Mitogen response of peripheral blood and splenic lymphocytes and effect of 2-mercaptoethanol in tumor-bearing mice

1982 ◽  
Vol 12 (3) ◽  
Author(s):  
Yoshihiro Kikuchi ◽  
RaymondN. Hiramoto ◽  
VithalK. Ghanta
Keyword(s):  
Peripheral Blood ◽  
Splenic Lymphocytes ◽  
Tumor Bearing ◽  
Mitogen Response

The Effect of Partial Splenectomy on Platelet Production in Mice

1981 ◽  
Vol 46 (03) ◽  
pp. 602-603 ◽  
Author(s):  
H Bessler ◽  
I Notti ◽  
M Djaldetti
Keyword(s):  
Peripheral Blood ◽  
Blood Platelets ◽  
Operative Procedures ◽  
Partial Splenectomy ◽  
Splenic Lymphocytes ◽  
Platelet Production ◽  
Platelet Number ◽  
Spleen Lymphocytes

SummaryThe effect of total and partial splenectomy on the number and production of circulating platelets was studied in mice. Five days after total and partial splenectomy the number of the peripheral blood platelets increased by 87% and 60%, respectively and the incorporation of 75selenium methionine (75Se-Met) into platelets was enhanced indicating that the thrombocytosis was due to increased platelet production. The results obtained by the two operative procedures were compared.Since previous work from our laboratory has shown that a factor produced by splenic lymphocytes affects the platelet number in mice, it is suggested that the differences in the number of circulating platelets observed in animals after total and partial splenectomy may reflect a difference in the number of spleen lymphocytes removed.

scholarly journals Immunologic abnormalities in an animal model of chronic hypoplastic marrow failure induced by busulfan

Blood ◽  
1978 ◽  
Vol 51 (4) ◽  
pp. 601-610 ◽  
Author(s):  
CA Pugsley ◽  
IJ Forbes ◽  
AA Morley
Keyword(s):  
B Lymphocytes ◽  
Peripheral Blood ◽  
Blood Cells ◽  
Cell Injury ◽  
Cell Types ◽  
Peripheral Blood Lymphocytes ◽  
Delayed Type Hypersensitivity ◽  
Splenic Lymphocytes ◽  
Hypoplastic Marrow ◽  
Experimental Murine Model

Abstract The immunology of chronic hypoplastic marrow failure (CHMF, aplastic anemia) was studied in an experimental murine model of the disease induced by busulfan. B lymphocytes of peripheral blood, spleen, and bone marrow were reduced to 30%–40% and T lymphocytes of thymus, spleen, marrow, and blood were decreased to 20%–70% of control values. IgG and IgM antibody titer to sheep red blood cells were reduced to one- third of control levels, and splenic IgG, but not IgM, plaque-forming cells were fewer on day 7 after antigen stimulation. The proliferative responses to phytohemagglutinin or concanavalin A were reduced in cultures of peripheral blood lymphocytes, splenic lymphocytes, and thymocytes, and cutaneous delayed-type hypersensitivity induced by dinitrofluorobenze was not detected in mice with CHMF. The results demonstrate disturbance of a variety of cellular and humoral functions and suggest that the disturbance was due to quantitative and possibly qualitative abnormalities of the cell types subserving these functions. The results suggest that residual cell injury, the lesion underlying experimental CHMF, is not confined to the myeloid stem cell but also involved cells of the lymphoid series.

scholarly journals Etiologic aspects of cold agglutinin disease: evidence for cytogenetically defined clones of lymphoid cells and the demonstration that an anti-Pr cold autoantibody is derived from a chromosomally aberrant B cell clone

Blood ◽  
1986 ◽  
Vol 67 (6) ◽  
pp. 1705-1709 ◽  
Author(s):  
LE Silberstein ◽  
GA Robertson ◽  
AC Harris ◽  
L Moreau ◽  
E Besa ◽  
...  
Keyword(s):  
B Cell ◽  
Peripheral Blood ◽  
Cell Clone ◽  
Peripheral Blood Lymphocytes ◽  
Lymphoid Cells ◽  
Cold Agglutinin ◽  
Additional Patient ◽  
Splenic Lymphocytes ◽  
Cold Agglutinin Disease ◽  
Karyotypic Analysis

