Acquired tolerance of turkeys to Rous sarcoma agent

1956 ◽  
Vol 146 (922) ◽  
pp. 59-66 ◽  
Keyword(s):  
Blood Cells ◽  
Intramuscular Injection ◽  
Strong Support ◽  
Skin Transplantation ◽  
Turkey Poult ◽  
Rous Sarcoma ◽  
Virus Tolerance ◽  
Transplantation Antigens ◽  
Intravenous Inoculation ◽  
Host Component

Five- to eight-weeks old A.M.B. turkeys cannot be infected by intramuscular injection with cell-free Rous tumour agent unless they have been made tolerant by intravenous inoculation at 1 day old with whole blood or with washed blood cells from young normal chickens of the strain in which the sarcoma is usually propagated. The duration of the immunologically null period in the turkey poult has been investigated together with the specificity and stability of the tolerance-producing antigens and their relationship to skin transplantation antigens. The results afford strong support for the existence of at least one immunologically distinctive host component for the Rous agent, and this method of investigation, i.e. the production of virus tolerance in another species with identifiable antigens (possible sources of which are discussed), appears to offer an opportunity for identifying such a component or components.

scholarly journals INCREASING NONSPECIFIC STABILITY OF SERVICE DOGS

2021 ◽  
Vol 245 (1) ◽  
pp. 64-71
Author(s):  
A.A. Ishtudov ◽  
◽  
V.G. Semenov ◽  
D.A. Nikitin ◽  
E.N. Ivanova ◽  
...  
Keyword(s):  
Blood Cells ◽  
Intramuscular Injection ◽  
White Blood Cells ◽  
Service Dogs ◽  
German Shepherd ◽  
Nonspecific Resistance ◽  
Humoral Factors ◽  
Wide Range ◽  
Biochemical Profiles ◽  
The Right

A biopreparation Dog-Stim-N-B was developed and a scientific and practical justification was given for its feasibility in the canine center for raising dogs of the German shepherd breed. Se-lective mobilization of morphological and biochemical profiles of blood, cellular and humoral factors of nonspecific resistance of dog organism is established against the background of intramuscular injection of first-tested biopreparation Dog-Stim-N-B and previously tested Prevention-N-E. The biologics used in the experiments showed a wide range of bio-effects: activated the production of red blood cells and increased the concentration of hemoglobin in the blood of dogs, that is, im-proved hematopoiesis, but did not have a stimulating effect on the production of white blood cells; caused physiological eosinophilia, moderate neutrophylopenia with neutrophilic nucleus shift to the right and lymphocytosis; increased protein metabolism, mainly due to synthesis of albumin and γ-globulin fractions; activated cellular and humoral factors of nonspecific resistance of the organism.

scholarly journals Critical requirement for Stat5 in a mouse model of polycythemia vera

Blood ◽  
2012 ◽  
Vol 119 (15) ◽  
pp. 3539-3549 ◽  
Author(s):  
Dongqing Yan ◽  
Robert E. Hutchison ◽  
Golam Mohi
Keyword(s):  
Polycythemia Vera ◽  
Blood Cells ◽  
Myeloproliferative Neoplasms ◽  
White Blood Cells ◽  
Strong Support ◽  
Primary Myelofibrosis ◽  
Blood Parameters ◽  
Critical Function ◽  
Critical Requirement ◽  
Multiple Signaling

The JAK2V617F mutation has been identified in most cases of Ph-negative myeloproliferative neoplasms (MPNs) including polycythemia vera (PV), essential thrombocythemia (ET), and primary myelofibrosis (PMF). Expression of JAK2V617F results in constitutive activation of multiple signaling molecules/pathways. However, the key signaling downstream of JAK2V617F required for transformation and induction of MPNs remains elusive. Using a mouse genetic strategy, we show here that Stat5 is absolutely required for the pathogenesis of PV induced by Jak2V617F. Whereas expression of Jak2V617F in mice resulted in all the features of human PV, including an increase in red blood cells, hemoglobin, hematocrit, white blood cells, platelets, and splenomegaly, deletion of Stat5 in the Jak2V617F knockin mice normalized all the blood parameters and the spleen size. Furthermore, deletion of Stat5 completely abrogated erythropoietin (Epo)–independent erythroid colony formation evoked by Jak2V617F, a hallmark feature of PV. Re-expression of Stat5 in Stat5-deficient Jak2V617F knockin mice completely rescued the defects in transformation of hematopoietic progenitors and the PV phenotype. Together, these results indicate a critical function for Stat5 in the pathogenesis of PV. These findings also provide strong support for the development of Stat5 inhibitors as targeted therapies for the treatment of PV and other JAK2V617F-positive MPNs.

