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Biomedical subjects

K D Cooper

Publications and source records attributed to K D Cooper.

At least 91 records · Page 5Linked to original sources
PubMed1993

Pemphigoid vegetans represents a bullous pemphigoid variant. Patient's IgG autoantibodies identify the major bullous pemphigoid antigen.

Pemphigoid vegetans is a rare disease; only four cases have been reported. The relationship of pemphigoid vegetans to bullous pemphigoid is not completely defined. We describe a case in a 77-year-old woman who had multiple well-circumscribed, erythematous, erosive, and vegetating plaques in the axillae and inframammary areas and in the neck. Microscopic examination revealed epidermal hyperplasia, dermoepidermal junctional separation, and prominent dermal eosinophilia. In the perilesional skin IgG was deposited linearly at the basement membrane zone. In addition, our patient's IgG autoantibodies, primarily the IgG4 subclass, reacted with the epidermal side of salt-split normal human skin and with the 230 kd major bullous pemphigoid antigen. We conclude that pemphigoid vegetans is best classified as a bullous pemphigoid variant.

Aged↗
PubMed1993

Cutaneous T-cell lymphoma associated with HIV infection.

BACKGROUND: Mycosis fungoides-type cutaneous T-cell lymphoma is uncommon in association with human immunodeficiency virus type 1 (HIV-1) infection. Reported patients have a high incidence of CD8+ T-cell lymphomas and erythroderma, are usually severely immunocompromised, and rapidly die. Chronic, more typical patch-plaque mycosis fungoides-type cutaneous T-cell lymphoma in association with HIV-1 infection has not been reported. OBJECTIVE: We report two cases of stage 1B epidermotropic mycosis fungoides-type cutaneous T-cell lymphoma in HIV-1-infected men with no history of the acquired immunodeficiency syndrome. METHODS: Clinical and laboratory data, including lesional immunophenotypic and immunogenotypic findings of two patients with HIV-1-associated cutaneous T-cell lymphoma, were studied. RESULTS: Immunohistochemical analysis of skin determined the lesional infiltrate of one patient to be CD8+ (Leu-2+), CD7- (Leu-9-), and Leu-8- with germline lesional skin and blood T-cell receptor genes. The other was CD4- (Leu-3+), CD2- (Leu-5-), CD7- (Leu-9-), and Leu-8- with beta-chain T-cell receptor gene rearrangement in lesional skin and blood. Circulating Sézary cells were not detected in either patient. Peripheral CD4/CD8 T lymphocyte numbers did not appear to correlate with cutaneous disease activity or the predominant lesional T-cell subtype. Both patients were responsive to standard therapies and have experienced prolonged survival in excess of that generally reported for HIV-1-associated systemic peripheral and cutaneous T-cell lymphomas. CONCLUSION: In the absence of severe immunodeficiency, HIV-1-infected patients with concomitant cutaneous T-cell lymphoma may follow a more typical slowly progressive course.

Adult↗
PubMed1993

CD1 gene expression in human skin.

In human epidermis, expression of CD1a is confined to Langerhans cells (LC), whereas CD1c expression has been observed in dendritic cells of the dermis, as well as the epidermis. In transfected fibroblasts, expression of CD1c at the cell surface appears to exclude expression of either CD1b or CD1a, despite continued transcription of the latter genes. In order to determine whether this mechanism might be operative in human skin, we have compared the expression of CD1a and CD1c on the surface of dermal and epidermal dendritic cells to their expression at the level of mRNA using a combination of dual-label immunofluorescence microscopy, northern blot hybridization, and reverse transcriptase-polymerase chain reaction (RT-PCR). By both immunofluorescence and Northern blotting, CD1c expression was observed in both dermal and epidermal cells, whereas expression of CD1a was confined largely to the epidermis. Moreover, as shown by immunomagnetic bead selection and RT-PCR, CD1a and CD1c were both expressed on epidermal LC, but were absent from other epidermal cell types. These results argue against cell surface exclusion as a mechanism for selective expression of CD1c in human dermis.

