Viewing affirmative mentions of gene expression of IL2 (H. sapiens) in skin

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Flexner et al. (1990)IL-2skinWild type and a control vaccinia recombinant produced large (greater than 5000 mm2) skin ulcers in this species, but the IL-2 expressing recombinant produced no ulceration.
Flexner et al. (1990)IL-2skinIL-2 expression accelerated the resolution of skin lesions in rhesus but not squirrel monkeys.
Flexner et al. (1990)IL-2skinIL-2 expression can greatly reduce the skin lesions formed by live recombinant vaccinia vectors in primates, indicating significant attenuation, without reducing the immunogenicity of the vaccine.
Zunich and Kirkpatrick (1988)interleukin-2skinEvaluation of cellular immunity (T-cell subsets, in vitro interleukin-2 production and interleukin-2 receptor expression, T-cell responses to mitogens and antigens, and delayed-hypersensitivity skin tests) as well as clinical and toxicity monitoring was performed prior to treatment, at 2-week intervals during treatment, and after the cessation of treatment.
Vonderheid et al. (1990)interleukin 2skinHowever, prolonged treatment with extracorporeal photopheresis/methotrexate was accompanied by a decrease in skin reactivity to recall antigens and by decreased capacity of lymphocytes to produce interleukin 2 in response to polyclonal stimuli in vitro.
Szczepa?ski and Kaczmarski (1995)IL-2skinThese results suggest that the increased IL-2 production in food sensitive atopic dermatitis can be very important factor in pathogenesis of skin lesions.
Morita et al. (1990)IL-2SkinPatients with atopic dermatitis (AD) were treated with Tranilast, Interleukin-2 (IL-2) (production of T cells in vitro) and blood histamine values, before and after Tranilast therapy, were measured, and the following results were obtained: 1) Compared with healthy controls, the IL-2 producing ability of T cells in patients with AD was increased. 2) After Tranilast therapy, IL-2 production of T cells in AD decreased in quantity to the control level. 3) Skin lesion severities of AD were correlated with the quantity of IL-2 production of T cells. 4) Serum histamine levels were not significantly different between AD patients and healthy controls, before or after Tranilast therapy.
Watanabe et al. (1990)interleukin-2skinDelayed hypersensitivity skin tests, lymphoblastogenesis, natural killer (NK) cell activity, and interleukin-2 (IL-2) production were employed to assess immune competence.
Sadick et al. (1984)interleukin 2skinInduction of lymphocyte proliferation and interleukin 2 production by soluble L. tropica antigens appeared within five weeks of infection and reached maximal levels coincident with ulceration of the skin lesion.
Vonderheid et al. (1989)IL-2skinAll patients, however, exhibited decreased intradermal skin responses to recall antigens and a decreased capacity of peripheral lymphocytes to produce interleukin 2 (IL-2) in response to polyclonal stimuli in vitro.
Abernethy et al. (2000)IL-2skinDysregulated expression of CD69 and IL-2 receptor alpha and beta chains on CD8+ T lymphocytes in flaky skin mice.
Bos et al. (1987)interleukin 2skinThird, the majority of skin perivascular T cells were activated as they expressed HLA-DR and interleukin 2 receptors.
Christ (1999)interleukin 2skinThe skin manifestations are a result of overstimulation of superficial skin cells (Langerhans cells) due to increased production of interleukin 2, 6 and 8 as well as transforming growth-factor-alpha.
Martinez et al. (1995)interleukin-2skinAssociation of interleukin-2 and interferon-gamma production by blood mononuclear cells in infancy with parental allergy skin tests and with subsequent development of atopy.
Martinez et al. (1995)IL-2skinMononuclear cell production of both IFN-gamma and IL-2 at 9 months, but not at birth, was found to be inversely related to parental immediate skin test reactivity to seven local aeroallergens.
Martinez et al. (1995)IL-2SkinSkin test reactivity at the age of 6 years was also inversely related to IFN-gamma and IL-2 production at 9 months of age.
Martinez et al. (1995)IL-2skinThese data suggest that mechanisms regulating skin test reactivity to inhaled allergens may involve deficient IFN-gamma production, deficient IL-2 production, or both during or preceding the time of initial sensitization and that additional mechanisms are involved in regulating total serum IgE level.
Mitsuishi et al. (2003)IL-2skinCimetidine treatment for viral warts enhances IL-2 and IFN-gamma expression but not IL-18 expression in lesional skin.
Dreno et al. (1986)IL-2skinTwo other anti-IL-2 moABs, one directed against unglycosylated recombinant IL-2 (17-2 moAB) and one against glycosylated natural IL-2 (9B11 IE5 moAB), were unreactive on skin.