Critical Role for Stat5 in the Initiation and Maintenance of Polycythemia Vera in a Jak2V617F Knock-In Mouse Model

Blood ◽  
2011 ◽  
Vol 118 (21) ◽  
pp. 121-121 ◽  
Author(s):  
Dongqing Yan ◽  
Golam Mohi
Keyword(s):  
Polycythemia Vera ◽  
Blood Cells ◽  
Conflicts Of Interest ◽  
Myeloproliferative Neoplasms ◽  
Critical Role ◽  
Flow Cytometric Analysis ◽  
Strong Support ◽  
Blood Parameters ◽  
Cyclin D2 ◽  
P70s6 Kinase

Abstract Abstract 121 Version:1.0 StartHTML:0000000207 EndHTML:0000006199 StartFragment:0000002599 EndFragment:0000006163 SourceURL:file://localhost/Users/mohim/Desktop/ASH%202011/Dongqing%20Yan%202011%20ASH%20Abstract.doc The JAK2V617F mutation has been identified in most cases of Ph-negative myeloproliferative neoplasms (MPNs) including polycythemia vera (PV), essential thrombocythemia (ET) and primary myelofibrosis (PMF). Expression of JAK2V617F results in constitutive activation of multiple signaling molecules/pathways. However, the key signaling downstream of JAK2V617F required for transformation, induction and maintenance of MPNs remains elusive. Using a mouse genetic strategy, we found that Stat5 is absolutely required for the pathogenesis of PV induced by Jak2V617F. Whereas inducible expression of Jak2V617F in mice resulted in all the features of human PV, including increase in red blood cells, hemoglobin, hematocrit, white blood cells, platelets, and splenomegaly, deletion of Stat5 in the Jak2V617F knock-in mice normalized all the blood parameters and the spleen size. Histopathologic analyses revealed that Stat5 deficiency blocked the development of PV in mice expressing Jak2V617F. In addition, deletion of Stat5 completely abrogated erythropoietin (Epo)-independent erythroid colony formation evoked by Jak2V617F, a hallmark feature of PV. Flow cytometric analysis revealed that concomitant deletion of Stat5 reduced the Jak2V617F-induced expansion of LSK (lin−Sca-1+c-kit+) and MEP (megakaryocyte-erythroid progenitors) as well as CD71+Ter119+ and Gr-1+Mac-1+ populations to normal levels. Unlike Jak2V617F knock-in mice, which developed myelofibrosis at old age, Stat5-deficient Jak2V617F-expressing mice failed to develop myelofibrosis. Re-expression of Stat5 in Stat5-deficient Jak2V617F knock-in mice bone marrow by retroviral transduction completely rescued the defects in transformation of hematopoietic progenitors and the PV phenotype. Furthermore, deletion of Stat5 after establishment of PV disease in the transplanted animals expressing Jak2V617F by injection with polyinosine:polycytosine (pI:pC) normalized the blood parameters and inhibited the progression of the disease. Together, these results indicate a critical function for Stat5 in the induction and maintenance of PV. Biochemical analyses revealed that Stat5 deficiency significantly inhibited constitutive phosphorylation of p70S6 kinase and markedly reduced expression of Bcl-xL, Cyclin-D2 and Pim-1 mediated by Jak2V617F. These suggest that p70S6 kinase, Bcl-xL, Cyclin-D2 and Pim-1 are downstream targets of Jak2V617F-Stat5 signaling, and they may play a role in hematopoietic transformation induced by Jak2V617F. These findings provide strong support for the development of Stat5 inhibitors as targeted therapies for the treatment of PV and other JAK2V617F-positive MPNs. Disclosures: No relevant conflicts of interest to declare.

scholarly journals Genetic Studies of the β-Hairpin Loop of Rous Sarcoma Virus Capsid Protein

2006 ◽  
Vol 81 (3) ◽  
pp. 1288-1296 ◽  
Author(s):  
Jared L. Spidel ◽  
Carol B. Wilson ◽  
Rebecca C. Craven ◽  
John W. Wills
Keyword(s):  
Binding Site ◽  
Rous Sarcoma Virus ◽  
Critical Role ◽  
Strong Support ◽  
Genome Replication ◽  
Consensus Binding Site ◽  
Rous Sarcoma ◽  
Capsid Shell ◽  
Sarcoma Virus

ABSTRACT The first few residues of the Rous sarcoma virus (RSV) CA protein comprise a structurally dynamic region that forms part of a Gag-Gag interface in immature virus particles. Dissociation of this interaction during maturation allows refolding and formation of a β-hairpin structure important for assembly of CA monomers into the mature capsid shell. A consensus binding site for the cellular Ubc9 protein was previously identified within this region, suggesting that binding of Ubc9 and subsequent small ubiquitin-like modifier protein 1 (SUMO-1) modification of CA may play a role either in regulating the assembly activity of CA in immature particles or mature cores or in controlling postentry function(s) during the establishment of infection. In the present study, mutations designed to eliminate the consensus binding site were used to dissect the potentially overlapping functions of these residues. The resulting replication defects could not be traced to a failure to form particles of normal composition but, rather, to a deficit in genome replication. Genetic suppressors of two detrimental β-hairpin mutations improved infectivity without restoring the consensus site or creating a novel one elsewhere. Optimal restoration of infectivity to a Lys-to-Arg mutant required a combination of secondary changes, one on the surface of each domain of CA. Rather than arguing for a critical role of Ubc9 and SUMO in RSV replication, these findings provide strong support for a structural role of the N-terminal residues and a particularly striking example of long-range interactions between regions of CA in achieving a functional core competent for genome replication.

