scholarly journals ROLE OF THE THYMUS IN IMMUNE REACTIONS IN RATS

1962 ◽  
Vol 116 (2) ◽  
pp. 187-206 ◽  
Author(s):  
Byron H. Waksman ◽  
Barry G. Arnason ◽  
Branislav D. Janković
Keyword(s):  
Lymph Nodes ◽  
Plasma Cells ◽  
Germinal Centers ◽  
White Pulp ◽  
Size Number ◽  
Splenic White Pulp ◽  
Spleen And Lymph Nodes ◽  
Lymphoid Nodules ◽  
Lymphatic Organs

In rats thymectomized at birth, there was a profound depletion of small lymphocytes in various lymphatic organs. In the spleen, these cells were completely lacking from the Malpighian bodies and splenic white pulp. Empty reticular structures remained surrounding the white pulp arterioles. In the lymph nodes, large masses and nodules of small lymphocytes (primary lymphoid nodules) were either markedly depleted or absent, as were the zones of these cells normally surrounding germinal centers. In both spleen and nodes, germinal centers appeared normal in size, number, and cellular make-up; and plasma cells were found in normal or even increased number in their customary position. Rats which in spite of thymectomy developed intense Arthus or delayed reactivity showed incomplete depletion of the lymphoid tissue. It is concluded that small lymphocytes of the spleen and lymph nodes may come, in large part, directly from the thymus and are not derived from medium and large lymphocytes of the germinal centers. It is suggested that there may be a second population of small lymphocytes whose function is unrelated to the thymus lymphocytes.

scholarly journals Fc chimeric protein containing the cysteine-rich domain of the murine mannose receptor binds to macrophages from splenic marginal zone and lymph node subcapsular sinus and to germinal centers.

1996 ◽  
Vol 184 (5) ◽  
pp. 1927-1937 ◽  
Author(s):  
L Martínez-Pomares ◽  
M Kosco-Vilbois ◽  
E Darley ◽  
P Tree ◽  
S Herren ◽  
...  
Keyword(s):  
Lymph Node ◽  
Lymph Nodes ◽  
B Cell ◽  
Marginal Zone ◽  
Chimeric Protein ◽  
Mannose Receptor ◽  
Germinal Centers ◽  
White Pulp ◽  
Subcapsular Sinus ◽  
Splenic White Pulp

Ligands for the cysteine-rich (CR) domain of the mannose receptor (MR) were detected by incubating murine tissues with a chimeric protein containing CR fused to the Fc region of human IgG1 (CR-Fc). In naive mice, CR-Fc bound to sialoadhesin+, F4/80low/-, macrosialin+ macrophages (M phi) in spleen marginal zone (metallophilic M phi) and lymph node subcapsular sinus. Labeling was also observed in B cell areas of splenic white pulp. Western blotting analysis of spleen and lymph nodes lysates revealed a restricted number of molecules that interacted specifically with CR-Fc. In immunized mice, labeling was upregulated on germinal centers in splenic white pulp and follicular areas of lymph nodes. Kinetic analysis of the pattern of CR-Fc labeling in lymph nodes during a secondary immune response to ovalbumin showed that CR ligand expression migrated towards B cell areas, associated with cells displaying distinctive dendritic morphology, and accumulated in developing germinal centers. These studies suggest that MR+ cells or MR-carbohydrate-containing antigen complexes could be directed towards areas where humoral immune responses take place, through the interaction of the MR CR domain with molecules expressed in specialized macrophage populations and antigen transporting cells.

scholarly journals Crucial Role of Tumor Necrosis Factor Receptor 1 Expression on Nonhematopoietic Cells for B Cell Localization within the Splenic White Pulp

1998 ◽  
Vol 187 (4) ◽  
pp. 469-477 ◽  
Author(s):  
Maria Tkachuk ◽  
Stephan Bolliger ◽  
Bernhard Ryffel ◽  
Gerd Pluschke ◽  
Theresa A. Banks ◽  
...  
Keyword(s):  
B Cells ◽  
Tumor Necrosis ◽  
Plasma Cells ◽  
Tumor Necrosis Factor Receptor ◽  
White Pulp ◽  
Splenic White Pulp ◽  
Initial Activation ◽  
Deficient Mice ◽  
Necrosis Factor