Dreno et al. (1986)IL-2skinAmong several monoclonal antibodies (moABs) directed against human interleukin 2 (IL-2), the 15-2 moAB raised in our laboratory against unglycosylated recombinant IL-2 (produced in Escherichia coli) cross-reacted with a human skin epitope.
Szczepa?ski and Kaczmarski (1995)IL-2skinThe level of interleukin-2 (IL-2) in the blood serum in 28 patients with different degree of skin lesions severity of food sensitive atopic dermatitis (AD), was studied.
Gramatzki et al. (1986)IL 2skinShortly after termination of IL 2 application in two patients an increase of lectin responsiveness as well as improved reactivity in skin testing was noted, encouraging further exploration of IL 2 as an immunostimulatory drug in AIDS patients.
Vonderheid et al. (1989)IL-2skinAll patients, however, exhibited decreased intradermal skin responses to recall antigens and a decreased capacity of peripheral lymphocytes to produce interleukin 2 (IL-2) in response to polyclonal stimuli in vitro.
Bujía et al. (1996)IL-2skinWhereas IL-1 activity was not detected in skin samples, all cholesteatoma specimens studied showed a stimulation effect on the production of IL-2 when incubated with the cell line LBRM-33.
Roy et al. (1995)IL-2skinConsistent with the PBMC data, IL-2 and IL-4 RNA were also more frequently detectable in skin biopsies with GVHD (n = 10): 70% of samples expressed IL-2 vs. 25% of normal controls (n = 8; P < 0.05); 60% had detectable IL-4 RNA vs. 0% of controls (P < 0.05).
Liu et al. (2009)IL-2skinIn vivo experiments: The emodin-treated group showed prolonged MST of skin grafts and decreased serum IL-2 production.
Zwingenberger et al. (1989)lymphokineskinIn conclusion, evidence is presented for severe, antigen-unspecific suppression of lymphokine production and skin reactivity against recall antigens.
Kimura et al. (1990)lymphokineskinWhen stimulated with crude antigen, the group of patients showed elevated proliferation and production of lymphokine in comparison with the healthy skin test-negative individuals (P less than 0.01).
Coeugniet and Elek (1987)lymphokineskinThese observations were confirmed by lymphokine production and assay, 3H-thymidine incorporation and a skin test with recall antigens (Multitest Merieux).
Coeugniet (1987)lymphokineskinThe depression of cell-mediated immunity (CMI) was determined in patients with ovarian and breast carcinomas by lymphokine production under Con-A-stimulation (migration inhibitory factor), T-lymphocyte-transformation test under PHA-stimulation and with a skin reactivity test with a viscum album extract (Plenosol, Dr.
Powell et al. (1975)lymphokineskinTiming of skin reactivity, lymphokine production, and blastogenesis following rechallenge with dinitrochlorobenzene using an automated microassay.
Miller et al. (1991)lymphokineskinImmunocompetence in 25 severely head injured patients was investigated by measuring: (1) delayed-type hypersensitivity (DTH) skin test responses to common antigens; (2) phytohaemagglutinin (PHA) stimulated peripheral blood lymphocyte (PBL): blastogenesis, phenotype expression, and lymphokine production; (3) lymphokine-activated killer (LAK) cytotoxicity, antibody dependent cellular cytotoxicity (ADCC) and natural killer (NK) cytotoxicity; and (4) immunoglobulin and complement levels.
Toossi et al. (1990)IL 2skinWe studied monocytes from patients with tuberculosis and healthy skin test reactive controls for expression and function of IL 2 receptors (IL 2R).
Kunstfeld et al. (1997)IL-2skinIL-2 and IFN-gamma expression and allogeneic vessel destruction were present within both superficial and deep vascular plexus skin.
Koga et al. (1993)IL-2skinThese findings indicate that this patient has peripheral T-lymphocytes that produced IFN-gamma, IL-2 and GM-CSF, which may play roles in the development of delayed-type hypersensitivity (DTH) reaction in the skin.
van Haelst Pisani et al. (1991)IL-2skinBy the time of the third IL-2 infusion, high concentrations of major basic protein were present in all five patients (up to 5,600 ng/mL) and skin biopsies showed major basic protein deposition in the dermis.
Denton et al. (1999)IL-2skinAddition of anti-CD86 but not anti-CD80 monoclonal antibodies to cocultures inhibited IL-2 production and the proliferation of CD4(+) T cells to allogeneic donor human umbilical vein ECs (HUVECs), as well as to skin and lung microvascular ECs.
Sparkes (1991)IL2skinIn the added presence of the lipid-protein complex (LPC) derived from burned skin, PHA and ConA produced much less bioavailable IL2, the combination with PHA being more inhibitory of its production than that with ConA at concentrations of 1 microgram and 5 micrograms lectin/ml.
