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Query: UMLS:C0021051 (immunodeficiency)
 71,517 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The pathways leading to the development of the allergic state and subsequently to the characteristic inflammatory response are complex in nature and result from an interplay between immunologic and biochemical events. Along these pathways a number of intrinsic factors, i.e., handling of antigens at mucosal level, transient immunodeficiency states, especially in the secretory IgA system, impairment in the IgE regulatory mechanism, modulation of cyclic nucleotides leading to mediator release and a "feedback" inhibition control provided by histamine and eosinophil derived products greatly dictate the outcome of events associated with allergic inflammation.
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PMID:Immune and biochemical mechanisms in the allergic disease of the upper respiratory tract; role of antibodies, target cells, mediators and eosinophils. 6 31

Two cases of combined immunodeficiency with lymphopenia, thymic dysplasia, and defective immunoglobulin production are reported. Both show selective hypo-gammaglobulinemia (IgG and IgA respectively) and selective hyper-gammaglobulinemia (both IgE, IgA, and IgM respectively). The cases are classified, by correlation of clinical and histopathological data as a variant of Fireman's disease.
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PMID:Combined immune deficiency syndromes with primary T-cell defect and partial B-cell reactive hyperactivity. Immunological and morphological analysis of two unusual cases. 15 Jan 19

Allergy often begins with a subtle and/or transient T cell defect. This defect is first responsible for an IgA deficiency. The normal function of IgA is immune exclusion. In its absence, allergens can pass through the mucosa and stimulate the immunocompetent cells. The T cell defect may also be implied by the synthesis of IgE directed against the allergens which passed through. Clinical, biological and immunological findings (T cell defect in allergic disease, low range of IgA in the early life of atopics) are in agreement. The genetic factor for pollinosis and house dust allergy are segregated. In ragweed allergy there is an Ir gene coding for antigen-specific Ig of different classes and a group of non-linked major histocompatibility complex alleles coding for non antigen-specific IgE. There are some links with HLA. In house dust allergy the Ir gene is very common and almost everyone can produce an allergy under some conditions (T cell defect). Whatever the immunologic and genetic factors are, they need allergens and environmental factors to induce allergy. Allergy is a complex state in which several mechanisms, often associated and sometimes unclear, are involved. Some of them may be an abnormality of the autonomic nervous system, and/or an increase in the mucous membrane permeability, and/or a subtle immunodeficiency. All these mechanisms are regulated by genetic factors and modulated by environmental ones.
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PMID:Immunologic and genetic factors predisposing to allergy. 37 74

Intestinal mucosal biopsy immunoglobulin content in a patient with eosinophilia, allergic gastroenteropathy (atopy, food sensitivities, protein-losing enteropathy, iron deficiency anemia, and growth retardation), and hyperimmunoglobulinemia E (68,000 units) was compared with that of a control group and a group with eosinophilic gastroenteritis who had no atopic features. The patient had no evidence of cellular or humoral immunodeficiency but was severely hypersensitive to multiple inhalant and dietary allergens. In contrast to the findings in patients with nonallergic eosinophilic gastroenteritis, whose intestinal immunoglobulin content was similar to that of controls, tissue immunoglobulin IgE and IgG was markedly increased in the allergic patient. These results support an intestinal reaginic mechanism in the etiology of the allergic form of eosinophilic gastroenteritis.
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PMID:Eosinophilic gastroenteritis in extreme allergy. Immunopathological comparison with nonallergic gastrointestinal disease. 45 50

A six-year old boy who had suffered from the age of two with chronic diarrhea has been found to be severely retarded in statural growth. Examinations discovered marked lymphopenia with a T lymphocyte defect accompanied by absent IgA and IgE. In contrast with other cases described in literature, in this case the immunodeficiency was not accompanied by bone or cartilage alterations. The only factor apparently responsible for his lack of growth was the malabsorption.
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PMID:Harmonic dwarfism, lymphopenia, deficit of IgA and IgE in a 6-year old boy. 61 Apr 13

Concentrations of IgD and IgE were measured in sera from 165 patients with well-defined immunodeficiency in an effort to find information possibly relevant to the roles of antibodies of these classes in host defense. Values for both immunoglobulins were generally quite low in patients who had marked deficiencies of all three major immunoglobulins, although occasional normal or high normal values for IgD were seen in hypogammaglobulinemic patients. Group mean IgD concentrations were also depressed in patients with Wiskott-Aldrich syndrome and in those with selective IgA deficiency; IgE concentrations were depressed in patients with X-linked immunodeficiency with hyper-IgM and in those with ataxia telangiectasia. IgD and IgE were both significantly elevated in patients with extreme hyperimmunoglobulinemia E and undue susceptibility to infection and in a patient with the Nezelof syndrome; none of these patients had histories suggestive of atopy. In addition, the mean IgE concentration was significantly elevated in patients with selective IgA deficiency, many of whom were atopic, and in those with the Wiskott-Aldrich syndrome. The highest IgD concentration (163 mg/100 ml) was found in serum from a boy with variable immunodeficiency who had a lifelong history of severe recurrent pharyngeal infections, primarily streptococcal in etiology. Recurrent staphylococcal infection was a feature common to many but not all patients with elevated serum IgE concentration. These data may prove useful in the future delineation of biologic roles for antibodies in these two immunoglobulin classes.
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PMID:Serum IgD and IgE concentrations in immunodeficiency diseases. 80 18

Seventy-five patients with multiple sclerosis (MS) were treated for complement components C3, after factor B, C4, and tested for HLA-A and B-determinants. Levels of IgG, IgA, IgD, IgE and titres of measles antibodies were also determined. Correlations between these immunological values and HLA determinants could be obtained in siblings, parents and/or children of the patients in 13 families. B18 frequency is strongly associated with the hypocomplementaemic group (x2 = 8.9). An association of B18 with the population of cases with low B levels is also found (x2 = 8.02). Familial data showed that low C3 and/or low B levels are associated with the HLA haplotyes, especially with those containing B18. A "complement abnormality susceptibility gene", linked to the HLA genes, is postulated. Infections are significantly more frequent in families of hypocomplementaemic MS, the existence of a genetic immunodeficiency affecting the synthesis of the complement components, linked to the HLA determinants. In 1 case studied in this article, a heterozygous C2 deficiency linked to HLA-A10, B18 was found and might confirm this hypothesis.
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PMID:Hypocomplementaemic and normocomplementaemic multiple sclerosis. Genetic determinism and association with specific HLA determinants (B18 and B7). 88 65

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

Ataxia-telangiectasia is characterized by endocrine, neurologic, hematologic, hepatic, cutaneous and immunologic abnormalities. The immunologic deficiencies vary considerably from patient to patient, and in each patient with respect to time. The most frequent deficiencies of humoral immunity are diminished or absent serum and salivary IgA, diminished or absent serum IgE and impaired antibody responses to a variety of bacterial and viral antigens. Deficiencies of cellular immunity are commonly found by both in vivo and in vitro analyses. Histologic confirmation of these immunodeficiencies is readily observed in the lymphoid tissue. The thymus, which may be the seat of the primary abnormality in the immunodeficiency syndrome, regularly shows morphologic characteristics of an embryonic thymus.
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PMID:immunodeficiency in ataxia-telangiectasia. 109 83

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


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