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)

Salmonella typhimurium infection was diagnosed in 186 patients aged 18-56. The clinical picture was that of gastroenteritis (73.1%), enteritis (14.0%), gastritis (6.45%), gastroenterocolitis (6.45%). Salmonellosis of moderate severity presented in 88.7% of patients, a severe course occurred in 11.3%. Concomitant disorders arose in 22.6% of cases. Immunological investigation disclosed T-lymphopenia, reduced number of multireceptor RFC, both T-helpers and T-suppressors. The levels of 0-lymphocytes and CIC were on the increase. Salmonellosis of long duration was characterized by hyperactivity of autoimmune reactions.
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PMID:[Immunologic status of patients with Salmonella infections]. 269 21

BB rats were found to have autoantibodies to gastric parietal cells, thyroid colloid antigens, smooth muscle, and thymocytes. No autoantibodies reactive with pancreatic islet cells (cytoplasmic), thyroid epithelial cells, adrenal cortex, testes, or anterior pituitary sections were identified. BB rats with gastric parietal autoantibodies had modest degrees of lymphocytic gastritis, but none developed iron or vitamin B12 deficiencies. These results suggest that BB rats have an underlying autoimmune diathesis. In addition, reports of peripheral T lymphopenia in such rats were confirmed, and markedly reduced helper T cell and cytotoxic-suppressor T cell subsets were demonstrated. Histological studies also revealed depletions of the T cell areas of spleen and lymph nodes. Furthermore, BB rats exhibited a profound inability to reject skin grafts across major and minor histocompatibility barriers. This was confirmed by mixed lymphocyte culture studies in vitro. BB-rat lymphocytes from either spleen or peripheral blood also showed profoundly reduced responses to T cell mitogens. Although BB-rat lymphocytes could produce normal levels of interleukin-2, they were unable to respond to this T cell growth factor. However, examination of thymuses from BB rats showed largely normal histologies, normal numbers of thymocyte subsets, and good mitogenic responses to con A. Thus, it appears that BB rats may have a thymic or post thymic defect in T lymphocyte maturation. The relevance of the immunologic lesion to the etiology of IDD in BB rats remains to be shown.
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PMID:Autoimmune diatheses and T lymphocyte immunoincompetences in BB rats. 634 99

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.
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PMID:Organ-specific autoimmunity induced by adult thymectomy and cyclophosphamide-induced lymphopenia. 784 36

It was shown that in patients with hypertension, duodenal and gastric ulcers and erosive gastritis leukopenia and lymphopenia are seen. At the same time contents of T- and B-lymphocytes are decreased and contents of C- lymphocytes are increased in circulation blood. Peroral daily intake of 20 mg of beta-carotene during 3-4 weeks caused increasing the contents of B- and T-cells and decreasing contents of C-lymphocytes in blood of patients.
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PMID:[Study of immunomodulating properties of beta-carotene in patients]. 856 Aug 70

We report the case of a 63 year-old female who presented with a seven-year history of epigastric pain and a sudden overall deterioration. Gastroscopy demonstrated inflammatory aspect and ulceration in the antrum and fundus. Histology showed a lymphocytic infiltrate consistent with low grade mucosa-associated lymphoid tissue lymphoma and cytomegalovirus gastritis. There was no evidence of Helicobacter pylori infection. Other investigations demonstrated two pulmonary foci consistent with lymphomatous infiltration and a reduced CD4 + T-lymphocyte count (85/mm3). Other screening tests including HIV serology were negative. This case of idiopathic CD4 lymphopenia, in conjunction with the other rare cases in the literature, allows us to reevaluate this condition and its unusual clinical presentation with two opportunistic pathologies.
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PMID:[Multifocal MALT lymphoma and acute cytomegalovirus gastritis revealing CD4 lymphopenia without HIV infection]. 1021 14

A number of experimental models of organ-specific autoimmunity involve a period of peripheral T cell lymphopenia prior to disease onset. In particular, experimental autoimmune gastritis, induced in susceptible mouse strains by neonatal thymectomy, is a CD4+ T cell mediated autoimmune disease. We have previously demonstrated that this disease displays the hallmarks of a Th1-mediated DTH inflammatory response with an essential role for IFN-gamma very early in the pathogenesis of disease. Given the interplay between the innate and adaptive immune responses, a potential source of early IFN-gamma production in these lymphopenic mice is the innate immune response. Here we have assessed the contribution of innate immunity to the induction of experimental autoimmune gastritis, in particular, the role of natural killer (NK) cells in production of IFN-gamma. Analysis of NK cells and macrophages revealed no difference in either the number or activation status between euthymic and neonatally thymectomised mice. Furthermore, in vivo depletion of NK cells immediately after neonatal thymectomy of (BALB/cCrSlcxC57BL/6) F1 mice demonstrated no reduction in disease incidence compared to control groups of neonatally thymectomised mice. Therefore, we conclude that NK cells are not the primary source of IFN-gamma required for the pathogenesis of autoimmune gastritis following neonatal thymectomy but rather the small cohort of T cells in the periphery of lymphopenic mice are likely to be responsible for the IFN-gamma production.
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PMID:The role of natural killer cells in the induction of autoimmune gastritis. 1190 44

