THE EFFECT OF HYPOPHYSECTOMY, ADRENALECTOMY AND CORTISONE ON THE INCORPORATION OF TRITIATED THYMIDINE IN RAT ORGANS, WITH SPECIAL REFERENCES TO THE LYMPHOID TISSUES

ABSTRACT After hypophysectomy, the incorporation of tritiated thymidine decreases in the thymus and spleen, but not in the lymph nodes. Adrenalectomy has no apparent influence on this incorporation. After prolonged treatment with moderate amounts of cortisone, the incorporation is significantly decreased in the thymus and spleen, but the slight decrease in the lymph nodes is not significant. In untreated animals the incorporation is of the same magnitude in all three lymphoid tissues. These results are compared with those obtained with 32P O4 – a method that gives a relatively higher incorporation in the thymus than in the spleen and lymph nodes. These values are more consistent with the mitotic indices of these organs. The reutilization of thymidine in the lymphoid organs is discussed. It is concluded that such a reutilization is a normal mechanism in the lymphoid tissues, and that it is markedly increased while under the influence of corticosteroids, particularly in the thymus.

Download Full-text

Histological Lesions and Replication Sites of PCV3 in Naturally Infected Pigs

Animals ◽

10.3390/ani11061520 ◽

2021 ◽

Vol 11 (6) ◽

pp. 1520

Author(s):

Elisa Rigo De Conti ◽

Talita Pilar Resende ◽

Lacey Marshall-Lund ◽

Albert Rovira ◽

Fabio Augusto Vannucci

Keyword(s):

In Situ Hybridization ◽

Lymph Nodes ◽

Real Time ◽

Real Time Pcr ◽

Systemic Vasculitis ◽

Tissue Type ◽

Lymphoid Tissues ◽

Associated Diseases ◽

Spleen And Lymph Nodes

Porcine circovirus type 3 (PCV3) has been recently described as a potential cause of abortions and systemic vasculitis in pigs. Although the virus has been detected by real-time PCR in several porcine tissues from countries worldwide, PCV3-associated diseases have not been satisfactorily clarified. The objective of this study was to investigate the association between the presence of PCV3 mRNA detected by in situ hybridization (ISH) within histological lesions and PCV3 DNA detected by real-time PCR in naturally infected pigs. A total of 25 PCV3 PCR-positive cases were analyzed. Formalin-fixed tissues from these cases were evaluated for histologic lesions and for ISH-RNA positive signals for PCV3. The most frequent tissue type with histopathologic lesions was heart, 76.2%, with lymphoplasmacytic myocarditis and epicarditis as the most frequent lesions observed. Lymphoplasmacytic interstitial pneumonia was also a frequent finding, 47.6%. There were also lesions in kidney, liver, spleen and lymph nodes. PCV3-ISH-RNA positive signals were mostly observed in association with lymphoplasmacytic inflammatory infiltrate in various tissues, including arteries. Based on our results, the minimum set of specimens to be submitted for histopathology and mRNA in situ hybridization to confirm or exclude a diagnosis of PCV3 are heart, lung and lymphoid tissues (i.e., spleen and lymph nodes), especially for differential diagnosis related with PCV2-associated diseases.

Download Full-text

Deoxynivalenol in the liver and lymphoid organs of rats: effects of dose and duration on immunohistological changes

World Mycotoxin Journal ◽

10.3920/wmj2016.2094 ◽

2017 ◽

Vol 10 (1) ◽

pp. 89-96 ◽

Cited By ~ 7

Author(s):

A.P.F.L. Bracarense ◽

K.M. Basso ◽

E.O. Da Silva ◽

D. Payros ◽

I.P. Oswald

Keyword(s):

