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S Goerdt

Publications and source records attributed to S Goerdt.

At least 91 records · Page 5Linked to original sources
PubMed1997

Cutaneous involvement in prelymphomatous angioimmunoblastic lymphadenopathy.

We describe prelymphomatous angioimmunoblastic lymphadenopathy with cutaneous involvement in a 73-year-old female patient. A maculopapular skin eruption was the first sign of the disease. Skin histology showed extensive perivascular and periadnexal mixed lymphoid infiltrates including centroblasts and immunoblasts with a high proliferative index and with focal erythrocyte extravasation. Lymph node histology confirmed the diagnosis, showing nearly complete effacement of the follicular architecture, a mixed lymphoid infiltrate, and numberous high endothelial venules in an expanded T-cell zone. Immunohistochemistry, however, demonstrated preservation of at least some follicular structures. T-cell receptor gene rearrangement analysis revealed oligoclonal patterns in both lymph node and skin specimens. In contrast, immunoglobulin heavy-chain gene rearrangement analysis revealed a polyclonal pattern. Accordingly, the disease was classified as a prelymphomatous stage of angioimmunoblastic lymphadenopathy with dysproteinemia (AILD) with specific involvement of both lymph node and skin. The patient was treated with high-dose corticosteroids, and long-lasting remission was induced. In contrast to our case, most reported cases of AILD show a monoclonal T-cell pattern indicating AILD-type lymphoma. Therefore we discuss the concept of prelymphomatous AILD developing into AILD-type lymphoma. Persistence of some antigenic stimulus may induce the proliferation of a monoclonal population of lymphoid cells from a polyclonal background in a multistep fashion. Proper treatment of AILD at an early, prelymphomatous stage may protract or inhibit development of full-blown, fatal AILD-type lymphoma.

Aged↗
PubMed1997

Alternatively activated macrophages actively inhibit proliferation of peripheral blood lymphocytes and CD4+ T cells in vitro.

We compared the immunological functions of interferon-gamma (IFN-gamma)-induced, classically activated macrophages (caM phi) and of interleukin-4 (IL-4)- and glucocorticoid-induced, alternatively activated macrophages (aaM phi) in a human co-culture system in vitro. Proliferation of peripheral blood leucocytes (PBL) or CD4+ T cells mediated by optimal doses of phytohaemagglutinin (PHA) or concanavalin A (Con A) was only marginally influenced by caM phi, but was strongly inhibited by aaM phi. The degree of lymphocyte proliferation sustained in the presence of caM phi was gradually reduced in a dose-dependent fashion by the addition of aaM phi. Flow cytometric analysis revealed that expression of costimulatory molecules such as CD11a, CD40, CD54, CD58, CD80 and CD86 did not vary significantly between caM phi and aaM phi and was low for CD58, CD80 and CD86. As shown by reverse transcriptase-polymerase chain reaction (RT-PCR) analysis, IL-10 was expressed in caM phi, aaM phi and control macrophages; the level of expression of IL-10 was slightly enhanced in aaM phi. Neither neutralizing anti-IL-10 antibodies, indomethacin nor NG-monomethyl-L-arginine (NMMLA) was able to reverse aaM phi-mediated inhibition of lymphocyte proliferation. Of several agents interfering with various second messenger pathways, cAMP and the Ca(2+)-ionophore A23187 inhibited differentiation of cultured human monocytes into phenotypically mature aaM phi expressing MS-1 high molecular weight protein (MS-1-HMWP) and RM 3/1 antigen, and prevented the suppressive action of aaM phi on lymphocyte proliferation. In conclusion, these results who that aaM phi actively inhibit mitogen-mediated proliferation of PBL and CD4+ T cells independently of the expression of costimulatory molecules and of IL-10, NO or prostaglandin synthesis, and that inhibition of phenotypic differentiation of aaM phi is paralleled by a lack of functional maturation. Thus, fully matured aaM phi may be functional in down-regulating CD4+ T-cell-mediated immune reactions by an as yet unknown mechanism.

