Immunohistochemical identification of type II alternatively activated dendritic macrophages (RM 3/1 +++ , MS-1 ± , 25F9 - ) in psoriatic dermis

Djemadji-Oudjiel, Noel; Goerdt, S.; Kodelja, Vitam; Schmuth, Matthias; Orfanos, Constantin E.

doi:10.1007/s004030050137

Cited by 32 publications

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“…All sections were examined by light microscopy (×40); 3 consecutive high-power fields were chosen. As previously described [32, 33], the dermal lymphocytes were evaluated semiquantitatively by two independent observers using a graded scale, based on the percentage of cells reactive with each antibody as compared to the total number of infiltrating cells: 0 = 0%, 1 = <10%, 2 = 10–30%, 3 = >30%. Values are given as means ± SD.…”

Section: Methodsmentioning

confidence: 99%

Overexpression of c-<i>myb</i> in Leukaemic and Non-Leukaemic Variants of Cutaneous T-Cell Lymphoma

et al. 2005

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Background: The c-myb oncogene is a transcription factor that regulates proliferation, differentiation and apoptosis of haematopoietic cells and activated T cells by binding to promoter sequences of such genes as c-myc or bcl-2 that are expressed in cutaneous T-cell lymphoma (CTCL). Objective: Our study was performed in order to evaluate c-myb expression as a quantitative parameter for differential diagnosis in leukaemic and non-leukaemic variants of CTCL. Methods: c-myb expression was analysed in lesional skin and in the peripheral blood of 21 patients with mycosis fungoides (MF), 15 patients with Sézary syndrome (SS) and 15 patients with inflammatory skin diseases using immunohistochemistry and semiquantitative as well as quantitative RT-PCR. Results: Immunohistochemistry confirmed expression of c-myb in the lesional skin of the majority of CTCL patients with a tendency towards higher expression in SS (1.86 ± 0.5) versus MF (1.2 ± 0.7) while c-myb was absent from the lesional skin of patients with inflammatory skin diseases. c-myb was overexpressed in the peripheral blood in all SS patients (100% SS vs. 35.7% MF) at a high expression level (51,335.31 ± 31,960.32 AU in SS vs. 1,226.35 ± 1,258.29 AU in MF using semiquantitative RT-PCR, and 5.72 × 10^–2 ± 2.27 × 10^–2 in SS vs. 0.91 × 10^–2 ± 1.18 × 10^–2 in MF vs. 0.24 × 10^–2 ± 0.11 × 10^–2 in inflammatory skin disease using quantitative RT-PCR). CD4+ cells from the peripheral blood of SS patients and cell lines in vitro showed the highest c-myb expression levels upon quantitative RT-PCR (23.27 × 10^–2 and 10.78 × 10^–2 ± 7.24 × 10^–2). Conclusion: Overexpression of c-myb in skin lesions of both non-leukaemic and leukaemic CTCL independent of the stage of the disease indicates that it acts early in disease development. Nevertheless, if positive, c-myb expression in lesional skin is a clear-cut diagnostic marker for CTCL as compared to inflammatory skin diseases. High-level expression of c-myb in the peripheral blood as assessed by quantitative RT-PCR constitutes an additional diagnostic parameter for SS and may be especially useful in cases in which morphological determination of Sézary cells or FACS analysis of CD7 and CD26 remain inconclusive.

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Section: Methodsmentioning

confidence: 99%

Overexpression of c-<i>myb</i> in Leukaemic and Non-Leukaemic Variants of Cutaneous T-Cell Lymphoma

et al. 2005

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“…All sections were examined by light microscopy (×160), 3 consecutive high-power fields were chosen. As previously described by Djemadji-Oudjiel et al [12], the dermal lymphocytes were evaluated semiquantitatively by 2 independent observers using a graded scale, based on the percentage of cells reactive to each antibody as compared to the total number of infiltrating cells: 4 = >75%; 3 = 75–50%; 2 = 50–25%; 1 = 25–5%; 0 = 5–0%. Values are given as means ± SD.…”

