Elevated serum levels of soluble CD30 in patients with atopic dermatitis (AD)

Bengtsson, Å.; Holm, L. E.; Bäck, Ove; Fransson, Jessica; Scheynius, A.

doi:10.1046/j.1365-2249.1997.4731373.x

Cited by 55 publications

(65 citation statements)

References 24 publications

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“…If so, blockade of CD30-CD30 ligand signals might reflect the prolongation of eosinophil survival. Clinical observations that the level of sCD30 correlates positively with eosinophilia in Hodgkin's disease (51) and the serum eosinophil cationic protein level in patients with atopic dermatitis (41,42) are quite plausible if sCD30 can inhibit CD30-CD30 ligand signals in vivo (52). Needless to say, secretion of Th2-type cytokines might also participate the eosinophilia seen in these patients (77,78).…”

Section: Discussionmentioning

confidence: 99%

“…Soluble levels of CD30 are elevated and are associated with the prognosis in Hodgkin's disease and AIDS (38). Elevated levels were also reported in patients with adult T cell leukemia and some of those with non-Hodgkin's lymphoma, rheumatoid arthritis (39), chronic renal failure with primary growth retardation (40), atopic dermatitis (41)(42)(43), bullous pemphigoid (44), polymyositis/dermatomyositis (45), and helminth infection (46). Interestingly, some of these diseases are associated with eosinophilia (47)(48)(49)(50), and an especially positive correlation between the levels of soluble CD30 (sCD30) and eosinophilia was found in Hodgkin's disease (51).…”

mentioning

confidence: 99%

“…Interestingly, some of these diseases are associated with eosinophilia (47)(48)(49)(50), and an especially positive correlation between the levels of soluble CD30 (sCD30) and eosinophilia was found in Hodgkin's disease (51). A positive correlation between the level of sCD30 and the serum eosinophil cationic protein level was also found in patients with atopic dermatitis (41,42).…”

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confidence: 99%

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Extremely Rapid and Intense Induction of Apoptosis in Human Eosinophils by Anti-CD30 Antibody Treatment In Vitro

Matsumoto

Terakawa

Miura

et al. 2004

The Journal of Immunology

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Apoptosis is an important cellular mechanism for controlling cell viability and proliferation. With respect to eosinophils, cytokines prolong their survival, whereas corticosteroids reduce their survival in vitro. CD30, a member of the TNFR family, is expressed on the surface of many cell types, including Hodgkin’s lymphoma cells. CD30 is capable of inducing apoptosis after Ab treatment in some cell lines. To determine whether this surface structure is involved in apoptosis of human eosinophils, we examined its expression and the effect of anti-CD30 Ab treatment on the viability of eosinophils. Purified human eosinophils expressed low, but consistently detectable, levels of CD30. Immobilized, but not soluble, forms of anti-CD30 Abs (HRS-4 and Ber-H8) or recombinant mouse CD30 ligand exhibited an extremely rapid and intense survival-reducing effect on the eosinophils in the presence of exogenous IL-5; this effect was both concentration and time dependent. Furthermore, high concentrations of IL-5 could not reverse the reduced survival rates. After treatment with anti-CD30 Ab, gel electrophoresis of DNA extracted from the eosinophils demonstrated changes consistent with apoptosis. The immobilized F(ab′)2 of the anti-CD30 Ab failed to induce eosinophil apoptosis. The addition of anti-CD18 Ab also completely abrogated the induction of eosinophil apoptosis. Further examination using specific signal transduction inhibitors suggested the involvement of p38, mitogen-activated protein kinase kinase 1/2, and specific tyrosine kinase, but not NF-κB, in the induction of CD30-mediated eosinophil apoptosis. These data demonstrate that CD30 can modify eosinophil survival by causing an extremely rapid and intense induction of apoptosis through a tightly regulated intracellular signaling pathway.

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

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Extremely Rapid and Intense Induction of Apoptosis in Human Eosinophils by Anti-CD30 Antibody Treatment In Vitro

Matsumoto

Terakawa

Miura

et al. 2004

The Journal of Immunology

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“…CD30 was shown to be consistently expressed on a subset of lymphocytes known as Th2 cells (16), and accordingly, CD30 expression has been associated primarily with inflammatory disorders, such as atopic dermatitis (AD), that have a Th2 profile (17)(18)(19). However, it is now clear that Th1 and Th0 lymphocytes also express CD30 (20,21), and the distinction between Th1 and Th2 disorders based on CD30 expression is not absolute.…”

Section: Introductionmentioning

confidence: 99%

Mast cell CD30 ligand is upregulated in cutaneous inflammation and mediates degranulation-independent chemokine secretion