Lymph Nodes ◽

Control Diet ◽

Lymphoid Organs ◽

Hepatocyte Proliferation ◽

Dependent Manner ◽

Histological Changes ◽

Lymphoid Depletion ◽

Spleen And Lymph Nodes ◽

Cytoplasmic Vacuolisation ◽

Immunohistochemical Analyses

Deoxynivalenol (DON) is one of the most prevalent type B trichothecenes present in food inducing adverse effects, including intestinal changes and immunosuppression. The aim of the present study was to investigate the effects of DON on rats exposed for 7, 14 and 28 days to mycotoxin-contaminated diets, using histological and immunohistochemical analyses on liver and lymphoid organs. Fifty rats received a control diet, or a diet contaminated with 1.75 mg/kg of DON for 30 days, or a diet contaminated with 11.4 mg/kg of DON for 7, 14 or 30 days. Ingestion of contaminated feed induced a significant increase in the lesional score in the liver, spleen, and lymph nodes. The main histological findings observed in the liver were cytoplasmic vacuolisation and hepatocelular megalocytosis. A significant increase in hepatocyte proliferation was observed in rats that received 1.75 mg/kg of DON. Lymphoid depletion was the main histological alteration observed in lymphoid organs, resulting in a significant increase in the lesional score in all groups that received the contaminated diets. The histological changes and lymphocyte apoptosis were more severe in lymph nodes of rats fed 11.4 mg/kg of DON during 30 days. The results of the morphological and immunohistochemical analyses suggest that the ingestion of DON can induce functional hepatic impairment and immunosuppression in a dose- and time-dependent manner.

Download Full-text

RESISTANCE OF LONG-LIVED LYMPHOCYTES AND PLASMA CELLS IN RAT LYMPH NODES TO TREATMENT WITH PREDNISONE, CYCLOPHOSPHAMIDE, 6-MERCAPTOPURINE, AND ACTINOMYCIN D

Journal of Experimental Medicine ◽

10.1084/jem.126.1.109 ◽

1967 ◽

Vol 126 (1) ◽

pp. 109-125 ◽

Cited By ~ 71

Author(s):

John J. Miller ◽

Leonard J. Cole

Keyword(s):

Lymph Nodes ◽

Autoimmune Diseases ◽

Actinomycin D ◽

Plasma Cells ◽

Tritiated Thymidine ◽

Lymphoid Tissues ◽

Organ Transplants ◽

Appreciable Effect ◽

Low Doses ◽

Popliteal Lymph Nodes

The cells of the popliteal lymph nodes of rats were labeled for 4 days after a secondary immunological stimulus. 31 days after the last dose of tritiated thymidine, groups of rats were started on courses of daily, intraperitoneal injections of prednisone, cyclophosphamide, 6-mercaptopurine, or actinomycin D. The initially low doses of these agents were doubled in successive weeks until either lymphoid hypoplasia or death occurred. Rats from each group were killed weekly, and the percentages of persisting, labeled small lymphocytes in the popliteal nodes were determined. Sections of these nodes were examined for persisting, labeled plasma cells. The per cent of lymphocytes labeled increased while the total number of lymphocytes decreased during treatment with prednisone and cyclophosphamide. Prednisone decreased the numbers of long-lived plasma cells, but these cells were preferentially resistant to cyclophosphamide. Neither 6-mercaptopurine nor actinomycin D had an appreciable effect on lymphoid tissues histologically nor on the proportions of labeled, long-lived lymphocytes and plasma cells before causing the deaths of the rats receiving them. These results indicate that long-lived lymphocytes and plasma cells survive treatment with the immunolytic drugs studied, and that long-lived lymphocytes are specifically resistant to prednisone and cyclophosphamide. We believe these results have an application to the attempts to find drugs useful in the treatment of immunologic rejections of organ transplants, and for therapy of autoimmune diseases.

Download Full-text

Regulation of murine lymphokine production in vivo. III. The lymphoid tissue microenvironment exerts regulatory influences over T helper cell function.