Antigens, CD↗
PubMed1993

Neutrophils, differentiated macrophages, and monocyte/macrophage antigen presenting cells infiltrate murine epidermis after UV injury.

We asked whether, as in humans, a population of antigen-presenting macrophages infiltrates the epidermis of ultraviolet (UV)-exposed BALB/c mice. Using three-color flow cytometry on cell suspensions plus in situ immunofluorescence microscopy, the phenotype of normal Langerhans cells was class II major histocompatibility complex (MHC+), CD11b+, NLDC-145+, BM8+ CD45+ and homogeneous. By contrast, in epidermal cells harvested 3 d following UV (UV-EC), there were two subsets of class II MHC+ cells: 1) class II MHChi CD11b+, and 2) class II MHClo CD11b-. Neither expressed the Langerhans cell markers BM8 and NLDC-145. In addition, there were two major populations of class II MHC- CD11b+ cells; half of these expressed the GR-1 neutrophil marker. Langerhans and dendritic epidermal T cells were markedly reduced after UV injury. By electron microscopy, immunomagnetic bead-purified CD11b+ cells in UV-EC were comprised of neutrophils, differentiated macrophages, and mononuclear cells with prominent lysosomes, but no Birbeck granules; the class II MHC+ subset resembled a monocytic cell in between differentiated macrophages and indeterminate dendritic cells. Functionally, immediately following in vivo UV exposure, the allogeneic antigen-presenting cell capacity of UV-EC was reduced to 21 +/- 6% of control epidermal cells (C-EC); by 3 d, antigen-presenting cell activity of UV-EC had recovered to 59 +/- 11% of C-EC, although at this time NLDC-145+ Langerhans cells had reached their lowest number. The recovered antigen-presenting cell activity was critically dependent upon the class II MHChiCD11b+ cells. Sensitization of BALB/c mice through skin that contained these antigen-presenting cells (3 d after UV) resulted in tolerance to dinitrofluorobenzene. By contrast, sensitization through UV-exposed skin immediately after the exposure resulted in unresponsiveness without tolerance, demonstrating temporal association of tolerance with leukocytic infiltration. In summary, murine epidermis responds to an acute UV injury in vivo with an initial abrogation of antigen-presenting activity followed by epidermal infiltration with neutrophils, differentiated macrophages, and monocytic antigen-presenting cells that are distinct from Langerhans cells with regard to expression of Langerhans cell markers and ultrastructure.

Animals↗
PubMed1993

Identification and partial characterization of a novel 105-kDalton lower lamina lucida autoantigen associated with a novel immune-mediated subepidermal blistering disease.

Certain skin basement membrane components, such as bullous pemphigoid antigens and epidermolysis bullosa acquisita antigen, were discovered as a result of an autoimmune reaction. In this report, we describe a unique lamina lucida determinant associated with a novel immune-mediated subepidermal bullous dermatosis. This unique bullous dermatosis resembled severe toxic epidermal necrolysis clinically. The histologic findings resemble dermatitis herpetiformis. Direct immunofluorescence microscopy detected linear immunoglobulin G (IgG) and C3 deposition at the cutaneous basement membrane zone of lesional and perilesional skin. Direct and indirect immunoelectron microscopy localized the IgG deposits to the lowest portion of the lamina lucida. The patient's autoantibodies, belonging to the IgG1 subclass, labeled basement membrane zone of normal intact human skin, oral mucosa, and conjunctiva, and localized to the dermal side of salt-split normal adult and neonatal human skin, but failed to react with human fetal skin up to 142 gestational days. The patient's autoantibodies failed to react with bullous pemphigoid antigens or epidermolysis bullosa acquisita antigen (type VII collagen) by immunoblotting. Instead, the patient's autoantibodies unequivocally labeled a 105-kilodalton (kD) protein in cellular extracts and conditioned media of human cultured keratinocytes and dermal fibroblasts. The titer of the patient's antibody against the cutaneous basement membrane zone and the intensity of the antibody reactivity against the 105-kD protein paralleled the patient's disease activity. Thus, this 105-kD lower lamina lucida protein represents a novel autoantigen and this patient's disease represents a novel autoantigen and this patient's disease represents a deep lamina lucida pemphigoid, distinguishable from all other known autoimmune bullous dermatoses.

