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Query: UMLS:C0024312 (lymphopenia)
 4,859 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A number of immunological parameters have been monitored for up to 6 weeks following 131I treatment for hyperthyroidism in Graves' disease. The aim was to examine whether this isotope treatment normalizes or further accentuates some immunological abnormalities which may be a manifestation of autoimmune reactions in these patients. It was confirmed that both the cellular composition and immunological reactivities of the patients' blood lymphocytes were abnormal before treatment. After 131I administration a slight lymphopenia occurred and the ratio between CD4 and CD8 positive T lymphocytes (helper-inducer/suppressor-cytotoxic), which was increased before treatment, increased further. Moreover, PWM-triggered IgM secretion in vitro was reduced by 50%. No other immunological parameters studied, such as secretion of other Ig classes, mitogenic responses of lymphocytes, and distribution of other lymphocyte subsets, changed to any detectable extent. It remains speculative whether the 131I-induced changes of the immune system may further accelerate the underlying autoimmune disease processes.
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PMID:Blood lymphocyte population following 131I treatment for hyperthyroidism. 182 98

We analysed the clinical and pathologic features of 42 patients with immunologically confirmed peripheral T-cell lymphoma. The median age was 60 years and the male to female ratio was 1:1. A prior lymphoproliferative or autoimmune disorder was present in 14 per cent of the patients. Signs of advanced disease were usually present from the onset, such as B symptoms (55 per cent), generalized lymphadenopathy (57 per cent), stage III/IV disease (62 per cent), and elevated levels of serum lactate dehydrogenase (68 per cent). Primary extranodal disease (14 per cent), hepatomegaly (12 per cent), splenomegaly (12 per cent), lung/pleural involvement (12 per cent), skin involvement (21 per cent), and bone marrow involvement (28 per cent) were uncommon. Lymphocytopenia was present in 64 per cent of the patients, and none of nine patients tested were serologically positive for human T-cell leukemia/lymphoma virus (HTLV-I) infection. Among 38 patients receiving combination chemotherapy, 20 (53 per cent) achieved a complete remission. The actuarial median survival of all patients was 17 months. Age greater than 60 years and stage III/IV disease predicted a poor clinical outcome, whereas the large cell histological subtype predicted a favourable outcome. Prospective clinical studies using uniform treatments and a uniform histologic classification scheme are needed to confirm these findings.
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PMID:Peripheral T-cell lymphoma: a clinicopathologic study of 42 cases. 288 15

Insulin-dependent diabetes is a chronic autoimmune disease probably mediated by T cells. We examined the alpha chain of the T-cell antigen receptor in two models of this illness (man and BB rat) to determine any association with autoimmune diabetes. We conducted a population study in man, using a human alpha chain probe, pGA-5, and restriction enzyme Bgl 11. Two allelic forms and three RFLP patterns, 2.8 and 3.0 kb homozygous and 2.8/3.0 heterozygous, were detected. There was no difference in the frequency of these RFLPs among the 50 Type I diabetic patients and 48 controls tested. BB rats develop a spontaneous T-cell mediated autoimmune diabetes. The diabetes has been linked in several breeding studies to an undetermined autosomal recessive gene causing T-cell lymphopenia. We were able to differentiate the T-cell antigen receptor alpha chain of the diabetic BB and control BBN rats using the restriction enzyme EcoR1 and a murine alpha chain probe, TT11. The BB rat had a haplotype characterized by the presence of 4.7 and 5.8 kb bands, and the absence of 1.4, 2.2, 2.6, 3.6, 3.9, 4.1, and 6.1 kb bands. In a breeding study with BB and BBN rats, diabetic animals of the F2 generation demonstrated no linkage with the BBs' alpha chain, nor was lymphopenia linked to the alpha chain of the BB rat. These results suggest that autoimmune diabetes is not linked to the T-cell antigen receptor alpha chain in the BB rat, nor is it associated with alpha chain constant region polymorphisms in Type I diabetes in man.
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PMID:T-cell antigen receptor alpha chain polymorphisms in insulin-dependent diabetes. 290 75

An 8-year-old girl with combined immunodeficiency secondary to adenosine deaminase deficiency developed thyroid failure of probable autoimmune origin manifested by linear growth deceleration, marked bone-age delay, and myxedema. To our knowledge, this association has not been previously reported. Immunologic abnormalities included absolute T-cell lymphopenia and markedly reduced in vitro lymphocyte responses to phytohemagglutinin and to alloantigen in the mixed lymphocyte reaction. The diagnosis of autoimmune thyroid disease was suggested by the presence of antithyroglobulin antibodies in the serum and by decreased, patchy uptake of iodine 123 on a thyroid scan. Autoimmune thyroid disease may have developed because the immunodeficient state, with its greater deficiency of suppressor/cytotoxic T cells, allowed expression of a clone of helper T lymphocytes specific for thyroidal antigens. Thus, autoimmune disease may be more common in immunodeficient states and appropriate surveillance should be instituted.
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PMID:Probable autoimmune thyroid disease and combined immunodeficiency disease. 349 Jan 77