During immune responses the initial activation of B cells takes place in T cell zones of periarteriolar lymphoid sheaths (PALS) of the splenic white pulp. After initial activation, B cells migrate into the primary follicles and, in association with follicular dendritic cells (FDCs), undergo clonal expansion and differentiation giving rise to germinal centers (GCs). Peanut agglutinin binding (PNA+) cells of the GC differentiate further into memory or plasma cells. Here we report that in tumor necrosis factor receptor 1–deficient mice (TNFR1−/−), the location of B cells was altered and that plasma cells were abnormally distributed in the splenic PALS. In contrast to lymphotoxin α–deficient mice (LTα−/−), bone marrow or fetal liver transplantation did not correct the abnormal organization of the spleen, location of B cells, the lack of an FDC network, nor the antibody response in TNFR1−/− mice. These results argue for a crucial role of TNFR1 expression on nonhematopoietic cells for the maintenance of the splenic architecture and proper B cell location. In addition, the lack in development of an FDC network after adoptive transfer suggests that either FDCs are not of bone marrow origin or that they depend on signals from nonhematopoietic cells for maturation.

DEFICIENCY OF IgM

PEDIATRICS ◽  
1971 ◽  
Vol 47 (2) ◽  
pp. 399-404
Author(s):  
W. P. Faulk ◽  
W. S. Kiyasu ◽  
M. D. Cooper ◽  
H. H. Fudenberg
Keyword(s):  
Lymph Nodes ◽  
Plasma Cells ◽  
Germinal Centers ◽  
Peyer's Patches ◽  
Peyer’S Patches ◽  
Pseudomonas Infection ◽  
Spleen And Lymph Nodes ◽  
Genetically Determined

An 8½-month-old infant with absent IgM had recurrent Pseudomonas infections. IgG and IgA, but no IgM-containing plasma cells, were identified in the spleen by immunofluorescence. The spleen and lymph nodes lacked germinal centers, but Peyer's patches and the appendix were normal. The absence of IgM was perhaps genetically determined because the father's serum IgM was also low. This may have predisposed to the Pseudomonas infection, since antibodies to Pseudomonas are predominantly IgM.

Experimental Trypanosoma brucei Infection in Deer Mice: Splenic Changes

1980 ◽  
Vol 17 (2) ◽  
pp. 218-225 ◽  
Author(s):  
J. E. Moulton
Keyword(s):  
Nervous System ◽  
Lymph Node ◽  
Lymph Nodes ◽  
Trypanosoma Brucei ◽  
Peromyscus Maniculatus ◽  
Plasma Cells ◽  
Germinal Centers ◽  
Deer Mice ◽  
Spleen And Lymph Nodes ◽  
Red Pulp

Forty deer mice (Peromyscus maniculatus) were infected with Trypanosoma brucei organisms and were killed 33 to 83 days after inoculation (average, 63). The outstanding lesion was infiltration of plasma cells in various tissues. These cells caused disruption of the periarteriolar lymphocytic sheaths and thickening of red pulp cords in the spleen. The lymph node was almost completely replaced by plasma cells. The spleen and lymph nodes also had marked hyperplasia of germinal centers and granulomatous-like proliferation of macrophages. The nervous system showed meningoencephalitis characterized by accumulations of plasma cells.

scholarly journals Morphometric and Histopathologic Analysis of Lymphoid Depletion in Murine Spleens Following Infection with Brucella abortus strains 2308 or RB51 or an htrA Deletion Mutant

1996 ◽  
Vol 33 (3) ◽  
pp. 282-289 ◽  
Author(s):  
M. V. Palmer ◽  
N. F. Cheville ◽  
F. M. Tatum
Keyword(s):  
Morphometric Analysis ◽  
Brucella Abortus ◽  
Marginal Zone ◽  
White Pulp ◽  
Splenic White Pulp ◽  
Lymphoid Depletion ◽  
Histopathologic Changes ◽  
Histopathologic Analysis ◽  
Marginal Zones