CD4-Positive T-Lymphocytes↗
PubMed1996

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

Immunological mechanisms play an important role in the pathogenesis of psoriasis. Lesional psoriatic skin-derived T-cell clones have been shown to stimulate keratinocyte proliferation and to predominantly express a T-helper type 1 cytokine pattern. However, T-helper type 2-like cytokines have also been identified in some psoriatic T-cell clones. In parallel to the T-helper type 1/type 2 dichotomy, a distinction between interferon-gamma-induced (classically activated) macrophages and interleukin-4/glucocorticoid-induced (alternatively activated) macrophages has been put forward as a conceptual framework for a better understanding of immunopathological processes. In the present study, the phenotype of mononuclear phagocytes in psoriatic skin lesions (n = 21), allergic contact dermatitis (n = 4) and normal skin (n = 2) was investigated using a panel of monoclonal antibodies (mAb) against monocytes/macrophages and dendritic cells (mAb MS-1, RM 3/1, and 25F9 against subsets of in vitro alternatively activated macrophages, and mAb against myeloid antigens CD1a, CD11b, CD11c, CD34, CD36, and CD68). With regard to mononuclear phagocytes, psoriatic skin was found to be compartmentalized into epidermis, subepidermal space, and upper and lower dermis. RM 3/1++ +, MS-1+/-, 25F9- dendritic macrophages previously classified as type II alternatively activated macrophages were the dominant dermal macrophage population in psoriatic skin, while intraepidermal and epithelium-lining macrophages expressed a different, presumably classically activated, macrophage phenotype (RM 3/1-, MS-1-, 25F9-, CD68+2, CD11b+2). In allergic contact dermatitis, a classical T-helper type 1 disease, RM 3/1++ + macrophages were less prominent. Since MS-1 high molecular weight protein is much more sensitive to interferon-gamma-induced suppression than RM 3/1 antigen, a predominance of T-helper type 1 cytokines in psoriasis could explain why dermal dendritic macrophages do not express the fully induced MS-1++ +, RM 3/1++ +, 25F9+/- phenotype of type I alternatively activated macrophages.

Antibodies, Monoclonal↗
PubMed1996

[Rare variants of cutaneous T-cell lymphomas].

Besides the classical forms of cutaneous T-cell lymphoma (C-CTCL), such as mycosis fungoides and Sézary's syndrome, unique variants may be encountered. The classification of these rare cutaneous T cell lymphomas is problematic and controversial. Newer classifications of lymphoma in general, such as the Revised European-American Lymphoma (REAL) Classification, emphasize well-established clinico-pathological entities. It seems appropriate to attempt to bring greater clarity to the classification of cutaneous T-cell lymphomas using the same principles. In this review, we list and characterize the rare variants of cutaneous T-cell lymphoma, such as (1) clinical, histological and immunological variants of mycosis fungoides; (2) progressive cutaneous T-cell lymphoma (P-CTCL) including transformed classical cutaneous T-cell lymphoma (TC-CTCL) and primary progressive cutaneous T-cell lymphoma (PP-CTCL); (3) angiocentric and angioimmunoblastic cutaneous T-cell lymphomas; (4) large cell anaplastic, CD30+ cutaneous T-cell lymphoma; (5) HTLV-I-associated adult T-cell leukemia/lymphoma (ATLL); (6) cutaneous manifestations of primary extracutaneous T-cell neoplasias; (7) unclassifiable cutaneous T-cell lymphoma.

Antigens, CD↗
PubMed1996

[Interferon-alpha-induced psoriasis vulgaris].