Autoantigens↗
PubMed1993

Differential expression of protein kinase C isoenzymes in normal and psoriatic adult human skin: reduced expression of protein kinase C-beta II in psoriasis.

Psoriatic lesions contain elevated levels of 1,2-diacylglycerol, the physiologic activator of protein kinase C (PKC), suggesting that PKC activation may be aberrant in psoriasis. We therefore have investigated the expression and properties of PKC isozymes in normal and psoriatic skin and in human skin cells. Chromatographic and immunoblot analyses revealed the presence of the calcium-dependent PKC isozymes PKC-alpha and -beta, but not -gamma, in normal human epidermis. PKC-beta was more prominent, constituting two thirds of the total calcium-dependent PKC activity. In psoriatic lesions, expression of both PKC-alpha and -beta was decreased, with preferential reduction (80%) of PKC-beta. Northern analysis and semi-quantitative polymerase chain reaction (PCR) indicated no change in the mRNA levels of PKC-alpha and -beta between normal and psoriatic epidermis. In normal epidermis, PKC-alpha was expressed mainly in the lower epidermis, whereas PKC-beta was localized to the upper cell layers, with very intense staining of CD1a+ Langerhans cells. In psoriasis, PKC-alpha staining was present in the lower epidermis, whereas PKC-beta staining was essentially absent, with the exception of some positive inflammatory cells. In addition to PKC-alpha and beta, immunoblot and Northern/PCR analysis revealed expression of four calcium-independent PKC isozymes, delta, epsilon, zeta, and eta, in both normal and psoriatic skin. There were no significant differences in mRNA levels among any of these PKC isozymes, between normal and psoriatic skin. Soluble PKC-zeta protein was modestly increased (twofold) in psoriatic, compared to normal, skin, whereas the levels of PKC-delta, epsilon, and eta were unchanged. Analysis of PKC isozyme expression in the three major cell types of human epidermis revealed that Langerhans cells and keratinocytes were the major sources of PKC-beta and PKC-zeta, respectively. These data demonstrate the diversity of PKC isozyme expression in human skin, and suggest that alterations of PKC-beta and -zeta may participate in the aberrant regulation of growth and differentiation observed in psoriasis.

Adult↗
PubMed1993

T-lymphocyte clones initiated from lesional psoriatic skin release growth factors that induce keratinocyte proliferation.

To investigate whether growth factors derived from T cells in psoriatic lesions are able to stimulate keratinocyte growth, T-cell lines were initiated from lesional psoriasis skin and cloned by limiting dilution. Eight clones with good proliferative capacity out of 40 clones from one patient were stimulated. After 24 h, the conditioned medium was harvested and the growth modulatory effect of the conditioned medium on keratinocytes was assessed. Seven of the eight T-cell clones stimulated keratinocyte growth to an extent ranging from 22% +/- 19 to 64% +/- 9 (mean +/- SD of three experiments) of maximal inducible keratinocyte growth, and one T-cell clone had no effect (-5% +/- 2) on keratinocyte growth. Keratinocyte growth was also induced by T-cell clones obtained from two other patients. Several cytokines were tested in this system to determine which T-cell growth factor may induce the keratinocyte growth. None of the cytokines interferon-g, transforming growth factor-beta, interleukin (IL)-2, IL-3, IL-4, IL-6, IL-8, or granulocyte-macrophage colony stimulating factor alone was found to possibly be responsible for the T-cell-induced keratinocyte growth. Thus the nature of the T-cell keratinocyte growth-promoting stimulus remains to be elucidated.

