Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0021051 (immunodeficiency)
 71,517 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Atopic dermatitis is a recognizable phenotype that most likely results from several mechanisms. An increasing number of children with atopic dermatitis are recognized as having immune defects, although the exact incidence of such immunodeficiency states among patients with atopic dermatitis is unknown. Children with atopic dermatitis who suffer recurrent or persistent infections should undergo immunologic evaluation. Ideally, this should include evaluation of cell-mediated immunity as well as neutrophil and monocyte chemotaxis. Further investigation into the beta-blockade theory may enhance our understanding of atopic dermatitis. Careful attention to factors exacerbating atopic dermatitis is essential in understanding this problem. Abnormal sweating, dry skin, sensitivity to contactants, and emotional stress should always be considered in evaluation of children with atopic dermatitis.
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PMID:Atopic dermatitis: etiology and pathogenesis. 18 47

Assays for the production of leukocyte migration inhibition factor (LMIF) activity by cultured lymphocytes in the presence of the T-cell mitogen concanavalin A (ConA) have been shown to be highly sensitive for detecting decreases in cell-mediated immunity in patients with malignant diseases and primary and secondary immunodeficiency diseases. We have applied the leukocyte migration inhibition test in agarose using supernatants from ConA-stimulated lymphocyte cultures (indirect leukocyte migration inhibition test in agarose for studying patients with atopic dermatitis. Only 5 of 14 lymphocyte cultures from atopic dermatitis patients produced LMIF when stimulated with ConA, as compared with 34 of 34 controls. This difference is highly significant.
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PMID:Leukocyte migration inhibition factor in atopic dermatitis: induction by concanavalin A in vitro. 31 68

Parameters of humoral and cellular immunity have been measured in 91 asthmatic patients. Mean serum levels of IgG and IgE were raised. IgG levels were higher in those with a family history of asthma. IgE levels were higher in those with a past history of atopic eczema, but intrinsic and extrinsic asthma could not be differentiated on the basis of IgE levels. Thirteen of 74 patients failed to respond to tetanus immunization, while only 1 failed to respond to Salmonella typhi H antigen. Tetanus nonresponders had a raised mean serum IgA level, reduced spontaneous lymphocyte tritiated thymidine uptake, and reduced thymidine uptake in fetal calf serum. Eight of 87 patients failed to mount delayed hypersensitivity reactions to a battery of five intradermal antigens. The tritiated thymidine uptake of lymphocytes stimulated with phytohemagglutinin was normal in autologous serum, but reduced in fetal calf serum. The data support the hypothesis that asthma may be associated with immunodeficiency states.
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PMID:Humoral and cellular immunity in asthma. 108 97

Parameters of humoral and cellular immunity were measured in thirty-five patients with atopic eczema. The mean serum IgE level was raised but levels of the other major immunoglobulin classes were normal. Ten per cent of patients failed to respond to tetanus immunization. All patients responded to S. typhi H antigen. Fourteen per cent of patients failed to mount delayed hypersensitivity reactions to a battery of three intradermal antigens. The phytohaemagglutinin-stimulated uptake of 3H thymidine by lymphocytes was normal in the presence of autologous or of fetal calf serum, as was the spontaneous lymphocyte uptake. T and B lymphocyte numbers in the peripheral blood were normal. These results are similar to those found in asthmatic patients and support the hypothesis that, in some patients, atopic eczema is associated with an immunodeficiency state.
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PMID:Humoral and cellular immunity in atopic eczema. 110 39

We present a patient with Smith-Lemli-Opitz syndrome with immunodeficiency. The patient suffered numerous infectious episodes, atopic dermatitis and wheezing. Immunological investigations demonstrated severely reduced oxidative burst-responsiveness of the blood monocytes, whereas chemotaxis, phagocytosis and interleukin-1 production were normal. Tests of neutrophils and lymphocytes were normal excluding previously described immune deficiency disorders. The father proved to have diminished monocyte oxidative metabolism as well, whereas the mother had normal monocyte function. The genetic and immunological aspects are discussed in relation to the syndrome.
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PMID:Defective monocyte oxidative metabolism in a child with Smith-Lemli-Opitz syndrome. 135 58