BALB/C mice were inoculated intraperitoneally with suspensions of Brucella abortus strains 2308 or RB51 or an htrA mutant. Spleens were examined on postinoculation day (PID) 2, 4, 7, 10, 15, 21, 30, and 60. Brucellae were cultured in high numbers from the spleens of mice infected with strains 2308 or htrA through PID 60; however, mice infected with strain RB51 cleared the infection between PID 30 and PID 60. Histopathologic changes in spleens from 2308-infected mice were characterized by marked accumulations of macrophages, which expanded marginal zones beginning as early as PID 7 and persisting through PID 60. Morphometric analysis showed a decrease in splenic white pulp in 2308-infected mice at PID 10, which correlated with the peak of bacterial infection. Although this decrease was significant ( P < 0.05) when compared with values at the previous (PID 7) and the following (PID 15) time periods, it was not significantly different from white pulp values noted at PID 2 or PID 4 or the values for control spleens. Spleens from RB51-infected mice showed only mild to moderate accumulations of macrophages in marginal zone areas during the peak of RB51 infection (PID 7-10). Morphometric analysis of RB51-infected spleens showed a decrease in white pulp area, which coincided with peak bacterial numbers. However, this decrease was not significant ( P > 0.05). Spleens from mice infected with the htrA mutant showed moderate to marked accumulations of macrophages in marginal zone areas, which persisted through PID 60. Multifocal necrosis in lymphoid follicles as early as PID 4 was seen in both htrA and 2308 infection. Morphometric analysis of htrA-infected spleens revealed no significant decrease in white pulp and no obvious correlation with bacterial numbers in the spleen. These results suggest that virulent B. abortus does not induce lymphoid depletion significantly below those values seen in noninfected mice; thus, the possible role of lymphoid depletion in the pathogenesis of brucellosis remains questionable.

scholarly journals Cyclical modulation of sphingosine-1-phosphate receptor 1 surface expression during lymphocyte recirculation and relationship to lymphoid organ transit

2005 ◽  
Vol 201 (2) ◽  
pp. 291-301 ◽  
Author(s):  
Charles G. Lo ◽  
Ying Xu ◽  
Richard L. Proia ◽  
Jason G. Cyster
Keyword(s):  
Lymph Nodes ◽  
Surface Expression ◽  
Lymphoid Organ ◽  
Lymphoid Organs ◽  
White Pulp ◽  
Activated T Cells ◽  
Circulating Lymphocytes ◽  
Sphingosine 1 Phosphate ◽  
Splenic White Pulp ◽  
Lymphocyte Egress

Sphingosine-1-phosphate receptor 1 (S1P1) was recently shown to be required for lymphocyte egress from lymphoid organs. Here we have examined the relationship between S1P1 abundance on the cell and egress efficiency. Using an integrin neutralization approach to separate the processes of entry and exit, we show that pertussis toxin treatment reduces lymphocyte egress from lymph nodes. Retrovirally mediated S1P1 overexpression is sufficient to reduce B cell accumulation in the splenic white pulp and to promote egress of activated T cells from lymph nodes, whereas S1P1+/−cells have reduced lymph node exit efficiency. Furthermore, lymphocyte S1P1 is down-regulated in the blood, up-regulated in lymphoid organs, and down-regulated again in the lymph. We propose that cyclical ligand-induced modulation of S1P1 on circulating lymphocytes contributes to establishing their lymphoid organ transit time.