In recent years, interferon-alpha has become widely used for systemic therapy of tumours and infectious diseases. Well-known cutaneous side effects include dry skin, pruritus and hair loss. Since 1986, 17 patients with renal cell carcinoma, malignant melanoma, hepatitis B and C, carcinoid syndrome and hairy cell leukemia have been reported in whom psoriasis with or without psoratic B joint involvement was induced or exacerbated by systemic interferon-alpha therapy. In these patients, the drug was discontinued because of the severity of the psoriatic symptoms induced. The psoriatic lesions then resolved in nearly all patients within 2 weeks to 6 months, but in 10 of 22 patients treated with interferon-alpha specifically for psoriasis exacerbation was reported. We report three new cases of interferon-alpha-induced psoriasis. The patients were treated with the drug for HIV-associated Kaposi's sarcoma, renal cell carcinoma, and hepatitis C. We conclude that interferon-alpha can provoke psoriatic skin and joint symptoms, especially when additional precipitating factors are involved. In patients in whom such risks are present careful consideration of the benefit/risk ratio and concomitant antipsoriatic treatment are essential if interferon-alpha therapy is to be continued.

Adult↗
PubMed1996

[2 unusual cutaneous T-cell lymphomas with extracutaneous involvement].

In this paper we present two patients with T-cell lymphomas, who presented with unique skin lesions, but later developed extracutaneous involvement. The first patient showed marked edematous infiltration of the trunk and legs as well as grouped, umbilicated red-to-blue papules limited to the body folds. The second patient had lesions reminiscent of poikiloderma vascular atrophicans, with erythema, teleangiectasia, hypo- and hyperpigmentation, and bizarre scarring, followed by development of papules and nodules. The first patient also had marked leukocytosis and lymph node enlargement. Histology, immunohistology, and immunophenotyping revealed an unclassifiable CD8+, alpha, beta +, CD10+ cutaneous T cell lymphoma with leukemic involvement. Unclassifiable cutaneous T-cell lymphoma was also diagnosed in the second patient: it was associated with a monoclonal proliferation of T-cell receptor V gamma 9, delta + large granular T lymphocytes and finally developed into frank, acute pre-T lymphatic leukemia.

Adult↗
PubMed1996

Hereditary progressive mucinous histiocytosis.

We describe hereditary progressive mucinous histiocytosis, a rare autosomal dominant non-Langerhans cell histiocytosis, in a mother and daughter. Both had similar, progressive eruptions of skin-colored to red-brown papules on the nose, hands, forearms, and thighs. Light microscopy showed small collections of epithelioid histiocytes and telangiectatic vessels in the upper dermis of early lesions. In the mid dermis of early and well-developed lesions, nodular aggregates of tightly packed spindle-shaped cells were seen. Moderate to extensive mucin production was demonstrated in epithelioid histiocytes and spindle-shaped cells. Electron microscopy of spindle-shaped cells revealed many dendritic histiocytes with abundant lysosomal storage organelles such as myelin bodies and zebra bodies. Immunohistochemistry showed expression of macrophage antigens (CD68; MS-1 high-molecular-weight protein) in epithelioid histiocytes and in some of the spindle-shaped cells. The histologic and immunohistochemical features of hereditary progressive mucinous histiocytosis most closely resemble solitary histiocytoma/cellular-type dermatofibroma.

Adult↗
PubMed1996

The mononuclear phagocyte-dendritic cell dichotomy: myths, facts, and a revised concept.

Since Aschoff's reticuloendothelial system was abandoned a few decades ago, classification and characterization of the mononuclear phagocyte and dendritic cell systems have evolved separately or even in competition with one another. New information has now become available indicating that monocytes/macrophages and dendritic cells have a common origin in the bone marrow, and may even transdifferentiate. Morphological and functional distinctions-although valid under certain conditions-have been blurred by revelation of the versatility of monocytes/macrophages and dendritic cells in response to different contextual needs in inflammation and immunity. Monocytes/macrophages and dendritic cells share a sentinel, receptor/effector, and presentation mode, and may either activate or silence specific immune reactions. In keeping with the view of monocytes/macrophages and dendritic cells as interactive sentinels, we suggest that the mono-nuclear phagocyte and dendritic cell systems be replaced by the custocyte system (custos, Lat = sentinel, guard) as a unifying concept. Within the custocyte system, we recognize type I, type II, and type III custocytes. Type I and II custocytes exhibit predominance of presentation or effector/presenter interdependency, respectively, while type III custocytes are bipolar, passing through type I- and type II-like phases during their development and in inflammatory responses. The custocyte system brings into view monocytes/macrophages and dendritic cells as dynamic players in immunity and inflammation with a high degree of derivational, phenotypic, functional, and molecular plasticity.