Cell Division↗
PubMed1993

Cyclosporin A rapidly inhibits epidermal cytokine expression in psoriasis lesions, but not in cytokine-stimulated cultured keratinocytes.

To better understand the cellular target(s) of cyclosporin action in psoriasis, we have studied the effects of systemic short-term (7 d), low-dose (3-7.5 mg/kg) cyclosporin A administration on the expression of the cytokines interleukin (IL)-8 and IL-1 beta in psoriatic lesions. RNA blot hybridization analysis of pretreatment keratome biopsies revealed that expression of both cytokine mRNAs was highly variable from patient to patient. Significant covariation of both cytokine mRNA levels was noted (r = 0.86, p < 0.0001). However, there was no significant correlation between expression of either cytokine and clinical severity, as measured by the pretreatment Psoriasis Area and Severity Index (PASI). IL-1 beta protein levels measured by enzyme-linked immunosorbent assay (ELISA) were highly correlated with IL-1 beta mRNA levels, indicating that the differences in transcript levels accurately reflect differences in epidermal cytokine protein. Significant reductions in both cytokine transcripts and in IL-1 beta immunoreactive protein were noted in the high expression subgroup after 1 week of cyclosporin A therapy, prior to detectable clinical improvement. In contrast to its pronounced effects on epidermal cytokine expression in vivo and the allogeneic mixed lymphocyte reaction in vitro, cyclosporine A did not inhibit the induction of intercellular adhesion molecule (ICAM)-1 or IL-8 mRNAs by cultured keratinocytes in response to IL-1 beta or the combination of tumor necrosis factor (TNF)-alpha and interferon (IFN)-gamma. These data suggest that epidermal keratinocytes respond to signals produced by activated T cells by coordinate expression of multiple cytokines, and that cyclosporin A acts primarily through blockade of T cells, rather than through keratinocyte activation.

Blotting, Northern↗
PubMed1993

Leukemic T cells from patients with cutaneous T-cell lymphoma demonstrate enhanced activation through CDw60, CD2, and CD28 relative to activation through the T-cell antigen receptor complex.

Antigen-dependent activation of T cells occurs through the T-cell antigen-receptor complex (TCR/CD3). Antigen-independent T-cell activation may occur through the surface molecules CDw60, CD2, and CD28. We wished to determine whether these antigen-independent T-cell-activation pathways could be involved in proliferation of leukemic T cells from patients with cutaneous T-cell lymphoma (CTCL). Whereas CDw60 was only expressed on 28% +/- 7% (mean +/- SEM) of blood T cells obtained from healthy control subjects (n = 4), CDw60 was expressed on 94% +/- 3% of blood T cells obtained from patients with CTCL (n = 4). Dual color immunofluorescence microscopy of the T-cell infiltrate in involved skin of these patients demonstrated that almost 100% of the T cells expressed CDw60. Not only did T cells in the patients with CTCL express CDw60, but triggering of the T cells with anti-CDw60 resulted in enhanced proliferation relative to anti-TCR/CD3 and mitogenic lectins. Other antigen-independent pathways also appeared highly active in the T cells from patients with CTCL because enhanced proliferation relative to anti-TCR/CD3 or mitogenic lectins was found when anti-CD2 or anti-CD28 plus phorbol ester was used as stimulant. Despite the brisk proliferation induced by anti-CDw60, anti-CD2, or anti-CD28, T cells from the patients did not produce detectable amounts of gamma-interferon. The inability to produce gamma-interferon correlates with our finding of absent (n = 3) or weak (n = 1) intercellular adhesion molecule-1 expression in the lesional keratinocytes in these patients. In conclusion, T cells of patients with CTCL demonstrate elevated expression of a T-cell-independent signaling molecule CDw60 and respond to antigen-independent activating signals.

Aged↗
PubMed1993

Cutaneous T-cell lymphoma: CT in evaluation and staging.

