RESUMO
Sickle Cell Anemia (SCA) is the most common genetic disorder around the world. The mutation in the ß-globin gene is responsible for a higher hemolysis rate, with further involvement of immunological molecules, especially cytokines, chemokines, growth factors, and anaphylatoxins. These molecules are responsible for inducing and attracting immune cells into circulation, thus contributing to increases in leukocytes and other pro-inflammatory mediators, and can culminate in a vaso-occlusive crisis (VOC). This study aimed to characterize the levels of these molecules in SCA patients in different clinical conditions in order to identify potential hallmarks of inflammation in these patients. An analytical prospective study was conducted using the serum of SCA patients in steady-state (StSt; n = 27) and VOC (n = 22), along with 53 healthy donors (HD). Samples from the VOC group were obtained on admission and on discharge, in the convalescent phase (CV). Levels of chemokines (CXCL8, CXCL10, CL2, CLL3, CCL4, CL5, and CCL11), cytokines (IL-1ß, IL-1ra, IL-2, IL-4, IL-5, IL-6, IL-7, IL-10, IL-12p70, IL-13, IL-17A, TNF-α, and IFN-γ) and growth factors (VEGF, FGFb, PDGF-BB, GM-CSF, and G-CSF) were measured using a Luminex assay, and anaphylatoxins (C3a, C4a, and C5a) were measured using Cytometric Bead Array. SCA patients in StSt showed a pro-inflammatory profile, and were indicated as being higher producers of CCL2, IL-1ß, IL-12p70, IFN-γ, IL-17A, and GM-CSF, while VOC is highlighted by molecules IL-4 and IL-5, but also IL-2, IL-7, PDGF-BB, and G-CSF. PDGF-BB and IL-1ra seemed to be two important hallmarks for the acute-to-chronic stage, due to their significant decrease after crisis inflammation and statistical difference in VOC and CV groups. These molecules show higher levels and a strong correlation with other molecules in VOC. Furthermore, they remain at higher levels even after crisis recovery, which suggest their importance in the role of inflammation during crisis and participation in immune cell adhesion and activation. These results support a relevant role of cytokines, neutrophil and monocytes, since these may act as markers of VOC inflammation in SCA patients.
Assuntos
Anemia Falciforme/imunologia , Citocinas/imunologia , Mediadores da Inflamação/imunologia , Inflamação/imunologia , Doenças Vasculares/imunologia , Adolescente , Adulto , Anemia Falciforme/metabolismo , Quimiocinas/imunologia , Quimiocinas/metabolismo , Citocinas/metabolismo , Feminino , Humanos , Inflamação/metabolismo , Mediadores da Inflamação/metabolismo , Masculino , Modelos Imunológicos , Monócitos/imunologia , Monócitos/metabolismo , Neutrófilos/imunologia , Neutrófilos/metabolismo , Mapas de Interação de Proteínas/imunologia , Doenças Vasculares/metabolismo , Adulto JovemRESUMO
Immunoglobulin A nephropathy (IgAN) is considered as mesangiopathy since it initiates in the mesangium; however, other glomerular components are involved and the glomerular capillary wall offers the first contact to circulating macromolecular IgA1. Acute and active forms of IgAN are associated with endocapillary hypercellularity and vascular damage of various degrees, in severe cases with microangiopathy (MA) without or with thrombosis [thrombotic microangiopathy (TMA)]. Vascular damage activates complement and coagulation cascades. A defective complement regulation has recently been detected in active and progressive cases of IgAN. C4d deposits in renal biopsies have been found to be an early risk factor. These observations have raised interest in manifestation of MA and TMA in progressive cases of IgAN. MA-TMA lesions have been found in various percentages (2-53%) of patients with IgAN according to patients' selection and pathology definition of TMA. The association with hypertension (HTN) was so strong that it led to the hypothesis that MA/TMA in IgAN was a mere consequence of severe HTN. Old and new clinical and experimental data indicate that in IgAN the interaction of the glomerular capillary wall with immune reactants and complement uncontrolled activation leading to C4b deposits favours the development of MA-TMA, which plays a role in progression and renal function decline. The central role of complement activation is relevant also for the new therapeutic interventions offered by the pharma.