Animals↗
PubMed1995

[Possibilities and limits of paraffin-embedded cell markers in diagnosis of primary cutaneous histiocytosis].

To date, the rare primary histiocytoses of the skin are diagnosed definitively on the basis of the clinical symptoms, H&E-stained sections, and demonstration of CD1 positivity in frozen sections and of Birbeck granules on electron microscopy. The improvement and analysis of antibodies with the ability to react in paraffin tissue allow retrospective evaluation and classification of these disorders. The antibodies for S-100-protein, peanut agglutinin (PNA) and PCNA (proliferating cell nuclear antigen) have been advocated for differentiation of the specific cells of Langerhans cell histiocytosis (LCH) from other histiocytic cell systems. To date the non-Langerhans cell histiocytoses (non-LCH) have no common ultrastructural and immunohistochemical characteristics. The infiltrate is made up of multiple cell populations, which are of significance for the cellular pathobiology (subtypes of monocytes/macrophages and dendritic cells). The number and distribution of the different monocyte/macrophages and dendritic cells and their ability to react with immunohistochemical markers in paraffin tissue can be completely different in different clinical entities. The antibodies against factor XIIIa (shown on xanthoma disseminatum) and the monoclonal antibody Ki-M1P (shown on juvenile xanthogranuloma) seem to be valuable in discrimination between LCH and non-LCH. Both markers show a positive staining pattern with the characteristic large macrophages. In juvenile xanthogranuloma, the foam cells and giant cells express Ki-M1P, KP1 and anti-cathepsin B. Other monocyte/macrophage markers with the ability to react in paraffin tissue, such as Mac387, lysozyme, alpha 1-antitrypsin and Leu-M1 (Anti-CD 15), in contrast, did not show a typical staining pattern with the characteristic large macrophages dominating the histological picture.

Biomarkers, Tumor↗
PubMed1995

[Generalized granuloma annulare or diffuse dermal histiocytosis?].

Generalized granuloma annulare is a rare variant of granuloma annulare affecting the trunk and extremities with a multitude of lesions. In contrast to localized granuloma annulare, generalized granuloma annulare occurs in older patients, shows a stronger association with diabetes, and is characteristically chronic. Like our 55-year-old patient, most patients present with papules and annular plaques; less often, macular or non-annular lesions may be encountered. Histology often fails to show necrobiotic or necrotic connective tissue changes demarcated by a palisading granuloma. Instead, there are diffuse dermal, band-like or nodular aggregations of histiocytes intermingled with some multinucleated giant cells and a predominantly lymphocytic infiltrate in the periphery. Because of its special characteristics, it has been suggested that generalized granuloma annulare might constitute a separate disease entity and that it should be classed among the primary cutaneous histiocytoses as a diffuse dermal histiocytosis. Using immunohistochemistry to determine the macrophage phenotype of the lesional histiocytes, we have shown that generalized granuloma annulare is not a cutaneous histiocytosis. Neither MS-1 high-molecular-weight protein, a new specific marker for cutaneous non-Langerhans cell histiocytoses, nor CD1a, the well-known marker for Langerhans cells and Langerhans cell histiocytoses, is expressed by the lesional histiocytes of our patient. In contrast, the antigen expression pattern was diagnostic for non-infectious granulomas and was highly similar to that in localized granuloma annulare. In contrast to the successful treatment of localized granuloma annulare reported with intralesional interferon beta-1, systemic treatment with interferon alpha-2b (9 x 10(6) units three times a week) was ineffective.

Biopsy↗
PubMed1995

Normolipemic papular xanthomatosis in erythrodermic atopic dermatitis.

