Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0024312 (lymphopenia)
 4,859 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In rats with experimental pyelonephritis, cyclophosphamide leads to changes in the spleen and thymus lymphocyte populations. When cyclophosphamide was given five times a week from the fifth week of infection on, the population of electrophoretically slow moving spleen lymphocytes, which are believed to be B-lymphocytes, decreased in the seventh week. This effect is independent of autovaccination. During the same period the number of immature slow moving thymus lymphocytes decreased. Further treatment with cyclophosphamide until the twelfth week of infection led to the differences almost disappearing in the histogramm. Cyclophosphamide showed a slight effect on antibody production and did not influence the elimination of infective agents from the kidneys of animals with pyelonephritis.
 ...
PMID:[Autovaccination in chronic pyelonephritis in the animal experiment--effect of cyclophosphamide on splenic and thymus lymphocytes]. 331 18

Cyclophosphamide (Cy) treatment (150 mg/kg) of Sprague-Dawley rats 48 hr before immunization with a T-dependent antigen, ovalbumin (OVA), resulted in striking bone marrow, blood and tissue eosinophilia, maximal at 14 days and concurrent with profound lymphopenia. This phenomenon has been tentatively attributed to selective elimination by Cy of T-suppressor cells. In this study, T-cell subsets, B cells and monocytes/macrophages were enumerated following alkaline phosphatase-anti-alkaline phosphatase (APAAP) staining of mononuclear cells isolated from lymphoid tissues of rats exhibiting eosinophilia. In lymph nodes, a significant increase in the A3/25+:OX-8+ ratio compared with normal was maintained from Day 7 to Day 14; in the spleen, however, this effect was no longer apparent by Day 14, due to the emergence of a population of OX-8+, OX-19- large granular lymphocytes. A seven-fold rise in splenic B-cell numbers (OX-12+) between Day 7 and Day 14 coincided with the eosinophilia. These findings are consistent with the potentiated production of TH-cell derived soluble factors affecting eosinophil production and differentiation, including possibly a rat equivalent of eosinophil differentiation factor, which in the mouse has been reported to have B-cell growth factor activity linked with eosinophilia.
 ...
PMID:Cyclophosphamide-induced eosinophilia in the rat: concomitant changes in T-cell subsets, B cells and large granular lymphocytes within lymphoid tissues. 349 68

The subacute toxic effects of cyclopiazonic acid (CPA; given orally) were characterized in the dog (CPA was purified from cultures of Aspergillus flavus). Four groups of dogs were given CPA in gelatin capsules for 90 days at the following dosage levels: 0.05, 0.25, 0.5, and 1.0 mg/kg of body weight; a 5th group was used as controls. All dogs administered the 0.5 and 1.0 mg of CPA/kg dosages and 1 dog given the 0.25 mg of CPA/kg dosage died or were humanely killed before the scheduled termination of the study. Clinical signs of intoxication appeared 2 to 44 days after dosing was started and consisted of anorexia and, in 1 to 2 days, vomiting, diarrhea, pyrexia, dehydration, weight loss, and CNS depression. Grossly, the entire alimentary tract had diffuse hyperemia with focal areas of hemorrhage and ulceration. Other lesions were renal infarcts, necrotizing epididymitis, and ulcerative dermatitis. Microscopic lesions included ulceration, necrosis, vasculitis, lymphoid necrosis, karyomegaly in several organs, and decreased mitotic activity in intestinal crypt epithelium. Ulcerative and necrotic lesions were usually associated with vascular lesions. Clinical pathologic changes were leukocytosis, neutrophilia, lymphopenia, monocytosis, and increased serum alkaline phosphatase activity.
 ...
PMID:Cyclopiazonic acid mycotoxicosis in the dog. 392 55