Journal of Experimental Medicine ◽

10.1084/jem.171.4.979 ◽

1990 ◽

Vol 171 (4) ◽

pp. 979-996 ◽

Cited By ~ 221

Author(s):

R A Daynes ◽

B A Araneo ◽

T A Dowell ◽

K Huang ◽

D Dudley

Keyword(s):

T Cells ◽

T Cell ◽

Lymph Nodes ◽

Steroid Hormones ◽

Lymphoid Tissue ◽

Specific Antigen ◽

Distinct Species ◽

Lymphoid Organs ◽

Lymphoid Cells ◽

Lymphoid Tissues

We investigated the capacity of murine T lymphocytes, isolated from various lymphoid organs of normal or antigen-primed donors, to produce IL-2 or IL-4 after activation with anti-CD3 or specific antigen. Our results established that T cells resident within lymphoid organs being drained by nonmucosal tissue sites (e.g., axillary, inguinal, brachial lymph nodes, or spleen) produced IL-2 as the predominant T cell growth factor (TCGF) after activation. Conversely, activated T cells from lymphoid organs being drained by mucosal tissues (Peyer's patches, and cervical, periaortic, and parathymic lymph nodes) produced IL-4 as the major species of TCGF. Analysis of the lymphoid tissues obtained from adoptive recipients of antigen-primed lymphocytes provided by syngeneic donors provided evidence that direct influences were being exerted on T cells during their residence within defined lymphoid compartments. These lymphoid tissue influences appeared to be responsible for altering the potential of resident T cells to produce distinct species of TCGF. Steroid hormones, known transcriptional enhancers and repressors of specific cellular genes, were implicated in the controlling mechanisms over TCGF production. Glucocorticoids (GCs) were found to exert a systemic effect on all recirculating T cells, evidenced by a marked dominance in IL-4 production by T cells obtained from all lymphoid organs of GC-treated mice, or after a direct exposure of normal lymphoid cells to GCs in vitro before cellular activation with T cell mitogens. Further, the androgen steroid DHEA appeared to be responsible for providing an epigenetic influence to T cells trafficking through peripheral lymphoid organs. This steroid influence resulted in an enhanced potential for IL-2 secretion after activation. Anatomic compartmentalization of the DHEA-facilitated influence appears to be mediated by differential levels of DHEA-sulfatase in lymphoid tissues. DHEA-sulfatase is an enzyme capable of converting DHEA-sulfate (inactive) to the active hormone DHEA. We find very high activities of this enzyme isolated in murine macrophages. The implications of our findings to immunobiology are very great, and indicate that T cells, while clonally restricted for antigen peptide recognition, also appear to exhibit an extreme flexibility with regards to the species of lymphokines they produce after activation. Regulation of this highly conservative mechanism appears to be partially, if not exclusively, controlled by cellular influences being exerted by distinct species of steroid hormones, supplied in an endocrine or a paracrine manner where they mediate either systemic or tissue-localized influences, respectively.(ABSTRACT TRUNCATED AT 400 WORDS)

Download Full-text

Incidence of Apoptosis in the Lymphoid Organs of Normal or Malaria Infected Mice is Decreased in CD18 and Urokinase - Receptor (UPAR, CD87) Deficient Mice

Developmental Immunology ◽

10.1155/2001/75259 ◽

2001 ◽

Vol 8 (3-4) ◽

pp. 183-191 ◽

Cited By ~ 5

Author(s):

Pierre Francois Piguet ◽

Chen da Laperrousaz ◽

Christian Vesin ◽

Yves Donati

Keyword(s):