The route of re-circulation of lymphocytes in the rat

1964 ◽  
Vol 159 (975) ◽  
pp. 257-282 ◽  
Keyword(s):  
Lymph Nodes ◽  
Thoracic Duct ◽  
Large Scale ◽  
Plasma Cells ◽  
Tritiated Thymidine ◽  
Autoradiographic Study ◽  
Total Output ◽  
White Pulp ◽  
Radioactive Label

The experiments presented in this paper support the idea that the output of small lymphocytes from the thoracic duct of the rat (about 10 9 /day) is normally maintained by a large-scale re-circulation of cells from the blood to the lymph. It has been shown that the main channel from blood to lymph lies with in the lymph nodes and that small lymphocytes enter the nodes by crossing the walls of a specialized set of blood vessels, the post-capillary venules. In order to trace the fate of small lymphocytes, cells from the thoracic duct of rats were incubated for 1 h in vitro with tritiated adenosine. This labelled the RNA of about 65% of the small lymphocytes and more than 95% of the large lymphocytes; it also labelled the DNA of a proportion of the large lymphocytes. The mixture of small and large labelled lymphocytes was transfused into the blood of two groups of rats which belonged to the same highly inbred strain as the cell donors. At various times after the transfusions the thoracic ducts in one group of rats were cannulated to determine the proportion of labelled cells which could be recovered in the lymph; at corresponding times, the rats in the other group were killed and autoradiographs prepared from their tissues to determine the location of the labelled cells. The radioactive label in the RNA of small lymphocytes was stable enough to ensure that the labelled small lymphocytes which were recovered in the lymph several days after a transfusion were those which had originally been transfused into the blood. When the thoracic duct was cannulated 20 to 27 h after a transfusion, about 70% of the labelled small lymphocytes which had been transfused into the blood could be recovered from the thoracic duct over a 5-day period of lymph collection. During the first 36 to 48 h after cannulation, while the total output of small lymphocytes was falling rapidly, the proportion of labelled cells in the lymph remained approximately constant. The pool of the animal’s own cells with which the labelled cells had mixed contained between 1·5 and 2 × 10 9 small lymphocytes; this was identified as the re-circulating pool. An autoradiographic study showed that after their transfusion into the blood the labelled small lymphocytes ‘homed’ rapidly and in large numbers into the lymph nodes, the white pulp of the spleen and the Peyer’s patches of the intestine. The concentration of labelled cells in other tissues was trivial in comparison. Labelled small lymphocytes were seen penetrating the endothelium of the post-capillary venules in the lymph nodes within 15 min of the start of a transfusion; they were traced into the cortex of the nodes and finally into the medullary lymph sinuses. Labelled small lymphocytes did not migrate into the adult thymus but a few entered the thymus of newborn rats. It was concluded that the re-circulating pool of small lymphocytes was located in the lymphoid tissue, the thymus excepted, and that the rapid ‘homing’ of cells into the lymph nodes had its basis in the special affinity of small lymphocytes for the endothelium of the post-capillary venules. The interpretation of these experiments was not complicated by the presence of large, as well as of small lymphocytes in the suspensions of labelled cells which were transfused. Other experiments, in which the large lymphocytes alone were labelled with tritiated thymidine, showed that most of them migrated from the blood into the wall of the gut where they assumed the appearance of primitive plasma cells; very few divided to form small lymphocytes.

scholarly journals AN ELECTRON MICROSCOPE STUDY OF LYMPHATIC TISSUE IN RUNT DISEASE

1965 ◽  
Vol 25 (3) ◽  
pp. 149-177 ◽  
Author(s):  
Leon Weiss ◽  
Alan C. Aisenberg
Keyword(s):  
Lymph Nodes ◽  
Plasma Cells ◽  
Cell Types ◽  
Sprague Dawley ◽  
Connective Tissues ◽  
Splenic Cells ◽  
Reticular Cells ◽  
Spleen And Lymph Nodes ◽  
Myelin Figure ◽  
Rats And Mice