Cyclophosphamide (Cy; 150 mg/kg) was administered (i.p.) to groups of Sprague-Dawley rats, followed two days later by immunization with ovalbumin (OVA). From that time, cyclosporin A (CsA; 25 mg/kg) or its vehicle was given (p.o.) for a further 13 days. Control animals tested 14 days after immunization, showed strong Arthus-like and modest delayed-type skin reactions to OVA, in contrast to almost total inhibition in animals tested with Cy, CsA or both. Similar effects were observed with respect to serum anti-OVA antibody levels. Despite itself producing lymphopenia, CsA had no additional effect on the lymphocyte depletion caused by Cy. Both drugs, either alone or in combination, caused neutrophilia and monocytosis. An additional eosinophilia due to Cy was prevented by CsA. Cy induced splenomegaly, nodal extramedullary haemopoiesis and increases in both tissue eosinophils and marrow neutrophils. There was also lymphoid depletion in both spleen and lymph nodes which was enhanced by CsA. Thymic lymphoid atrophy was found only when CsA was given. Despite the powerful immunosuppressive properties of both drugs, detailed biochemical and structural analyses showed no other synergistic toxicity, apart from modest hepatic abnormalities. In particular, there was no enhancement of the nephrotoxicity of CsA.
 ...
PMID:Immunosuppressive activity and toxicity of cyclosporin A in rats pretreated with high dose cyclophosphamide. 408 81

Cyclophosphamide is widely used to induce a remission of minimal-change nephropathy, but concerns have been raised about whether its effects on cellular immunity persist after treatment is discontinued. We studied functional and numerical measures of cellular immunity in children who had minimal-change nephropathy with frequent steroid-responsive relapses and were receiving cyclophosphamide (2.5 mg per kilogram of body weight per day for eight weeks). Sequential studies during such treatment showed that cyclophosphamide caused lymphopenia, particularly among T helper cells, resulting in a significant fall in the immunoregulatory (helper/suppressor) cell ratio. This change persisted 1 to 3 months after cyclophosphamide was discontinued, but measures of immune function reverted to normal after 6 to 12 months. Children with minimal-change nephropathy in long-term remission had no difference in T-cell subpopulations, lymphocyte responses to mitogens, or suppressor-cell function that could be attributed to the disease itself or to the previous use of cyclophosphamide.
 ...
PMID:Modulation of cellular immune function by cyclophosphamide in children with minimal-change nephropathy. 622 99

Murine graft versus host (GVH) disease takes two forms depending upon the parental/F1 strain combination employed. Acute lethal GVH disease is characterized by anemia, lymphopenia, hypogammaglobulinemia, profound anti-F1 cytotoxicity, and the loss of cytotoxic potential against third-party alloantigen. In contrast to this, chronic GVH disease is characterized by polyclonal B cell activation, autoantibody production, no anti-F1 cytotoxicity, and retained cytotoxicity against allotargets. We have previously reported that this marked disparity in disease expression results from a radiosensitive host cell which protects the F1 mouse from parental anti-F1 CTX in mice undergoing CGVH disease. Using an in vitro system to induce the host protective cell, we now demonstrate that two distinct Thy-1+ cells emerge which regulate CTX against the host. One cell is of host origin, radiation sensitive, and functionally resembles a veto cell. The second regulatory cell, of parental origin, is radiation resistant and restricted in its ability to suppress anti-F1 CTX. We further demonstrate that the emergence of these cells is modulated by competitive immunoregulatory influences mediated by T contrasuppressor and I-J+ cells.
 ...
PMID:The host response in graft versus host disease. III. The in vitro induction of regulatory cells in chronic murine graft versus host disease. 763 39