We describe papular xanthomatosis that progressively developed in a patient with long-standing erythrodermic atopic dermatitis and normal lipid metabolism and without an associated systemic disease. Light microscopy showed a lobulated aggregate of sometimes foamy histiocytes. Ultrastructurally, these histiocytes contained lipid inclusions and lacked features of Langerhans or epithelioid cells. Other granulomatous skin diseases such as tuberculosis, sarcoidosis, or foreign body granuloma were excluded by histologic study, polarizing microscopic examination, electron microscopy, and microbiologic investigations. Nevertheless, these xanthomas showed an antigen expression pattern similar to that found in noninfectious granulomas (CD1a-, MS-1-, CD11c+, MRP-8/-14+, 25F9+, RM 3/1+/-, CD36(+), indicating that normolipemic papular xanthomatosis may be reactive process and should not be included among the true cutaneous non-Langerhans cell histiocytoses.

Adolescent↗
PubMed1995

Chronic urticaria, arthralgia, raised erythrocyte sedimentation rate and IgG paraproteinaemia: a variant of Schnitzler's syndrome?

Schnitzler's syndrome is a distinct disease entity characterized by the association of chronic urticaria, intermittent fever, arthralgia, elevated erythrocyte sedimentation rate and IgM macroglobulinaemia. We report a patient with the same symptoms, but a monoclonal IgG instead of IgM gammopathy. Histological examination of the urticarial lesions showed signs of mild leucocytoclastic vasculitis. Except for the different class of the monoclonal immunoglobulin, the clinical symptoms, laboratory findings and histology in this patient were identical with those in classical Schnitzler's syndrome. IgG and IgM paraproteins may be equivalent with regard to the putative pathophysiology of the disease process in Schnitzler's syndrome. We therefore suggest that the spectrum of Schnitzler's syndrome is expanded to include patients with chronic urticaria and monoclonal IgG gammopathy, as a closely related variant.

Arthralgia↗
PubMed1994

Differential distribution of intercellular adhesion molecules (ICAM-1, ICAM-2, and ICAM-3) and the MS-1 antigen in normal and diseased human synovia. Their possible pathogenetic and clinical significance in rheumatoid arthritis.

OBJECTIVE: Cellular adhesion and differentiation molecules (CAMs) may play a role in the recruitment and retention of inflammatory cells into rheumatoid arthritis synovial tissue (RA ST). In order to determine if certain CAMs are up-regulated in RA ST compared with normal ST, we studied the distribution of intercellular adhesion molecules (ICAMs) 1, 2, and 3 in ST. We also studied the MS-1 antigen since it is preferentially expressed on discontinuous endothelia, such as those found in RA ST; MS-1 is also expressed differentially upon cytokine activation of cells in vitro or in pathologic conditions in situ. Thus, we postulated a possible similarity between MS-1 and ICAM-1 expression in inflamed ST. METHODS: Immunohistochemical analysis was used to determine the distribution of ICAMs and MS-1 in ST from 10 patients with RA, 10 with osteoarthritis (OA), and 4 normal individuals. RESULTS: ICAM-1 expression was found on significantly more RA ST endothelial cells compared with normal cells, as well as on RA ST macrophages and lining cells. ICAM-2, also found on endothelial cells, showed no differential staining pattern. ICAM-3 was present on RA ST macrophages and lining cells as well as on some RA and OA endothelial cells. The MS-1 antigen was present on most RA and OA ST endothelia, lining cells, and macrophages. ICAM-1 expression and MS-1 expression in the lining layer were positively correlated in both RA and OA. CONCLUSION: ICAM-1, while found mainly on endothelial cells, is up-regulated on RA ST macrophages and lining cells, suggesting a role for these cells in the infiltration and tissue damage seen in the RA ST: ICAM-3, which is present mainly on normal resting leukocytes but not on normal endothelium, is expressed by some diseased ST leukocytes and endothelial cells. MS-1 is also found on the RA ST specialized, fenestrated endothelium, on macrophages, and in the lining layer. These results suggest that the differential expression of ICAMs and MS-1 in RA ST compared with normal ST might play a special role in the pathogenesis of RA.

