Mononuclear cells from patients with the hyperimmunoglobulin E-recurrent infection syndrome produce an inhibitor of leukocyte chemotaxis.

Donabedian, Haig; Gallin, John I.

doi:10.1172/jci110551

Cited by 51 publications

(15 citation statements)

References 28 publications

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“…The possibility of IgE production in response to Staphylococcus, as in Job's syndrome (Hill & Quie 1974, Scopfer et al 1980, Donabedian & Gallin 1982, Berger et al 1988, cannot be ruled out, because helminth infection can act as an adjuvant for IgE production against unrelated antigens (Turner et al 1979). It is thus possible that in helminth infections, chemotactic defects in leukocytes are induced by high tissue histamine levels, released (Hill & Quie 1974, Berger et al 1988.…”

Section: Discussionmentioning

confidence: 99%

Nematode Infections Are Risk Factors for Staphylococcal Infection in Children

Moreira-Silva

Leite

Brito

et al. 2002

Mem. Inst. Oswaldo Cruz

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Section: Discussionmentioning

confidence: 99%

Nematode Infections Are Risk Factors for Staphylococcal Infection in Children

Moreira-Silva

Leite

Brito

et al. 2002

Mem. Inst. Oswaldo Cruz

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“…In addition to the hallmark of increased serum IgE, reported immunologic abnormalities include the presence of anti-S. aureus and anti-Candida albicans IgE (3)(4)(5), elevated total IgD (6), and a neutrophil chemotactic defect (7)(8)(9) possibly caused by suppressive factors released from mononuclear cells (10,11). In addition, there are deficiencies of delayed hypersensitivity (2,12), in vitro proliferative responses to C. albicans (1,4,12), proliferative responses in mixed lymphocyte cultures (1), anamnestic antibody responses to tetanus and diphtheria antigens (1), in vitro response to pokeweed mitogen (13) and concanavalin A (12), and suppressor T cell number and function (14).…”

Section: Introductionmentioning

confidence: 99%

Immunoglobulins in the hyperimmunoglobulin E and recurrent infection (Job's) syndrome. Deficiency of anti-Staphylococcus aureus immunoglobulin A.

Dreskin¹,

Goldsmith²,

Gallin³

1985

J. Clin. Invest.

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Patients with the hyperimmunoglobulin E and recurrent infection syndrome (HIE) characteristically have frequent skin and respiratory infections caused by Staphylococcus aureus. We have developed a set of enzyme-linked immunosorbent assays that use whole S. aureus (Wood's strain) immobilized on 0.22-um filters and highly specific, affinity-purified enzyme conjugates of goat anti-human IgE, anti-human IgD, anti-human IgG, anti-human IgA, and anti-human IgM. These reagents were used to determine S. aureus-specific immunoglobulin (Ig) levels. As previously published, 10 patients with HIE had markedly higher levels of anti-S. aureus IgE than did 5 patients with eczema and recurrent superficial S. aureus infections (P < 0.001). The HIE patients were also found to have a deficit of anti-S. aureus serum IgA as compared with 12 normal subjects, 12 patients with chronic granulomatous disease, 5 patients with chronic eczema and recurrent superficial S. aureus infections, and 3 patients with the Chediak-Higashi syndrome (P < 0.01 for each comparison). In addition, the HIE patients had an excess of anti-S. aureus IgM as compared with normal subjects (P < 0.01). An expected excess of anti-S. aureus IgG was absent. These abnormalities cannot be explained by variations of total serum Ig levels or by a general inability to produce antigen-specific IgA because levels of naturally occurring IgA antibody against Escherichia coli lipopolysaccharide and the antigens of the pneumococcal vaccine are normal. Parotid saliva from patients with HIE contained less salivary IgA per milligram of protein (P < 0.01) and less salivary anti-S. aureus IgA per milligram of protein (P < 0.05) than did normal controls. The incidence of infection at mucosal surfaces and adjacent lymph nodes correlated inversely with serum anti-S. aureus IgA (r = -0.647, P = 0.034), serum anti-S. aureus IgE (r = -0.731, P = 0.016), total serum IgE (r = -0.714, P = 0.020), and total serum IgD (r = -0.597, P = 0.049). These findings are evidence of a previously undescribed immunoregulatory defect in patients with HIE, which may contribute to the increased susceptibility to infection in this syndrome.

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“…Elevated levels of urinary histamine have been reported in some patients, and correlate with the extent of the eczematoid dermatitis (80). Although impaired neutrophil chemotaxis has been documented in HIES patients, this defect is inconsistently present, even in the same patient at different times (37,81).…”

Section: Disorders Characterized By Excessive Ige Productionmentioning

confidence: 99%