Section: Methodsmentioning

confidence: 99%

Jessner’s Lymphocytic Infiltration of the Skin: A CD8+ Polyclonal Reactive Skin Condition

et al. 2003

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Background: Jessner’s lymphocytic infiltration of the skin (JLIS) is a clinically and histologically distinct disease entity. Conflicting results have been reported concerning its differentiation from cutaneous lupus erythematosus and polymorphous light eruption, its relationship to palpable migratory arciform erythema and its classification as a B-cell or a CD4+ T-cell lymphoproliferative disease. Objective: Our study was performed in order to re-evaluate JLIS clinically and by immunohistochemical and molecular analyses. Methods: Stringent inclusion/exclusion criteria were used to collect a cohort of 34 patients with JLIS that did not overlap with lupus erythematosus or polymorphous light eruption. Clinical data were analysed, and immunohistochemical and molecular studies were performed including TCR-γ PCR GeneScan software analysis of tissue and peripheral blood samples. Results: In the majority of the patients, the lesions consisted only of papules and plaques while in 12% annular lesions were also seen. The lesions were found on the face (38%), on the trunk and arms (50%) or at both sites (12%). Immunohistochemical analyses revealed a clear predominance of T cells in all patients, and of CD8+ T cells in 77% of the patients. As judged by TCR-γ PCR GeneScan analysis, 98 and 79% of the tissue and peripheral blood samples, respectively, showed a polyclonal T-cell population; identical T-cell clones were not detected concomitantly in both the skin and the peripheral blood of the same patient. Conclusions: JLIS occurs at 2 major predilection sites, that is the face and trunk. Therefore introduction of palpable migratory arciform erythema as a separate entity is not justified. The lymphoid infiltrates are dominated immunohistochemically by CD8+ T cells that do not show clonality on molecular analysis. Thus, JLIS represents a characteristic CD8+ polyclonal reactive skin condition.

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“…Functionally, aaMΦ are important players in down-modulating inflammation and immunity, and they exert Th2-associated effector functions [6]. aaMΦ are obtained during the healing phase of acute inflammatory reactions [23], in chronic inflammatory diseases, such as rheumatoid arthritis [24]and psoriasis [25], and in wound healing tissue [8], in vivo. In the present study, macrophages treated with serum of patients with BD, another chronic inflammatory disorder, showed neither AMAC-1 expression nor staining with mAb which identify proteins characteristic for aaMΦ.…”

Section: Discussionmentioning

confidence: 99%

Serum of Patients with Behçet’s Disease Induces Classical (Pro-Inflammatory) Activation of Human Macrophages in vitro

et al. 2003

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Background: Although several immunological abnormalities have been demonstrated in Behçet’s disease (BD), the exact mechanism of the inflammatory changes occurring is still unknown. Antigen-presenting cells, such as mononuclear phagocytes, play a major role in the regulation of immune-mediated as well as of non-specific inflammation. Objective: To investigate the serum activity of patients with BD on antigen and chemokine expression of human macrophages in vitro. Methods: Serum of 15 patients (8 women, 7 men; mean age 33 ± 10 years) with BD was incubated with cultured macrophages isolated from peripheral blood of healthy volunteers. Macrophages maintained in patients’ serum, fetal calf serum with/without dexamethasone and interleukin (IL)-4 or γ-interferon were investigated for alternative macrophage-activation-associated CC-chemokine 1 (AMAC-1) and IL-8 mRNA expression by Northern blotting. In addition, cytocentrifuge macrophage preparations were stained with monoclonal antibodies against proteins indicating alternative (anti-inflammatory) macrophage activation, such as MS-1 high-molecular-weight protein (MS-1-HMWP), RM3/1 antigen (CD163) and 25F9, as well as classical (pro-inflammatory) macrophage activation, such as CD11c, class I receptor binding the Fc part of IgG (FcγRI: CD64) and class III receptor binding the Fc part of IgG (FcγRIII: CD16). Results: Macrophages treated with patients’ serum showed neither AMAC-1 expression nor staining with monoclonal antibodies for MS-1-HMWP, CD163 or 25F9. Concomitant treatment with IL-4/dexamethasone up-regulated significantly the expression of CD163. In contrast, IL-8 mRNA expression and staining for CD11c and CD64 were strongly positive after treatment with serum of patients with BD. CD64 positivity and IL-8 mRNA expression were more prominent in patients with active BD than in patients with inactive disease. Conclusion: Taken together, our results indicate that serum of patients with BD induces classical (pro-inflammatory) activation of human peripheral blood macrophages in vitro. Our findings suggest that serum factor(s) may be responsible for inflammatory changes in BD.

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Immunohistochemical identification of type II alternatively activated dendritic macrophages (RM 3/1 +++ , MS-1 ± , 25F9 - ) in psoriatic dermis

Cited by 32 publications

References 0 publications

Overexpression of c-<i>myb</i> in Leukaemic and Non-Leukaemic Variants of Cutaneous T-Cell Lymphoma

Overexpression of c-<i>myb</i> in Leukaemic and Non-Leukaemic Variants of Cutaneous T-Cell Lymphoma

Jessner’s Lymphocytic Infiltration of the Skin: A CD8+ Polyclonal Reactive Skin Condition

Serum of Patients with Behçet’s Disease Induces Classical (Pro-Inflammatory) Activation of Human Macrophages in vitro

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