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

This paper summarizes previous in-flight infections and novel conditions of spaceflight that may suppress immune function. Granulocytosis, monocytosis, and lymphopenia are routinely observed following short duration orbital flights. Subtle changes within the monocyte and T cell populations can also be noted by flow cytometric analysis. The similarity between the immunological changes observed after spaceflight and other diverse environmental stressors suggest that most of these alterations may be neuroendocrine-mediated. Available data support the hypothesis that spaceflight and other environmental stressors modulate normal immune regulation via stress hormones, other than exclusively glucocorticoids. It will be essential to simultaneously collect in-flight endocrine, immunologic, and infectious illness data to determine the clinical significance of these results. Additional research that delineates the neuroendocrine mechanisms of stress-induced changes in normal immune regulation will allow clinicians in the future to initiate prophylactic immunomodulator therapy to restore immune competence altered by the stress of long-duration spaceflight and therefore reduce morbidity from infectious illness, autoimmune disease, or malignancy.
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PMID:The role of psychoneuroendocrine factors on spaceflight-induced immunological alterations. 837 Oct 53

During an infection with human immunodeficiency virus (HIV) the immune system is deregulated, even before real immunodeficiency, lymphopenia and AIDS occur. The immunologic alterations that have been described are a differentiation of a T-lymphocyte subclass, Th1 to Th0. Immunologic stimulation of these Th0 cells afterwards, makes them mature into Th2 cells. This causes a imbalance between the Th1 and Th2 cells, in favor of the second group. The clinical expression of this imbalance is an elevated risk of HIV-seropositive patients for allergies and for autoimmune disease, specially those autoimmune disease in which the production of autoantibodies prevails. Sometimes of differential diagnosis with systemic lupus erythematosus is difficult. There has been describes a major prevalence of allergic diseases, especially allergic rhinitis, in adult patients infected by HIV. Reports in pediatric patients are still sporadic, and the prevalence of allergies in children infected with HIV-AIDS is unknown. Only after recognizing the allergic nature of some symptoms, the treatment will be complete, reducing morbidity and infectious complications.
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PMID:[Allergic diseases and infection with human immunodeficiency virus (HIV)-AIDS in pediatric patients]. 929 27

Sjogren's syndrome (SS) is an autoimmune disease characterized by a chronic inflammatory response mainly localized to the lacrimal and salivary glands. However, it sometimes involves extraglandular organs culminating in systemic disorders. Hematological abnormalities are not uncommon, although they rarely have clinical significance. In this study we examined 99 patients with primary SS who visited our hospital during 1989 to 1999. Patient's mean age was 54.1 years and 95 out of 99 were female. Lymphopenia and leukopenia was noted in 35 patients (35.3%) and 26 patients (26.2%) respectively, and 7 patients (7.1%) had thrombocytopenia. 43 patients (43.4%) had either of these hematological abnormalities. Patients with lymphopenia showed significantly low frequency of arthralgia and anti-SS-A/B antibody was more common in this group. Only one patient in this group required prednisolone therapy because of polyarthritis and general fatigue while others needed no specific therapy. Patients with thrombocytopenia were significantly younger and a male/female ratio was higher than those without this abnormality. They had higher tendency to accompany with skin eruption, positive anti-SS-B antibody, anti-nuclear antibody and rheumatoid factor. Three out of 8 patients with thrombocytopenia were treated with prednisolone according to the protocol for idiopathic thrombocytopenic purpura. All of 3 patients had positive PA-IgG and normocellular bone marrow. Autoimmune mechanism such as polyclonal B cell activation may play a role in the pathogenesis of thrombocytopenia.
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PMID:[Hematological abnormalities of primary Sjogren's syndrome]. 1086 27

Homeostasis of T cell numbers in the periphery implies an ability of lymphocytes to sense cell numbers. Although the mechanisms are unknown, we find that the chemokine CCL21 (also known as TCA4, SLC, 6Ckine), a ligand for the chemokine receptor CCR7, can regulate homeostasis of CD4 (but not CD8) T cells. In the absence of CCR7 ligands, transferred CD4 T cells failed to expand in lymphopenic hosts, whereas in the presence of CCL21 overexpression, homeostatic CD4 T cell proliferation occurred even in nonlymphopenic recipients. Ag-specific CD4 T cells transferred into Ag-expressing mice proliferated and induced autoimmunity only in lymphopenic recipients. Pancreatic expression of CCL21 was sufficient to replace the requirement for lymphopenia in the progression of autoimmune disease. These results suggest that CD4 T cells use local concentrations of CCR7 ligands as an index of T cell steady state numbers and that homeostatic expansion of the T cell population may be a contributing factor in the development of autoimmune disease.
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PMID:A ligand for the chemokine receptor CCR7 can influence the homeostatic proliferation of CD4 T cells and progression of autoimmunity. 1173 86

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


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