Among 63 patients with cutaneous T-cell lymphoma (CTCL), 29% (n = 18) had positive computed tomographic (CT) findings, with frequencies of 65% (n = 13) among patients thought to have stages II-IV disease at clinical examination and 12% (n = 5) among patients thought to have stage I. Among eight patients with atypical CTCL variants such as cutaneous large-cell lymphoma, only one had negative findings at CT; extracutaneous disease was not suspected in five before they underwent CT. In contrast, CT findings were positive in only 5% (n = 2) of patients with classic early mycosis fungoides-type CTCL (scaling patches, small epidermotropic CD4+ cells), and CT is unlikely to provide substantial information in this patient subgroup. Contrary to earlier reports, the authors' data suggest that body CT is extremely useful in staging and evaluating patients with CTCL. CT should be included in the evaluation of atypical CTCL variants, Sézary syndrome, advanced-stage mycosis fungoides, and cases in which the CTCL subtype is unclear.

Aged↗
PubMed1993

New therapeutic approaches in atopic dermatitis.

Novel approaches to the therapy for atopic dermatitis (AD) can now be considered because of recent advances in the pathogenesis of the disease. Several of these concepts are being tested in clinical trials. The effectiveness of cyclosporin A, plus reports of adoptive transfer of AD, or its clearing, following bone marrow transplantation, verify the criticalness of immune cells in AD pathogenesis. Thus, there is renewed interest in immunosuppressives, such as azathioprine and methotrexate, as well as new adhesion molecule and T-cell activation inhibitors. Therapy with the T-cell lymphokine, interferon-gamma, or the thymic hormone, thymopentin, is designed to inhibit the IL-4-dominated response of AD T-cells. This approach, rather than directly suppressing all immune responsiveness, represents a more specific targeting to improve the balance of a chronically disordered immune response. Recent findings of a therapeutic advantage of longer-wavelength phototherapy over UVB therapy may relate to specific immunologic events following UVB vs UVA photoinjury that are critical to the exacerbation of AD. Complex herbal mixtures used in traditional Chinese medicine are currently being evaluated, but toxicity and palatability may be limiting. Other dietary approaches, such as modifying the lipid balance, have generally not had much benefit. Because the safety and efficacy of the above treatments need further exploration, the physician must continue to utilize fundamental methods, such as mitigating trigger factors (i.e., microbes and stress, and certain foods in persons with documented sensitivity), on improving the abnormal epidermal lipid barrier to irritation, and on reducing cutaneous inflammation with mild topical steroids.

Clinical Trials as Topic↗
PubMed1993

Gene rearrangements and T-cell lymphomas.

BACKGROUND: Cutaneous T-cell lymphomas comprise a broad spectrum of neoplasia ranging from indolent to highly aggressive types. To determine subset lineage and malignant vs benign nature, morphologic analysis, immunophenotyping, and flow cytometry have been used. However, given the shortcomings of these methods, molecular genetic techniques, which take particular advantage of the clonal nature of malignancy, are now being applied to better characterize and diagnose these lymphomas. RESULTS: Each antigen-specific T cell and its clonal progeny has a unique rearrangement of its T-cell receptor gene such that it can recognize very specific antigenic epitopes. By visualizing these particular T-cell receptor gene rearrangements, Southern hybridization techniques and polymerase chain reaction amplification can detect clonal populations of T cells in the skin, blood, and lymph nodes of patients with T-cell leukemias and lymphomas. Clonal T-cell populations have also been found in cases of benign disorders such as lymphomatoid papulosis and pityriasis lichenoides et varioliformis acuta. Although these disorders usually have a benign outcome, they may represent dysplastic clonal lymphoid expansions with a high incidence of spontaneous regression. CONCLUSIONS: Molecular genetic techniques have added to our ability to diagnose, characterize, and monitor the course of T-cell lymphomas and leukemias. In addition, they may provide insight into the pathogenesis of certain benign disorders.

Cloning, Molecular↗
PubMed1993

Paraneoplastic pemphigus presenting as a lichen planus pemphigoides-like eruption.