scholarly journals THE DIPHASIC NATURE OF TUBERCULOSIS IN RABBITS AFTER INTRAVENOUS INOCULATION WITH BOVINE TUBERCLE BACILLI

1932 ◽  
Vol 56 (2) ◽  
pp. 185-202 ◽  
Author(s):  
R. M. Thomas
Keyword(s):  
Mortality Rate ◽  
Blood Cells ◽  
The State ◽  
Infected Group ◽  
Entire Group ◽  
Large Group ◽  
Intravenous Inoculation

It has been shown that in a large group of rabbits inoculated intravenously with bovine tubercle bacilli the disease which follows resolves itself into two distinct phases. The first phase manifests itself in widespread diffuse lesions which subsequently regress. The mortality rate shows a rise and fall during this period, which have been correlated with the extent of lesions and with the changes in the blood cells. The duration of this phase is approximately 80 to 90 days. Following this period the mortality rate again rises and falls, during a period when all animals show lesions of a chronic nature. In an infected group the number of fatalities in the first phase is a function of the size of the dose. When the size of the dose and other conditions are held constant, a definite basis upon which to compare the reactions of treated animals is established. Studies of the blood cells during the course of the disease show that the changes in these cells reflect the course of the lesions in the first phase when other signs are lacking and offer a valuable means of making an estimate of the state of resistance of the animal from time to time. Studies of blood counts made on rabbits before their inoculation with tuberculosis were analyzed with regard to the relative longevity of the animals. It was found that those animals whose blood cells of various sorts deviated least from the modal value for the entire group survived longer than those animals whose counts were significantly high or low.

scholarly journals Domains of receptor mobility and endocytosis in the membranes of neonatal human erythrocytes in the membranes of neonatal human erythrocytes and reticulocytes are deficient in spectrin

1979 ◽  
Vol 80 (2) ◽  
pp. 481-486 ◽  
Author(s):  
KT Tokuyasu ◽  
R Schekman ◽  
SJ Singer
Keyword(s):  
Blood Cells ◽  
Strong Support ◽  
Human Erythrocytes ◽  
Frozen Sections ◽  
Con A ◽  
Neonatal Blood ◽  
Ultrathin Frozen Sections ◽  
Discrete Domains ◽  
Restricted Mobility ◽  
Endocytic Vesicles

It has previously shown (Schekman, R., and S.J. Singer, Proc. Natl. Acad. Sci. U.S.A. 73:4075-4079) that receptors in the membranes of neonatal human erythrocytes show a restricted degree of lateral mobility, whereas in adult human erythrocytes the receptors are essentially immobile. This restricted mobility is exhibited, for example, when concanavalin A (Con A) induces a limited clustering of its receptors in the neonatal erythrocyte membrane, resulting in the formation of invaginations and endocytic vesicles. This does not happen with adult cells. By the use of indirect immunoferritin labeling of ultrathin frozen sections of Con A-treated neonatal blood cells, we now show that the invaginations and endocytotic vesicles do not stain for spectrin, whereas the adjacent unperturbed membrane is heavily stained. The reticulocytes in the neonatal cell population undergo substantially more Con A-induced invagination and endocytosis than do the erythrocytes. These results lend strong support to the hypothesis that specialized discrete domains exist, or are induced, in the membranes of these neonatal cells, in which receptors are laterally mobile, whereas in the remaining (and predominant) part of the membrane the receptors are immobile. Such mobile domains are characterized by an absence of spectrin. During the maturation of the neonatal reticulocyte to erythrocyte, it is proposed that these domains are in large part, but not completely, eliminated.

scholarly journals TRANSMISSION OF MYELOID LEUKEMIA OF MICE

1935 ◽  
Vol 61 (3) ◽  
pp. 423-446 ◽  
Author(s):  
J. Furth
Keyword(s):  
Multiple Myeloma ◽  
Blood Cells ◽  
Myeloid Leukemia ◽  
Live Cells ◽  
X Rays ◽  
Diffuse Disease ◽  
Small Doses ◽  
Intravenous Inoculation ◽  
Intraperitoneal Inoculation

A transmissible strain of myeloid leukemia of mice is described. It can be readily passed from diseased to healthy mice by the transfer of tissues that contain live cells; but inoculation fails when the latter are not present. Inoculation is successful in almost every mouse whose resistance is lowered by X-rays. It is often successful in mice related to the animal in which the spontaneous leukemia took its origin, and occasionally successful in mice unrelated to it. The systemic diffuse disease (myeloid leukemia) is produced only by intravenous inoculation with relatively large doses, whereas subcutaneous or intraperitoneal inoculation results in the formation of tumors composed of myelocytes with basophile granules, in other words malignant blood cells of the strain described. Intravenous inoculation with small doses in susceptible mice, or similar inoculation with larger doses in somewhat resistant mice, results in the formation of tumors composed of myelocytes (multiple myeloma).

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