Autoimmune gastritis, a CD4+ T cell-mediated organ-specific autoimmune disease, can be induced by thymectomy of neonatal, but not of older, BALB/c mice. Here we have shown that autoimmune gastritis can also be induced in 6-8-week-old BALB/c mice by thymectomy combined with a single dose of cyclophosphamide (300 mg/kg). This treatment reduced the numbers of splenic T and B cells approximately 25-fold. However, by 8 days after treatment, the number of splenic lymphocytes had returned to normal adult levels. Approximately 50% of treated mice developed autoimmune gastritis after 10-12 weeks. These mice had mononuclear cellular infiltrates within the gastric mucosa and serum autoantibodies to the alpha and beta subunits of the gastric H+/K+ ATPase. Transgenic mice, expressing the gastric H+/K+ ATPase beta-subunit in the thymus (Alderuccio, F., Toh, B. H., Tan, S. S., Gleeson, P. A. and van Driel, I. R., J. Exp. Med. 1993. 178: 419), did not develop autoimmune gastritis after the adult thymectomy/cyclophosphamide treatment. Thus a T cell response to the H+/K+ ATPase beta-subunit is likely to be required for the onset of gastritis. These observations suggest that pathogenic autoreactive T cells exist in the periphery of normal adult mice and that autoimmunity can be induced by the activation of these autoreactive T cells following transient lymphopenia. Cyclophosphamide-treatment of adult mice without thymectomy did not induce autoimmune gastritis, suggesting thymic regulation of these pathogenic T cells.
 ...
PMID:Organ-specific autoimmunity induced by adult thymectomy and cyclophosphamide-induced lymphopenia. 784 36

Developments in the diagnosis and treatment of paratuberculosis is constrained by the lack of an experimental animal model. To investigate this problem conventional chicks immunodepressed by a Cyclophosphamide injection and concurrent inoculation of Infectious Bursal Disease Virus (IBDV) were infected with Mycobacterium paratuberculosis and kept for 4 months. The immunodepressed chicks eliminated mycobacteria with their faces from the first month until the third month and developed typical intestinal lesions of mycobacterial infection characterized by aggregation of macrophages with monocytes and lymphocytes. Diarrhoea was absent. The number of lymphocytes decreased by about 80%. The serological tests carried out with Complement Fixation test were negative. For the positive bacteriology and typical granulomatous lesions, the conventionally reared chicks proved to be a useful laboratory model for reproduction of Johne's disease.
 ...
PMID:Use of an experimental chicks model for paratuberculosis enteritis (Johne's disease). 920 44

Cyclophosphamide (CY), an alkylating cytostatic drug, is known for its ability to accelerate a number of experimental autoimmune diseases including spontaneous diabetes in NOD mice. The mechanism(s) by which CY renders autoreactive lymphocytes more pathogenic is largely unknown, but it has been postulated that the drug preferentially depletes regulatory (suppressor) T cells. It has been suggested that in cell-mediated autoimmune diseases, Th2-like lymphocytes secreting IL-4 and/or IL-10 provide protection, while Th1-like cells secreting IFN-gamma are pathogenic. In this study, we analysed the effects of CY on autoimmune diabetes and cytokines in two mouse models: the spontaneous diabetes of NOD mice and the diabetes induced in C57BL/KsJ mice by multiple injections of low dose streptozotocin (LD-STZ). In both models, CY induced severe lymphopenia and accelerated the progression to hyperglycemia. This was associated with changes in splenic cytokine patterns indicating a shift towards the IFN-gamma-secreting phenotype. We provide here evidence that IFN-gamma producers are relatively resistant to depletion by CY and that Th0 clones can be shifted towards Th1. However, direct exposure of T lymphocytes to CY may not be a necessary condition for exacerbation of diabetes; NOD.scid mice treated with CY before adoptive transfer of NOD splenocytes developed diabetes at a higher rate than did controls. Thus, the acceleration of diabetes by CY seems to be a complex event, which includes the relatively high resistance of IFN-gamma producers to the drug, their rapid reconstitution, and a Th1 shift of surviving T cell clones.
 ...
PMID:Acceleration of autoimmune diabetes by cyclophosphamide is associated with an enhanced IFN-gamma secretion pathway. 1058 54

Cyclophosphamide (CY) is an alkylating agent used in chemotherapy of tumors and autoimmune disorders. The drug causes a large number of side-effects including deep, transient lymphopenia and neutropenia, thus rendering the immune system susceptible to infections. In this review we focus on the effects of CY on the haematopoetic system and the immune response in rodents. In addition, we present approaches aimed at reconstitution of lympho- and myelopoiesis using a spectrum of immunotropic factors including: thymic hormones, cytokines, low-molecular weight compounds, bacterial products and lactoferrin.
 ...
PMID:[Reconstitution of cyclophosphamide-induced, impaired function of the immune system in animal models]. 1276 23


1 2 Next >>