BACKGROUND: Paraneoplastic pemphigus refers to a specific disease entity in which neoplasia is associated with severe mucosal ulceration and polymorphous cutaneous eruptions, sometimes resembling erythema multiforme. Direct immunofluorescence and indirect immunofluorescence on standard substrates are similar to pemphigus vulgaris; however, paraneoplastic pemphigus serum uniquely binds to all epithelia and has distinctive immunoprecipitation characteristics. OBSERVATIONS: A 63-year-old woman with chronic lymphocytic leukemia developed a severe, mucocutaneous, vesiculobullous eruption with the clinical and histopathologic characteristics of lichen planus pemphigoides evolving into a Stevens-Johnson-like presentation and the immunofluorescence findings of pemphigus vulgaris. Evaluation of her serum confirmed the presence of autoantibodies specific for paraneoplastic pemphigus by indirect immunofluorescence and immunoprecipitation criteria. CONCLUSION: The spectrum of paraneoplastic pemphigus must now be expanded to include cases that present clinically and histologically as a lichen planus pemphigoides-like eruption.

Diagnosis, Differential↗
PubMed1993

Complete remissions in psoralen and UV-A (PUVA)-refractory mycosis fungoides-type cutaneous T-cell lymphoma with combined interferon alfa and PUVA.

UNLABELLED: BACKGROUND AND DESIGN--The optimal therapy for the mycosis fungoides type of cutaneous T-cell lymphoma has yet to be determined. Based on recent reports on the efficacy of high-dose interferon alfa in cutaneous T-cell lymphoma, we chose to test the hypothesis that systemic adjunctive therapy with low-dose interferon alfa along with psoralen and long-wave UV-A radiation (PUVA) could decrease the amount of PUVA necessary to achieve the best response, as well as improve the therapeutic effect of PUVA. Five patients with cutaneous T-cell lymphoma (mycosis fungoides type) were initially treated unsuccessfully with PUVA alone (three times a week for at least 3 months); PUVA was stopped, patients' diseases were re-staged, then interferon alfa (3 x 10(6) U/d for 1 week, then 6 x 10(6) U/d for 1 week) was initiated 2 weeks prior to restarting PUVA. Responses to treatment were graded as complete remission (skin clear, or negative biopsy specimens of remaining dermatitic lesions), partial remission (> 50% improvement), progression (> 25% worsening), or no change (failure to qualify for other categories) at 4, 8, 12, and 16 weeks. OBSERVATIONS--After 3 to 5 months of treatment with PUVA thrice weekly, none of the patients treated with PUVA alone had achieved complete remission. By contrast, systemic adjunctive therapy with low-dose interferon alfa along with PUVA resulted in complete remissions in all five (100%) patients in an average of 3.2 months (in three patients, lesions were cleared by 3 months). Average of 107 additional joules (68% more) and 1.6 additional months of PUVA administered thrice weekly was required to achieve the best response attainable with PUVA alone compared with complete remissions achieved with combined interferon alfa and PUVA therapy. CONCLUSION: --These data indicate that patients with disease refractory to PUVA alone can achieve a complete remission if they restart treatment with PUVA in combination with well-tolerated low doses of interferon alfa. In addition, the duration of PUVA exposure can be reduced with the addition of low-dose interferon alfa to the conventional PUVA treatment of cutaneous T-cell lymphoma of the mycosis fungoides type in such patients.

Adult↗
PubMed1992

UV exposure reduces immunization rates and promotes tolerance to epicutaneous antigens in humans: relationship to dose, CD1a-DR+ epidermal macrophage induction, and Langerhans cell depletion.

