate the relative contributions of each of these mech- anisms to the loss of CD4 ⫹ T-lymphocyte function during the period of primary infection, we characterized the functional capacity of the residual memory CD4 ⫹ T lymphocytes in these monkeys. The fraction of memory CD4 ⫹ T lymphocytes (CD95 ⫹ ) that produced IFN- ␥ or IL-2 in response to SEB was assessed by intracellular staining at regular intervals following infection. Production of Ki-67, perforin, and granzyme B in unstimulated memory CD4 ⫹ T lymphocytes was also moni- tored (Fig. 6A). The ability of memory CD4 ⫹ T lymphocytes to secrete IFN- ␥ and IL-2 was maintained in animals with low set point viral loads. In contrast, the capacity of this subpopulation of cells to express these cytokines was dramatically reduced by the time of peak viremia on day 14 in animals with moderate to high set point viral loads. Furthermore, this reduction in the FIG. 3. Loss of memory CD4 ⫹ T-lymphocyte subsets defined by various antibody combinations had similar correlations with set point plasma viral RNA levels. Total CD4 ⫹ T lymphocytes were divided into naı¨ve, central memory, effector memory, and intermediate memory subpopulations based on their expression of CD28/CD95, CD45RA/CD95, CD28/CCR7/CD95, or CCR7/CD45RA. The percentage of total CD4 ⫹ T lymphocytes represented by each of these subsets was assessed at various times during the course of primary infection. Comparable positive correlations were observed between the loss of memory CD4 ⫹ T-lymphocyte subsets defined by these different antibody combinations and the set point plasma viral RNA levels in these animals.
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Studies of T  and B Lymphocytes in Patients with Connective Tissue Diseases

Studies of T and B Lymphocytes in Patients with Connective Tissue Diseases

approximated 100%. The mean value for percent B-cells among 51 normals tested was 22.9%±7.1; mean T-cells value was 75.3±13.95%. T-cell-specific antiserum stained 18% of normal human bone marrow lymphocytes, 42.5% of lymphocytes from normal spleens, and 98% of cells obtained from thoracic duct drainage of patients with RA. Specificity of

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Role of the T and B lymphocytes in pathogenesis of autoimmune thyroid diseases

Role of the T and B lymphocytes in pathogenesis of autoimmune thyroid diseases

Furthermore, basing on past scientific reports, it has been noted that all Treg cells, mostly with expression of FoxP3, contribute to prevention and pathogenesis of autoimmune diseases, including AITD [63, 96, 97]. Mentioned contribution of Tregs was subsequently con- firmed by development of AITD in humans that have qualitative or quantitative disturbances of Foxp3 expres- sion [98–101] and lesser concentration or lack of pTregs and tTregs [102, 103]. Considering both tTregs and pTregs, it was observed that they have a tendency to ac- cumulate in inflammated thyroid tissue [97, 103–105], whereas their count in peripheral blood widely varies in patients suffering from AITD. Nevertheless, it is clear that they are dysfunctional and unable perform their immunosuppressive functions in afflicted subjects [99, 102, 106]. Presumably, the reason for that phenomenon might be connected with possible conver- sion of Tregs to pro-inflammatory cells (mainly Th17and Th1 lymphocytes) [107–109], in the presence of different cytokines in thyroid’s inflammatory microenvironment (IL-2/IL-15 and IL-21/IL-23) [110, 111]. Regardless, there is a need of conducting further studies to prove this thesis. Development of AITD also depends on vulnerability of immune-regulatory genes and their final products of tran- scription, which are located on the surface of T regulatory cells such as FOXP3, CD25, and CLTA-4 (Fig. 2). These genes and their products are involved in ensuring proper maintenance of peripheral tolerance (FOXP3 and CD25) and establishing an appropriate co-stimulation (CLTA-4). Due to various factors, improper activity of these immune-regulatory genes would potentially lead to a breakdown in immune tolerance and ultimately autoim- munologic disease such as AITD [112]. Forkhead box P3 (FOXP3) is a gene located on chromosome X (Xp11) [113]. T regulatory cells are characterized by an expres- sion of FOXP3, whose involvement in the processes of dif- ferentiation, maintenance, and function of Treg cells is essential [99, 114–117]. In humans, disruptions in FOXP3 gene or deficiencies of this molecule lead to the syndrome comprising immune dysregulation, polyendocrinopathy and enteropathy (IPEX) [118–120], which is more com- mon in men. Diverse polymorphisms of FOXP3 gene have
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