Wasik et al. (1996)IL-2skinThis increase in IL-2 appeared unique to this lymphoma because serum concentration of IL-2 was not increased in any of the cases of various types of cutaneous lymphoproliferative disorders tested: mycosis fungoides-related cutaneous T-cell lymphoma (CTCL: 28 patients), granulomatous slack-skin syndrome (GS-SS: 1 patient), anaplastic large cell lymphoma (ALCL: 2 patients), subcutaneous gamma/delta T-cell lymphoma (gamma/delta-TCL: 1 patient), adult-type leukemia/lymphoma (ATLL: 1 patient), and lymphomatoid papulosis (LyP: 4 patients).
Puissant-Lubrano et al. (2010)IL-2skinHere, we have shown that residual VV-specific IFN-gamma+TNF-alpha+ or IFN-gamma+IL-2+ CD4+ lymphocytes but not CD8+ effector/memory lymphocytes expressing a skin-homing marker are inversely associated with the size of the skin lesion formed in response to revaccination.
Gutiérrez et al. (1991)IL-2skinNo statistically significant differences were observed in the lymphocyte distribution nor in the IL-2 and BCDF-IgG production when comparing patients with or without scleroderma-like skin lesions.
Hawes et al. (1981)lymphokineskinStudies of cell-mediated immunity, comprising delayed hypersensitivity skin testing with four antigens, PHA and antigen-induced lymphocyte transformation and detection of the lymphokine, monocyte chemotactic factor, were undertaken in 14 women during pregnancy and in the post-natal period.
Cori?-Martinovi? and Basi?-Juki? (2008)interleukin-2skinThe mechanism underlying uremic pruritus is poorly understood; possibilities include histamin, proteases, interleukin-2 and TNF- produced by skin mast-cells, substance P, neuropathy and neurological changes, high level of Ca, P, PTH, Al, Mg, divalent ion abnormalities, hypervitaminosis A, inflammation, or some combination of these.
Mesret et al. (1995)lymphokineskinAnalysis of lymphokine production suggested that cultured cells from skin lesions had reduced IL-w and IL-4 production relative to PBMC generated under similar conditions.
Tsicopoulos et al. (1992)IL-2skinPreferential messenger RNA expression of Th1-type cells (IFN-gamma+, IL-2+) in classical delayed-type (tuberculin) hypersensitivity reactions in human skin.
Jegasothy and Humeniuk (1981)lymphokineskinOne Darier's patient and 6 controls showed positivity to at least one skin test antigen and produced lymphokine in vitro to the appropriate antigen.
Kubota et al. (1994)IL-2skinTo investigate possible involvement of Th1-type immunoreaction in the development of skin lesions of atopic dermatitis (AD), we measured mite-antigen-stimulated production of IL-2, IL-4 and IFN-gamma, using peripheral blood mononuclear cells (PBMC) obtained from 23 patients with AD who developed positive patch test reactions to house dust mite antigens extracted from Dermatophagoides pteronyssinus (Dp).
Bata-Csorgo et al. (1995)interleukin-2skinLesional psoriatic skin contains activated memory T lymphocytes with production of mRNA for lymphokines such as interleukin-2, interferon-gamma, and tumor necrosis factor-alpha that is elevated relative to normal or uninvolved psoriatic skin.
Furue et al. (1991)IL-2skinWe examined IL-4 responsiveness or interleukin 2 (IL-2) responsiveness of peripheral blood mononuclear cells of 31 patients with AD, 19 healthy individuals, and seven patients with other skin diseases.
Horroccks et al. (1989)interleukin-2skinInfluence of systemic cyclosporin A on interleukin-2 and epidermal growth factor receptor expression in psoriatic skin lesions.
Nuttall et al. (2002)IL-2 mRNAskinHigher levels of IFN-gamma, TNF-alpha and IL-2 mRNA were seen in lesional compared with non-lesional and healthy skin (P < 0.05).
Leonardi et al. (2004)IL-2skinThe soluble IL-2 receptor concentration decreased even after 8 weeks of treatment in all 3 patients, regardless of IgE levels (case 1: low IgE level; case 2: very high IgE level) as in several others T-cell mediated non IgE-related skin disease.
Stein et al. (1997)IL-2skinIFN-gamma and IL-10 mRNAs were found in all normal skin controls, whereas IL-2, IL-4, and IL-5 mRNAs were undetectable.
Dolan et al. (1995)interleukin-2skinHuman immunodeficiency virus type 1 (HIV-1)-infected patients (n = 335) in the US Air Force HIV Natural History Program were followed for 3 years (mean) after skin testing, immunophenotyping of CD4+ cell subsets, and measurement of in vitro interleukin-2 production after stimulation by phytohemagglutinin, alloantigens, tetanus toxoid, and influenza A virus.