Fischer

Harvima²,

Carvalho³

et al. 2006

J. Clin. Invest.

121

124

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Mast cells are involved in many disorders where the triggering mechanism that leads to degranulation and/or cytokine secretion has not been defined. Several chronic inflammatory diseases are associated with increased mast cell numbers and upregulation of the TNF receptor family member CD30, but the role of elevated CD30 expression is poorly understood. Here we report what we believe to be a novel way to activate mast cells with CD30 that leads to degranulation-independent secretion of chemokines. CD30 induced a de novo synthesis and secretion of the chemokines IL-8, macrophage inflammatory protein-1α (MIP-1α), and MIP-1β, a process involving the MAPK/ERK pathway. Mast cells were found to be the predominant CD30 ligand-positive (CD30L-positive) cell in the chronic inflammatory skin diseases psoriasis and atopic dermatitis, and both CD30 and CD30L expression were upregulated in lesional skin in these conditions. Furthermore, the number of IL-8-positive mast cells was elevated both in psoriatic and atopic dermatitis lesional skin as well as in ex vivo CD30-treated healthy skin organ cultures. In summary, characterization of CD30 activation of mast cells has uncovered an IgE-independent pathway that is of importance in understanding the entirety of the role of mast cells in diseases associated with mast cells and CD30 expression. These diseases include Hodgkin lymphoma, atopic dermatitis, and psoriasis.

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“…Determination of TNF-alpha plasma levels and production by mononuclear cells in AD patients gave controversial results (19)(20)(21)(22). It should also be mentioned that CD30, which is a marker ofTh2 cell activation and whose soluble form is significantly elevated in AD, belongs to the TNF-receptor family (23). Recently, it has been found that TNF-alpha is the main inducer of inducible protein-It), belonging to the CXC chemokine subfamily, by skin fibroblasts from patients with atopic dermatitis (24).…”

Section: Resultsmentioning

confidence: 99%

Infliximab in Recalcitrant Severe Atopic Eczema Associated with Contact Allergy

Cassano

Loconsole

Coviello

et al. 2006

Int J Immunopathol Pharmacol

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Inffiximab is an anti-tumour necrosis factor (TNF)-alpha chimeric monoclonal antibody which is effective in diseases associated with aT-helper (Th) 1 response, such as rheumatoid arthritis, Crohn's disease and psoriasis. There are sporadic case reports of atopic dermatitis (AD) induced or precipitated by anti-TNF-alpha therapy, which have been attributed to the switch towards Th2-mediated reactions. We report the case of a 30-year-old man with long-standing severe AD associated with contact allergy and poorly responding to conventional treatments. The use ofinffiximab resulted in a dramatic amelioration of AD lesions and pruritus, persisting at follow-up examinations over a 3-year period. Probably, the unexpected response to infliximab therapy in this case might be due to some peculiar features of AD in our patient (i,e. chronic-continuous course and concomitant contact allergy) which could have been responsible for a more preponderant recruitment ofThl cells as compared to "common" forms of AD.Infliximab is an anti-tumour necrosis factor (TNF)-alpha chimeric monoclonal antibody which is effective in diseases associated with aT-helper (Th) I response, such as rheumatoid arthritis, Crohn's disease and psoriasis (1-5). There are sporadic case reports of immune-mediated cutaneous eruptions induced or precipitated by anti-TNF-alpha therapy, including atopic dermatitis (AD) (6-8). Unaware of the possible risk of aggravating AD with anti-TNF-alpha therapy, in January 2003, we used infliximab in a case ofsevere recalcitrant AD associated with contact allergy. MATERIALS AND METHODSA 30-year-old man presentedwitha 22-yearhistoryofAD, which had notably worsened in the last 4 years, being characterized by a continuouscourse,long-lasting widespread lesions and incoercible pruritus, refractory to topical steroids and H I-receptorantagonists. The patientalso experiencedtwo episodes of erythrodermia associated with generalized lymphadenopathy. The deterioration of AD included pronounced impact on quality of life and mood disorders so that after two years the patient received treatment with paroxetine and benzodiazepines. He also presented a concomitant contact sensitisation to nickel sulphate and potassium bichromate but prevention did not cause any substantial benefit on skin manifestations and symptoms. On two separate occasions over the last three years, histopathological analysisof skin samplestaken from lesional skin showed the typical findings of an eczematousdermatitis.Systemic corticosteroids and cyclosporin gave only partial temporary relief of AD and had to be discontinued after a few months because of side effects, whereas leukotriene antagonists and high-dose immunoglobulinsdid not show any effects. Treatment with 0.1% tacrolimus

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Elevated serum levels of soluble CD30 in patients with atopic dermatitis (AD)

Cited by 55 publications

References 24 publications

Extremely Rapid and Intense Induction of Apoptosis in Human Eosinophils by Anti-CD30 Antibody Treatment In Vitro

Extremely Rapid and Intense Induction of Apoptosis in Human Eosinophils by Anti-CD30 Antibody Treatment In Vitro

Mast cell CD30 ligand is upregulated in cutaneous inflammation and mediates degranulation-independent chemokine secretion

Infliximab in Recalcitrant Severe Atopic Eczema Associated with Contact Allergy

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