Arthritis, Rheumatoid↗
PubMed1994

A unique non-Langerhans cell histiocytosis with some features of generalized eruptive histiocytoma.

A symmetric eruption of hundreds of coalescent small red macules and a few slightly elevated papules sparing the flexures was observed in a 73-year-old man. Light microscopic examination showed loose aggregates of small and large histiocytic cells. Electron microscopy showed an absence of Langerhans cell granules and lipid droplets. Features shared with generalized eruptive histiocytoma were the symmetry of the eruption sparing the flexures, the blue-red coloration, and the absence of lipid-containing foam cells and multinucleated giant cells. However, the primary occurrence of macules rather than papules or nodules, the tendency of the macules to coalesce, and the dimorphic histiocytoid infiltrate are not found in generalized eruptive histiocytoma. Nevertheless, immunohistochemistry confirmed that this unique condition is a form of MS-1+ cutaneous non-Langerhans cell histiocytosis.

Aged↗
PubMed1994

Dissection of macrophage differentiation pathways in cutaneous macrophage disorders and in vitro.

Macrophages play important roles in immunity and inflammation, and in allergic, granulomatous and neoplastic diseases. Here, we present the indepth results of an ongoing study of macrophage differentiation pathways in cutaneous macrophage disorders and in vitro. Up to now, a total of 40 cases of cutaneous macrophage disorders (histiocytoses and granulomas) and related diseases were examined using a panel of monoclonal and polyclonal antibodies to macrophage differentiation antigens (mAb MS-1, mAb alpha CD1a, mAb alpha CD34, mAb RM 3/1, mAb alpha CD11c, mAb alpha CD36, mAb MAC 387, mAb 27E10, polyclonal antibodies alpha MRP-8 and -14, mAb alpha CD68, mAb 25F9, mAb DRC1-R4/23, and mAb 1F10). Of these, MS-1 high molecular weight protein, synthesized by non-continuous sinusoidal endothelial cells and highly dendritic perivascular macrophages in normal human organs, is the most specific macrophage differentiation marker. MS-1 high molecular weight protein is selectively expressed by cutaneous non-Langerhans cell histocytoses, and proves to be a valuable diagnostic tool for these diseases. MS-1 high molecular weight protein is not found in Langerhans cell histiocytosis cells, epithelioid cells in sarcoidosis, and palisading histiocytes in granuloma annulare. MS-1+ macrophages may be found intermingled in cellular type dermatofibroma and in foreign body granulomas; they differ from MS-1+ non-Langerhans cell histiocytosis cells by their highly dendritic morphology, and thus rather resemble the MS-1+ macrophages in normal skin. RM 3/1 antigen shows a similar, but broader expression pattern including non-Langerhans cell histiocytoses, xanthelasmata palpebrarum, foreign body granulomas, granuloma annulare, and cellular type dermatofibroma. Moreover, xanthelasmata palpebrarum paradigmatically represent a class of macrophage lesions with strong RM 3/1, but little MS-1 antigen expression. In sarcoidosis, RM 3/1+ macrophages are only found at the very periphery of epithelioid cell granulomas. In contrast, 25F9 antigen is strongly and consistently expressed in epithelioid cells of sarcoidosis, and in foreign body granulomas. In cultured human monocytes/macrophages, RM 3/1 antigen is expressed early on, while MS-1 high molecular weight protein and 25F9 antigen are late and very late macrophage differentiation antigens, respectively. Expression of RM 3/1 antigen and MS-1 high molecular weight protein is inducible by glucocorticoid and interleukin-4, and less so by interleukin-13 and interleukin-10, and combinations thereof, while 25F9 antigen seems to be less influenced by these agents. Interferon-gamma (and less so tumor necrosis factor-alpha) inhibit expression of all three antigens in cultured human monocytes/macrophages.(ABSTRACT TRUNCATED AT 400 WORDS)

Antigens, CD↗