Lymph Nodes ◽

Annexin V ◽

Urokinase Receptor ◽

Lymphoid Organs ◽

White Pulp ◽

Facs Analysis ◽

Surface Molecules ◽

Spleen And Lymph Nodes ◽

Serum Igg Levels ◽

Deficient Mice

Incidence of apoptosis was investigated in the spleen and lymph nodes of +/+, CD18 -/- and urokinase receptor (uPAR, CD87) -/- mice, untreated orPlasmodium Berghei Anka(PbA) infected. In non infected mice, incidence of apoptosis was lower in the lymph nodes of CD18 -/- and uPAR -/- than in +/+ mice, as seen by FACS analysis to count the number of hypodiploid and Annexin-V binding cells. Infection of mice with PbA resulted in a marked increase in the size of spleen and lymph nodes 7–8 days after infection, which was slightly higher in uPAR -/- and CD18 -/- than in +/+ mice. PbA infection increased about 7 fold the incidence of apoptosis in the lymphoid organs of +/+, especially in the white pulp and germinal centers of the spleen and lymph nodes, while in contrast it was unchanged in PbA infected CD18 -/- or uPAR -/- mice. Serum IgG levels, and number of circulating leukocytes were significantly higher in both uPAR and CD18 -/- than in +/+ mice. These results indicate that the CD18 and uPAR surface molecules, which are known to be associated in the cell membrane, have an important influence upon the incidence of cell survival in both normal or stimulated lymphoid organs.

Download Full-text

HIV-1 infection and pathogenesis in a novel humanized mouse model

Blood ◽

10.1182/blood-2006-07-033159 ◽

2006 ◽

Vol 109 (7) ◽

pp. 2978-2981 ◽

Cited By ~ 113

Author(s):

Liguo Zhang ◽

Grigoriy I. Kovalev ◽

Lishan Su

Keyword(s):

T Cells ◽

Lymph Nodes ◽

Productive Infection ◽

In Vivo Model ◽

Lymphoid Tissues ◽

Dependent Manner ◽

Double Knockout ◽

Hematopoietic Stem ◽

Spleen And Lymph Nodes ◽

Hiv 1

Abstract The Rag2-γC double-knockout (DKO) mouse lacks T, B, and natural killer (NK) cells, and allows development of a functional human immune system with human CD34+ hematopoietic stem/progenitor cells (DKO-hu HSCs). Normal human T, B, and dendritic cells are present in peripheral blood, thymus, spleen, and lymph nodes. We report that both CCR5 and CXCR4 are expressed on human immature and mature T cells. DKO-hu HSC mice allow efficient HIV-1 infection with plasma high viremia. High levels of productive infection occur in the thymus, spleen, and lymph nodes. Human CD4+ T cells are gradually depleted by HIV-1 in a dose-dependent manner. In addition, HIV-1 infection persists in infected DKO-hu HSC mice for at least 19 weeks, with infectious HIV-1 in lymphoid tissues. Thus, the DKO-hu HSC mouse can serve as a relevant in vivo model to investigate mechanisms of HIV-1 infection and immunopathogenesis as well as to develop anti–HIV-1 therapeutics.

Download Full-text

Migration patterns of dendritic cells in the mouse. Traffic from the blood, and T cell-dependent and -independent entry to lymphoid tissues.

Journal of Experimental Medicine ◽

10.1084/jem.167.2.632 ◽

1988 ◽

Vol 167 (2) ◽

pp. 632-645 ◽

Cited By ~ 147

Author(s):

J W Kupiec-Weglinski ◽

J M Austyn ◽

P J Morris

Keyword(s):