Increasing UVB radiation at the earth's surface might have adverse effects on in vivo immunologic responses in humans. We prospectively randomized subjects to test whether epicutaneous immunization is altered by prior administration of biologically equalized doses of UV radiation. Multiple doses of antigens on upper inner arm skin (UV protected) were used to elicit contact sensitivity responses, which were quantitated by measuring increases in skin thickness. If a dose of UVB sufficient to induce redness (erythemagenic) was administered to the immunization site prior to sensitization with dinitrochlorobenzene (DNCB), we noted a marked reduction in the degree of sensitization (P less than 0.0006) that was highly dose responsive (r = 0.98). Even suberythemagenic UV (less than a visible sunburn) resulted in a decreased frequency of strongly positive responses (32%) as compared to controls (73%) (P = 0.019). The rate of immunologic tolerance to DNCB (active suppression of a subsequent repeat immunization) in the groups that were initially sensitized on skin receiving erythemagenic doses of UV was 31% (P = 0.0003). In addition, a localized moderate sunburn appeared to modulate immunization with diphenylcyclopropenone through a distant, unirradiated site (41% weak responses) as compared to the control group (9%) (P = 0.05). Monitoring antigen presenting cell content in the epidermis revealed that erythemagenic regimens induced CD1a-DR+ macrophages and depleted Langerhans cells. In conclusion, relevant and even subclinical levels of UV exposure have significant down modulatory effects on the ability of humans to generate a T-cell-mediated response to antigens introduced through irradiated skin.

Antigens, CD↗
PubMed1992

Psoriatic skin reveals the in vivo presence of an epidermal IL-1 inhibitor.

Production of inhibitor(s) of IL-1 activity can be induced in keratinocytes by exposure to UVB. We describe in this study the characterization of an endogenous constitutively expressed IL-1 inhibitor which is present in extracts of human psoriatic epidermal keratome biopsies. Size-fractionated extracts of normal human epidermis did not reveal IL-1 inhibitory factor(s) activity in normal epidermis. Psoriatic epidermal extracts, however, contained virtually no IL-1 bioactivity and inhibited the activity of recombinant human IL-1 beta. This IL-1 inhibitor has a molecular weight of approximately 30 kDa and a pI of 5.3, as revealed by fast protein liquid chromatography size fractionation and chromatofocusing of psoriatic epidermal extracts. IL-1 inhibitory activity was not blocked by neutralizing anti-TGF beta monoclonal antibody. It did not have any inhibitory effect upon normal cellular proliferation but could block the IL-1 induction of IL-2 production by LBRM.33 cells as late as 4 h after exposure of LBRM.33 cells to IL-1. Thus, in vivo human psoriatic epidermis expresses an IL-1 inhibitor that specifically inhibits IL-1 activity but which appears distinct from previously described UV-induced epidermal IL-1 inhibitory activity or TGF beta.

Biopsy↗
PubMed1992

Mycosis fungoides--type cutaneous T-cell lymphoma arising before 30 years of age. Immunophenotypic, immunogenotypic and clinicopathologic analysis of nine cases.

BACKGROUND: Cutaneous T-cell lymphomas (CTCLs) rarely arise before 30 years of age; therefore the characteristics of these lymphomas are largely unknown. OBJECTIVE: Our purpose was to assess the clinical and pathologic aspects of CTCL in young persons. METHODS: We identified nine patients who had epidermotropic CTCL by 30 years of age and analyzed their lymphoma phenotypes and genotypes. RESULTS: The diagnosis of CTCL was made an average of 6 years after the reported onset of the lesion. Histologic examination revealed the mycosis fungoides (MF) form of CTCL, and none of the patients underwent conversion to nonepidermotropic or large-cell variants of CTCL. The immunophenotypes were typical of MF-type CTCL; seven of eight lymphomas tested were predominantly CD4+ although in only three were abnormal CD4/CD8 ratios present. All four cases tested were CD7- (Leu-9-), and seven of eight specimens tested exhibited deficient Leu-8 expression. The loss of one or more pan-T-cell markers was found in four of eight patients tested. Clonal beta-chain T-cell receptor gene rearrangements occurred in skin samples from four of eight tested cases. CONCLUSION: A persistent eruption, even in youths and young adults, should be thoroughly evaluated for possible CTCL.

Age Factors↗