Abstract This study investigated the clonal nature of cold agglutinin disease in a series of nine patients, which included the benign or idiopathic form as well as cases with an underlying lymphoma. Surface marker phenotyping and karyotypic analysis were performed on peripheral blood lymphocytes. An increased proportion of B cells was found in four cases and in three of these patients a monoclonal B cell population was identified with a mu, kappa phenotype. In the same three cases, as well as an additional patient, an aberrant karyotype was demonstrated. The cytogenetic abnormality present in all four cases included trisomy 3; two patients also had a trisomy 12. One of these four patients had a well-differentiated lymphoma and underwent a splenectomy. Splenic lymphocytes were transformed with Epstein-Barr virus and cultured en masse. Eight clones were established producing the same cold agglutinin with identical specificity as that present in the patient's plasma. Five of these clones were studied cytogenetically, and all had the same abnormal karyotype (51,XX,+3,+9,+12,+13,+18) found in peripheral blood and splenic lymphocytes. Thus, in this case, the cold reactive autoantibody was produced by the chromosomally abnormal, neoplastic clone of lymphocytes. Our findings support the view that cold agglutinin disease represents a spectrum of clonal disorders.

In Vivo Visualization of Stat3 Activation in Myeloid Cells during Inflammation and Tumor Growth.

Blood ◽  
2004 ◽  
Vol 104 (11) ◽  
pp. 3434-3434
Author(s):  
Pedro Horna ◽  
Fengdong Cheng ◽  
Richard Jove ◽  
Linda Mora ◽  
Eduardo M. Sotomayor
Keyword(s):  
Steady State ◽  
Immune Responses ◽  
Tumor Growth ◽  
Peripheral Blood ◽  
Inflammatory Responses ◽  
Myeloid Cells ◽  
Tumor Bearing ◽  
Inflammatory Site ◽  
Number Of Cells

Abstract Signal transducer and activator of transcription 3 (Stat3) is a key mediator of several cytokine and growth factor signaling pathways. On myeloid cells, activation of Stat3 to its phosphorylated form (pStat3) has been shown to negatively regulate inflammatory responses and play a central role in the decision leading to immune activation versus immune tolerance of antigen-specific T-cells1. Little is still known however, about the status of Stat3 signaling in myeloid cells in the steady state and during ongoing immune responses in vivo. To address this question we recently developed flow-cytometric and immuno-histochemistry assays that have allowed us to visualize the in vivo dynamics of Stat3 activation in myeloid cells during immune responses leading to divergent outcomes: productive inflammatory response to adjuvant immunization and tumor-induced unresponsiveness or tolerance. In the steady state we found that in peripheral blood only Ly6G+ polymorphonuclear cells display a positive nuclear staining for pStat3. Analysis of lymphoid organs revealed that although Stat3 protein was expressed almost ubiquitously on spleen sections of normal mice, only a small number of cells were positive for pStat3. Following immunization with complete Freund adjuvant (CFA) a dramatic increase in the number of cells expressing pStat3 was observed in the peripheral blood and spleen of treated animals. Ly6G+ pStat3+ were rapidly recruited from the blood to the inflammatory site where they now displayed significantly decreased levels of pStat3. During the growth of a subcutaneous tumor, a similar increase in the number of cells expressing pStat3 was observed in the blood and spleen of tumor-bearing mice. Further analysis by flow cytometry revealed that pStat3 expression was restricted to two sub-populations: a) CD11b+ myeloid cells expressing the lineage marker Gr-1 and b) Ly6G− mononuclear cells unable to down-regulate Stat3 activity following their migration from the blood into peripheral tissues. In vivo depletion of Gr-1+ cells eliminated most of the pStat3+ cells in tumor bearing mice. The immunoregulatory properties of these Gr-1+ cells was highlighted by the demonstration that in their absence, in vivo immunization with a peptide derived from influenza hemagglutinin (HA) in CFA markedly enhanced the priming of anti-HA specific CD4+ T-cells. More importantly, in animals depleted of Gr-1+ cells, the outcome in response to a tolerogenic stimuli was T-cell activation rather than tolerance induction. Taken together, although similar changes in the number of cells expressing pStat3 was observed in response to adjuvant immunization and during tumor progression, an important difference might relate to the extent of Stat3 activation in myeloid cells following their migration to the site of stimuli. While down-regulation of Stat3 in myeloid cells at the inflammatory site is an early event during productive inflammatory responses, a sustained Stat3 activation in myeloid cells such as that observed during tumor growth may provide an explanation for the state of immune unresponsiveness associated with malignancies.

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