The thymus, spleen, and lymph nodes were studied in runt disease induced by a graft of intravenously injected homologous splenic cells into newborn rats and mice. Adult Long-Evans cells (70 x 106) were injected into Sprague-Dawley rats. Adult DBA cells (7 x 106) were injected into C57BL/6 mice. Runted rats were sacrificed at 14 to 28 days of age; mice at 10 to 20 days. The thymic cortex is depleted of small lymphocytes. Those remaining are severely damaged and phagocytized. Evidence of damage includes swelling of mitochondria, myelin figure formation, margination of chromatin, and sharp angulation in nuclear contour. Large numbers of macrophages are present. Epithelial-reticular cells which envelop small cortical blood vessels are often retracted, with the result that the most peripheral layer in the thymic-blood barrier suffers abnormally large gaps. Lymphocytes of the periarterial lymphatic sheaths of spleen and of the cortex of lymph nodes are reduced in number and damaged. Vast numbers of plasma cells and many lymphocytes are evident throughout lymph nodes, in the periarterial lymphatic sheaths, and in the marginal zone and red pulp of the spleen. Plasma cells are of different sizes, the larger having dilated sacs of endoplasmic reticulum. Lymphocytes are small to medium in size. They contain, in varying quantity, ribosomes and smooth membrane-bounded cytoplasmic vesicles approximately 350 to 500 A in diameter. Most plasma cells and lymphocytes are damaged and many of these are phagocytized. Many lymphocytes in lymph nodes, however, show no evidence of damage. Reticular cells and other fixed cells of the connective tissues seldom appear affected. Thus, the major cell types reacting in runt disease are lymphocytes, plasma cells, and histiocytes or macrophages. It appears, therefore, that both the delayed and immediate types of sensitivity play a part in this disease.

scholarly journals Histological and histochemical changes in the peripheral organs of the immune system of dogs in cases of isoniazid poisoning

2021 ◽  
Vol 12 (3) ◽  
pp. 537-544
Author(s):  
G. I. Kotsyumbas ◽  
N. P. Vretsona
Keyword(s):  
Immune System ◽  
Lymph Nodes ◽  
Clinical Course ◽  
Clinical Diagnostics ◽  
Pathological Examination ◽  
White Pulp ◽  
Peripheral Organs ◽  
Vascular Walls ◽  
Spleen And Lymph Nodes ◽  
Histochemical Changes

Most publications on isoniazid poisoning in dogs are devoted to clinical diagnostics, treatment, and prevention of the disease. Histological and histochemical changes are not fully described, though they are important in assessing the toxic effects of isoniazid. Isoniazid is used to treat tuberculosis in humans. Dogs are hypersensitive to this drug. The article highlights the results of macroscopic, histological, and histochemical studies of the dogs’ lymph nodes and spleen in cases of isoniazid poisoning. A pathological examination of 19 corpses of dogs of different ages was performed, during which isoniazid poisoning was posthumously diagnosed, based on anamnesis, clinical signs, pathological autopsy, histological, and histochemical examination. Samples of lymph nodes and spleen were fixed in a 10% aqueous neutral formalin solution, Carnoy’s solution, and Bouin’s fixative. Histoсuts were prepared using a sled microtome and stained with hematoxylin and eosin. Staining was also performed according to the techniques suggested by McManus, Brachet, and Perls. The pathomorphological changes in lymph nodes and spleen were characterized by disorganization of vascular walls and connective tissue fibers of the stroma, dilatation of veins, their overflow with hemolyzed blood, and, in cases of the long clinical course, thrombosis of small vessels. Intravascular hemolysis of erythrocytes resulted in an excessive formation of hemosiderin. Histochemically, the spleen and lymph nodes showed a significant increase in the number of hemosiderophages in the spleen’s red and white pulp and the lymph nodes’ central sinuses and pulp cords. In the spleen, mucoid swelling and necrobiotic changes in the wall structures of the arterioles and arteries progressed with a narrowing of their lumen in dogs suffering from the long clinical course. Increased permeability of the microcirculatory tract vessels of the spleen and lymph nodes, transudate formation, and the destructive changes in the reticular skeleton accompanied hemodynamic violations. A sharp change in blood rheology caused the violation of trophism and metabolism in the immune system. Lymphoid elements of the lymph nodes and white pulp of the spleen were in a state of karyorrhexis and karyolysis. The morphological study of the immune system’s peripheral organs suggests that dogs poisoned by isoniazid demonstrate hemodynamic disorders, changes in the physicochemical properties of blood (hemolysis of erythrocytes and thrombosis). This is the basis of trophic disorders, metabolic malfunctions, and the development of dystrophic processes in all structural elements of the spleen and lymph nodes.

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