Thymectomy of BALB/c mice on day 3 of life results in the development of autoimmune gastritis (AIG) due to the absence of CD4(+)CD25(+) regulatory T cells. However, depletion of CD4(+)CD25(+) T cells by treatment with anti-CD25 rarely resulted in AIG. Depletion was efficient, as transfer of splenocytes from depleted mice induced AIG in nu/nu mice. One explanation for this result is that CD4(+)CD25(-) T cells upon transfer to nude recipients undergo lymphopenia-induced proliferation, providing a signal for T cell activation. Cotransfer of CD25(+) T cells did not inhibit initial proliferation but did suppress AIG. Surprisingly, immunization with the AIG target Ag, H/K ATPase, in IFA failed to induce disease in normal animals but induced severe AIG in CD25-depleted mice. These results demonstrate that second signals (nonspecific proliferation, TCR activation, or inflammation) are needed for induction of autoimmunity in the absence of CD25(+) regulatory T cells.
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PMID:Cutting edge: depletion of CD4+CD25+ regulatory T cells is necessary, but not sufficient, for induction of organ-specific autoimmune disease. 1205 2

A number of experimental models of organ-specific autoimmunity involve a period of peripheral lymphopenia prior to disease onset. There is now considerable evidence that the development of autoimmune disease in these models is due to the absence of CD4+CD25+ regulatory T cells. However, the role of CD4+CD25+ regulatory T cells in the prevention of autoimmune disease in normal individuals has not been defined. Here we have assessed the affect of depletion of CD4+CD25+ regulatory T cells in BALB/c mice on the induction of autoimmune gastritis. The CD4+CD25+ T cell population was reduced to 95% of the original population in adult thymectomized mice by treatment with anti-CD25 mAb. By 48 days after the anti-CD25 treatment, the CD4+CD25+ regulatory T cell population had returned to a normal level. Treatment of thymectomized adult mice for up to 4 weeks with anti-CD25 mAb did not result in the development of autoimmune gastritis. Furthermore, we have demonstrated that depletion of CD4+CD25+ regulatory T cells, together with transient CD4+ T lymphopenia, also did not result in the development of autoimmune gastritis, indicating that peripheral expansion of the CD4+ T cell population, per se, does not result in autoimmunity in adult mice. On the other hand, depletion of CD4+CD25+ T cells in 10-day-old euthymic mice resulted in a 30% incidence of autoimmune gastritis. These data suggest that CD4+CD25+ regulatory T cells may be important in protection against autoimmunity while the immune system is being established in young animals, but subsequently other factors are required to initiate autoimmunity.
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PMID:The role of CD4+CD25+ immunoregulatory T cells in the induction of autoimmune gastritis. 1240 91

Interleukin (IL)-2 plays a crucial role in the maintenance of natural immunologic self-tolerance. Neutralization of circulating IL-2 by anti-IL-2 monoclonal antibody for a limited period elicits autoimmune gastritis in BALB/c mice. Similar treatment of diabetes-prone nonobese diabetic mice triggers early onset of diabetes and produces a wide spectrum of T cell-mediated autoimmune diseases, including gastritis, thyroiditis, sialadenitis, and notably, severe neuropathy. Such treatment selectively reduces the number of Foxp3-expressing CD25(+) CD4(+) T cells, but not CD25(-) CD4(+) T cells, in the thymus and periphery of normal and thymectomized mice. IL-2 neutralization inhibits physiological proliferation of peripheral CD25(+) CD4(+) T cells that are presumably responding to normal self-antigens, whereas it is unable to inhibit their lymphopenia-induced homeostatic expansion in a T cell-deficient environment. In normal naive mice, CD25(low) CD4(+) nonregulatory T cells actively transcribe the IL-2 gene and secrete IL-2 protein in the physiological state. IL-2 is thus indispensable for the peripheral maintenance of natural CD25(+) CD4(+) regulatory T cells (T reg cells). The principal physiological source of IL-2 for the maintenance of T reg cells appears to be other T cells, especially CD25(low) CD4(+) activated T cells, which include self-reactive T cells. Furthermore, impairment of this negative feedback loop via IL-2 can be a cause and a predisposing factor for autoimmune disease.
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PMID:Homeostatic maintenance of natural Foxp3(+) CD25(+) CD4(+) regulatory T cells by interleukin (IL)-2 and induction of autoimmune disease by IL-2 neutralization. 1575 6

The popularly exploited murine neonatal thymectomy experimental autoimmune gastritis (nTx:EAG) model requires the animal to be in a state of lymphopenia. Here we report on a novel murine immunization (without adjuvant) model that can establish a lasting gastritis. We demonstrate that the immunization model (imm:EAG) results in a bona fide autoimmune disease and define the resulting pathology and serology observed and compare it with that reported for human autoimmune gastritis. Immune cells present in the stomachs of imm:EAG gastritic mice include CD8 T cells, CD11b and Gr1 (granulocytes/monocytes) and B cells. We detected circulating antibodies of immunoglobulin G1 (IgG1) subclass, with some IgG(2a) and IgG(2b) reactive to stomach membranes and the parietal cell proton pump. The class and subclass of autoreactive antibodies resulting from imm:EAG suggest a T helper 1 (Th1)/Th2 immune response. We establish that both self-reactive T and B cells from BALB/cCrSlc imm:EAG gastritic mice have the potential to induce a gastritis in BALB/c syngeneic nu/nu recipients. We conclude that this model is likely to be superior to the currently popularly exploited nTx:EAG and provide insight into and an understanding of the mechanisms of and remedies for autoimmunity in an intact immune system.
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PMID:Gastritis in neonatal BALB/cCrSlc mice induced by immunization without adjuvant can be transferred to syngeneic nu/nu recipients. 1639 1


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