T Cells ◽

Dendritic Cells ◽

Lymph Nodes ◽

Nude Mice ◽

Specific Activity ◽

Lymphoid Tissues ◽

Migration Patterns ◽

Peripheral Lymph ◽

Accessory Cells ◽

Spleen And Lymph Nodes

Dendritic cells (DC) are critical accessory cells for primary immune responses and they may be important stimulators of transplantation reactions, but little is known of their traffic into the tissues. We have studied the migration of purified splenic DC and T lymphocytes, labeled with 111Indium-tropolone, in syngeneic and allogeneic mice. First we demonstrate that DC can migrate from the blood into some lymphoid and nonlymphoid tissues. Immediately after intravenous administration, radio-labeled DC were sequestered in the lungs, but they actively migrated into the liver and spleen and reached equilibrium levels between 3 and 24 h after transfer. At least half of the radiolabel accumulated in the liver, but the spleen was the principal site of DC localization in terms of specific activity (radiolabel per weight of tissue). DC were unable to enter Peyer's patches, or mesenteric and other peripheral lymph nodes from the bloodstream. This was also true in splenectomized recipients, where the otherwise spleen-seeking DC were quantitatively diverted to the liver. In contrast, T cells homed readily to the spleen and lymph nodes of normal mice and increased numbers were present in these tissues in splenectomized mice. Thus, unlike T cells, DC cannot recirculate from blood to lymph via the nodes. We then show that migration of DC from the blood into the spleen is dependent on the presence of T cells: DC did not enter the spleens of nude mice, but when they were reconstituted with T cells the numbers entering the spleen resembled those in euthymic mice. In nude mice, as in splenectomized recipients, the DC that would normally enter the spleen were quantitatively diverted to the liver. These findings suggest that there is a spleen-liver equilibrium for DC, that may be akin to that existing between spleen and lymph node for T cells. Finally, we followed the traffic of radiolabeled DC via the afferent lymphatics after subcutaneous footpad inoculation. DC accumulated in the popliteal nodes but did not migrate further to the inguinal nodes. There was no difference between euthymic and nude mice, showing that unlike traffic to the spleen, this route probably does not require T cells. These migration patterns were not affected by major histocompatibility barriers, and were only seen with viable, but not glutaraldehyde-fixed, DC.(ABSTRACT TRUNCATED AT 400 WORDS)

Download Full-text

Development of Accessory Cells in B-Cell Compartments Is Retarted in B-Cell-Depleted Fetal Sheep

Developmental Immunology ◽

10.1155/1998/27025 ◽

1998 ◽

Vol 6 (3-4) ◽

pp. 223-231 ◽

Cited By ~ 6

Author(s):

Charles Mcl. Press ◽

John D. Reynolds ◽

Susan J. McClure ◽

Thor Landsverk

Keyword(s):

Lymph Nodes ◽

B Cell ◽

Cell Populations ◽

Accessory Cell ◽

Lymphoid Tissues ◽

Peyer’S Patch ◽

Peyer's Patch ◽

Fetal Sheep ◽

Cell Compartments ◽

Spleen And Lymph Nodes

Accessory-cell populations in the lymphoid tissues of fetal sheep were investigated following depletion of B cells. An intraperitoneal injection of an anti-IgM antibody early in gestation resulted in a marked depletion of IgM+cells in lymphoid tissues. Immune and enzyme histochemical techniques were used to identify accessory-cell populations in the ileal Peyer's patch, spleen, and lymph nodes of B-cell-depleted fetal sheep. The rudimentary follicles in the ileal Peyer's patch showed strong enzyme reactivity for 5′ nucleotidase, indicating the presence of follicular dendritic cells (FDCs). Enzyme reactivities for FDCs in primary follicles of the spleen and lymph nodes were absent, as were reactivities for metallophilic macrophages in the marginal zone of the spleen. MgATPase reactivity associated with dendritic-cell populations in the gut-associated lymphoid tissues was detected. A monoclonal antibody against complement receptor-2 (CD21) reacted with FDCs in the rudimentary follicles of the ileal Peyer's patch and immature FDCs in lymph nodes. The results suggest that the development of accessory-cell populations in B-cell compartments of peripheral but not central lymphoid tissues is dependent on the presence of B cells.

Download Full-text

B1 Lymphocytes and Myeloid Dendritic Cells in Lymphoid Organs Are Preferential Extratumoral Sites of Parvovirus Minute Virus of Mice Prototype Strain Expression

Journal of Virology ◽

10.1128/jvi.79.6.3517-3524.2005 ◽

2005 ◽

Vol 79 (6) ◽

pp. 3517-3524 ◽

Cited By ~ 9

Author(s):

Zahari Raykov ◽

Larissa Savelyeva ◽

Ginette Balboni ◽

Thomas Giese ◽

Jean Rommelaere ◽

...