It is shown that patients suffering from eczema, atopic dermatitis and psoriasis demonstrate immunologic shifts related to genetic predisposition to allergic (atopic and autoimmune) responses, specific skin responses, clinical features of dermatoses, reactivity of the affected connective tissue. Immune defects of the above patients suggest a drop in T-lymphocyte count and T-suppressor dysfunction, i.e. T-cell immunodeficiency. This indicates possible benefit of pharmacological immunomodulators scheduled on the basis of pathogenetic characteristics of each variant of dermatosis and of dermal inflammation.
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PMID:[Disorders of T-cell immunity in patients with eczema, atopic dermatitis and psoriasis]. 183 23

In vitro effect of tactivin on E-rosette forming capacity of peripheral blood T lymphocytes of atopic dermatitis patients permits more accurate diagnosis of immunodeficiency degree, evaluation of the relations between T-cell immunity affection and immunomodulation results. Individual sensitivity of ERF cells to tactivin in vitro may be utilized for selection of patients in need for immunocorrection and the latter substantiation.
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PMID:[An in-vitro system study of the immunomodulating activity of taktivin in atopic dermatitis]. 228 71

Atopic dermatitis (AD) represents an inflammatory skin disorder which is characterized by many signs of immunodeficiency. Particularly, decreased lymphoproliferative responses upon stimulation with mitogens as well as bacterial antigens were reported repeatedly. Since there is increasing evidence for a network of immuno-modulating cytokines playing a crucial role in the regulation of immunity and inflammation, in the present study we investigated whether an altered production of these mediators is one of the pathomechanisms responsible for the altered immune response in AD. For this purpose the 24-h supernatants of LPS- and PHA-stimulated or unstimulated mononuclear cells (MNC) from patients with AD of a moderate to severe disease activity and from nonatopic healthy controls were tested for Interleukin-1 (IL-1) and Interleukin-2 (IL-2) activity. Whereas supernatants of unstimulated MNC of AD patients and controls did not contain significantly different levels of these cytokines, LPS-stimulated MNC of AD patients released significantly less IL-1 in the supernatants. Similarly, the production of IL-2 by PHA-stimulated MNC of AD patients was significantly decreased in comparison to the controls. Moreover, there was a strong correlation between IL-1 and IL-2 levels. These findings indicate that diminished lymphoproliferative responses in AD may partly be caused by a decreased capacity of MNC to release immuno-modulating cytokines, even upon appropriate stimulation.
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PMID:Altered production of immuno-modulating cytokines in patients with atopic dermatitis. 280 Sep 14

A 39-year-old black male who is an intravenous drug abuser developed certain clinical manifestations that were consistent with the hyper-IgE syndrome. These included an extremely elevated IgE (greater than 2000 IU/mL), extensive eczematoid dermatitis, and recurrent soft tissue infections. He had no history of atopic disease as a child. Immunophenotypic analysis of peripheral blood mononuclear cells showed a significant decrease in helper (CD 4) cells with a normal concentration of suppressor (CD 8) cells. Human immunodeficiency virus (HIV) antibody was detected in his serum. Previous studies of patients with atopic dermatitis as well as of patients with the hyper-IgE syndrome characteristically show decreases in total suppressor lymphocyte concentrations in peripheral blood. These results led some investigators to postulate that high IgE concentrations in patients with atopic dermatitis result from defective IgE specific suppression. More recent evidence suggests that helper cell function may be the more critical impairment in these disorders. The development of a hyper-IgE syndrome in this setting of T-helper cell viral affliction lends further support to the hypothesis that helper lymphocyte defects may have a key role in the development of atopic dermatitis and the hyper-IgE syndrome.
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PMID:Hyper-IgE and human immunodeficiency virus infection. 317 68

Atopic dermatitis (AD) is characterized by many signs of immunodeficiency. Our interest was to investigate if there are also alterations of the chemiluminescence (CL) response of polymorphonuclear leukocytes (PMN) as a measure of the release of toxic oxygen radicals. Isolated PMN of 13 patients with AD with mild to moderate disease activity were stimulated with a chemotactic peptide (f-met-phe), zymosan-activated serum (ZAS), zymosan particles and phorbolmyristate acetate. In the AD group, we found a significantly decreased response after stimulation with ZAS in comparison to the controls. With the other stimuli tested no significant difference was detected. The decreased response of PMN to stimulation with ZAS from patients with AD associated with a normal reactivity to the other stimuli could be due to specific desensitization of the PMN by C5a in vivo.
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PMID:Chemiluminescence response of polymorphonuclear leukocytes in atopic dermatitis. 357 May 2


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