Ishiyama et al. (1994)IL-2skinThese studies show: (1) a negative PPD skin test in 3/4 patients, (2) decreased IL-2 production in 3/4 patients, (3) decreased T cell colony formation in 3/4 patients, (4) decreased NK activity and NK cell number in 2/4 patients, (5) increased soluble IL-2 receptor in 4/4 patients, and (6) decreased CD4/CD8 ratio in 3/4 patients.
Soboslay et al. (1994)IL-2skinThese results suggest that onchocerciasis-associated immunosuppression is reversible following ivermectin-induced permanent clearance of microfilariae from the skin; and that a vigorous parasite-specific cellular reactivity and a sustained production of IL-2 and IFN-gamma in amicrofilaridermic individuals may contribute to controlling O. volvulus infection.
Hoefakker et al. (1995)IL-2skinAt 72 h after application of the agents, significantly enhanced frequencies of dermal infiltrating cells, producing IL-alpha, IL-2, and IFN-gamma per 100 infiltrating cells in the dermis, were observed in allergic as well as irritant test patch reactions, as compared to normal skin.
Markewitz et al. (1996)IL-2skinPostoperatively, group A patients showed a persistent, significant reduction of TH, IL-2 synthesis and DTH skin response as compared to baseline values, while IL-6 synthesis remained unaltered and AB production increased (P < 0.05).
Markewitz et al. (1996)IL-2skinIn group B patients no change in TH, IL-2 and IL-6 synthesis, or DTH skin response was observed (P < 0.05 vs A).
Jain et al. (2009)interleukin 2skinPsoriasis is an inflammatory skin disorder characterized by increased activation of CD4(+) T lymphocytes, and systemic and local overexpression of pro-inflammatory cytokines such as interleukin 2 (IL-2), gamma interferon (IFN-gamma), IL-6 and tumour necrosis factor alpha, indicating that immunopathogenesis of the disease is T helper 1 (Th1) mediated.
Blaschke et al. (1999)interleukin-2skinInterleukin-16 expression correlated positively with the expression of interleukin-2 and its receptor CD25 in individual skin lesions.
Nestle et al. (1994)IL-2skinUpon addition of PHA or superantigens, both PP skin-derived and NN skin-derived DDCs mediated high levels of IL-2 and IFN-gamma production, with induction of IL-4 particularly evident for PHA reactions.
Volc-Platzer et al. (1988)lymphokineskinCryostat sections of full-thickness skin biopsies from 21 patients along the whole spectrum of leprosy were subjected to immunohistological examination with special regard to defective lymphokine production.
Rook et al. (1996)IL-2skinWe have previously demonstrated aberrant cytokine production by peripheral blood mononuclear cells (PBMCs) in SzS characterized by increased IL-4 and deficient IL-2 and IFN-gamma production, as well as increased expression of mRNA for IL-4 and IL-5 within active skin lesions, indicating that the clonal T-cell population is likely derived from the T-helper type 2 (Th2) subset of helper T lymphocytes.
Hua et al. (2006)IL-2skinSerum LTB4, LTC4, IL-2, IFN-gamma and urinary LTE4 and skin tissue LTB4, LTC4, LTE4 levels in patients are higher than those in healthy volunteers significantly (P < 0.05).
Santos-Martínez et al. (1997)IL-2skinMETHODS: The cytokine production (IL-1 beta, IL-2, IL-4, IL-6, IL-10, IL-13, TNF-alpha, IFN-tau, and TGF-beta) in skin biopsies from 12 AP lesions was determined by a semiquantitative coupled reverse transcription-polymerase chain reaction.
Wicher et al. (1998)IL-2skinUsing a semi-quantitative multiplex reverse transcription-polymerase chain reaction assay, we examined cytokine mRNA expression for interleukin-1alpha (IL-1alpha), IL-2, IL-10, IL-12p40, tumour necrosis factor-alpha (TNF-alpha) and transforming growth factor-beta (TGF-beta) in skin samples obtained from C4-deficient (C4D) guinea-pigs inoculated intradermally with virulent Treponema pallidum (VTP).
Rook et al. (1997)IL-2skinWe also demonstrated increased production of T-helper type 2 (Th2) cytokines (IL-4, IL-5) and deficient Th1 cytokines (IL-2 and IFN-gamma) by their peripheral blood mononuclear cells (PBMC) and detected IL-4 and IL-5 mRNA within lesional skin of patients with all stages of CTCL.
Müllegger et al. (2000)interleukin-2skinIn an effort to understand pathogenic factors that lead to different outcomes in dermatoborrelioses, skin biopsy samples from 42 patients with erythema migrans and 27 patients with acrodermatitis chronica atrophicans were analyzed for mRNA expression of five pro-inflammatory cytokines (tumor necrosis factor alpha, interleukin-1 beta, interleukin-6, interferon-gamma, and interleukin-2) and two anti-inflammatory cytokines (interleukin-4 and interleukin-10) by in situ hybridization with cytokine-specific riboprobes.