Keyword(s):

Gene Expression ◽

Dendritic Cells ◽

Lymph Nodes ◽

Therapeutic Potential ◽

Prototype Strain ◽

Lymphoid Organs ◽

Lymphoid Tissues ◽

Myeloid Dendritic Cells ◽

Minute Virus Of Mice ◽

Minute Virus

ABSTRACT Due to their oncolytic properties and apathogenicity, autonomous parvoviruses have attracted significant interest as possible anticancer agents. Recent preclinical studies provided evidence of the therapeutic potential of minute virus of mice prototype strain (MVMp) and its recombinant derivatives. In a murine model of hemangiosarcoma, positive therapeutic outcome correlated with high intratumoral expression of MVMp-encoded genes in tumors and lymphoid organs, especially in tumor-draining lymph nodes. The source and relevance of this extratumoral expression, which came as a surprise because of the known fibrotropism of MVMp, remained unclear. In the present study, we investigated (i) whether the observed expression pattern occurs in different tumor models, (ii) which cell population is targeted by the virus, and (iii) the immunological consequences of this infection. Significant MVMp gene expression was detected in lymphoid tissues from infected tumor-free as well as melanoma-, lymphoma-, and hemangiosarcoma-bearing mice. This expression was especially marked in lymph nodes draining virus-injected tumors. Fluorescent in situ hybridization analysis, multicolor fluorescence-activated cell sorting, and quantitative reverse transcription-PCR revealed that MVMp was expressed in rare subpopulations of CD11b (Mac1)-positive cells displaying CD11c+ (myeloid dendritic cells [MDC]) or CD45B (B220+ [B1 lymphocytes]) markers. Apart from the late deletion of cytotoxic memory cells (CD8+ CD44+ CD62L−), this infection did not lead to significant alteration of the immunological profile of cells populating lymphoid organs. However, subtle changes were detected in the production of specific proinflammatory cytokines in lymph nodes from virus-treated animals. Considering the role of B1 lymphocytes and MDC in cancer and immunological surveillance, the specific ability of these cell types to sustain parvovirus-driven gene expression may be exploited in gene therapy protocols.

Download Full-text

Dynamics of CCR5 Expression by CD4+ T Cells in Lymphoid Tissues during Simian Immunodeficiency Virus Infection

Journal of Virology ◽

10.1128/jvi.74.23.11001-11007.2000 ◽

2000 ◽

Vol 74 (23) ◽

pp. 11001-11007 ◽

Cited By ~ 181

Author(s):

Ronald S. Veazey ◽

Keith G. Mansfield ◽

Irene C. Tham ◽

Angela C. Carville ◽

Daniel E. Shvetz ◽

...

Keyword(s):

T Cells ◽

T Cell ◽

Lymph Nodes ◽

Simian Immunodeficiency Virus ◽

Cell Loss ◽

Lymphoid Tissues ◽

Immunodeficiency Virus ◽

Siv Infection ◽

Spleen And Lymph Nodes

ABSTRACT Early viral replication and profound CD4+ T-cell depletion occur preferentially in intestinal tissues of macaques infected with simian immunodeficiency virus (SIV). Here we show that a much higher percentage of CD4+ T cells in the intestine express CCR5 compared with those found in the peripheral blood, spleen, or lymph nodes. In addition, the selectivity and extent of the CD4+ T-cell loss in SIV infection may depend upon these cells coexpressing CCR5 and having a “memory” phenotype (CD45RA−). Following intravenous infection with SIVmac251, memory CD4+ CCR5+ T cells were selectively eliminated within 14 days in all major lymphoid tissues (intestine, spleen, and lymph nodes). However, the effect on CD4+T-cell numbers was most profound in the intestine, where cells of this phenotype predominate. The CD4+ T cells that remain after 14 days of infection lacked CCR5 and/or were naive (CD45RA+). Furthermore, when animals in the terminal stages of SIV infection (with AIDS) were examined, virtually no CCR5-expressing CD4+ T cells were found in lymphoid tissues, and all of the remaining CD4+ T cells were naive and coexpressed CXCR4. These findings suggest that chemokine receptor usage determines which cells are targeted for SIV infection and elimination in vivo.

Download Full-text