Assuntos
Ativação do Complemento/imunologia , Complemento C4b/imunologia , Glomerulonefrite por IGA/patologia , Glomérulos Renais/patologia , Microangiopatias Trombóticas/patologia , Doenças Vasculares/patologia , Glomerulonefrite por IGA/imunologia , Humanos , Glomérulos Renais/imunologia , Microangiopatias Trombóticas/imunologia , Doenças Vasculares/imunologiaRESUMO
The aim of this study was to evaluate the impact of high-intensity strength training (ST) or low-intensity strength training with blood flow restriction (ST-BFR) on monocyte subsets, the expression of C-C chemokine receptor 5 (CCR5), and CD16 on monocytes, and tumor necrosis factor alpha (TNF-α) production of overweight men. Thirty overweight men were randomly assigned to conventional ST or ST-BFR. Both groups performed exercises of knee extension and biceps curl with equal volume (3 sessions/week) over 8 weeks, and the peripheral frequency of monocytes (CD14+CD16-, classical monocytes; CD14+CD16+, intermediate monocytes; CD14-CD16+, nonclassical monocytes), the mean fluorescence intensity (MFI) of CCR5 and CD16 on CD14+ monocytes; and the production of TNF-α by lipopolysaccharide (LPS)-stimulated cells were quantified. Eight weeks of ST increased the frequency of CD14+CD16- monocytes (p = 0.04) and reduced the percentage of CD14-CD16+ (p = 0.02) and the production of TNF-α by LPS-stimulated cells (p = 0.03). The MFI of CD16 on CD14+ monocytes decreased after the ST intervention (p = 0.02). No difference in monocyte subsets, CCR5 or CD16 expression, and TNF-α production were identified after ST-BFR intervention (p > 0.05). The adoption of ST promotes anti-inflammatory effects on monocyte subsets of overweight men, but this effect was lost when BFR was adopted. Novelty High-intensity strength training reduces the production of TNF-α and the peripheral frequency of CD16+ monocytes in overweight men. Blood flow restriction method blunts the strength training adaptations on monocyte subsets and pro-inflammatory TNF-α production in overweight men.
Assuntos
Inflamação , Sobrepeso , Condicionamento Físico Humano/fisiologia , Treinamento Resistido , Adaptação Fisiológica/imunologia , Adaptação Fisiológica/fisiologia , Adulto , Células Cultivadas , Humanos , Inflamação/imunologia , Inflamação/fisiopatologia , Masculino , Monócitos/imunologia , Monócitos/metabolismo , Sobrepeso/imunologia , Sobrepeso/fisiopatologia , Sobrepeso/terapia , Fator de Necrose Tumoral alfa/sangue , Doenças Vasculares/imunologia , Doenças Vasculares/fisiopatologia , Adulto JovemRESUMO
MPO (myeloperoxidase) is a peroxidase enzyme secreted by activated leukocytes that plays a pathogenic role in cardiovascular disease, mainly by initiating endothelial dysfunction. The molecular mechanisms of the endothelial damaging action of MPO remain though largely elusive. Calpain is a calcium-dependent protease expressed in the vascular wall. Activation of calpains has been implicated in inflammatory disorders of the vasculature. Using endothelial cells and genetically modified mice, this study identifies the µ-calpain isoform as novel downstream signaling target of MPO in endothelial dysfunction. Mouse lung microvascular endothelial cells were stimulated with 10 nmol/L MPO for 180 minutes. MPO denitrosylated µ-calpain C-terminus domain, and time dependently activated µ-calpain, but not the m-calpain isoform. MPO also reduced Thr172 AMPK (AMP-activated protein kinase) and Ser1177 eNOS (endothelial nitric oxide synthase) phosphorylation via upregulation of PP2A (protein phosphatase 2) expression. At the functional level, MPO increased endothelial VCAM-1 (vascular cell adhesion molecule 1) abundance and the adhesion of leukocytes to the mouse aorta. In MPO-treated endothelial cells, pharmacological inhibition of calpain activity attenuated expression of VCAM-1 and PP2A, and restored Thr172 AMPK and Ser1177 eNOS phosphorylation. Compared with wild-type mice, µ-calpain deficient mice experienced reduced leukocyte adhesion to the aortic endothelium in response to MPO. Our data first establish a role for calpain in the endothelial dysfunction and vascular inflammation of MPO. The MPO/calpain/PP2A signaling pathway may provide novel pharmacological targets for the treatment of inflammatory vascular disorders.
Assuntos
Calpaína/metabolismo , Células Endoteliais , Peroxidase/metabolismo , Proteína Fosfatase 2/metabolismo , Doenças Vasculares , Animais , Animais Geneticamente Modificados , Aorta/metabolismo , Aorta/patologia , Adesão Celular/fisiologia , Moléculas de Adesão Celular/metabolismo , Técnicas de Cultura de Células , Células Endoteliais/imunologia , Células Endoteliais/metabolismo , Inflamação/imunologia , Leucócitos/fisiologia , Camundongos , Transdução de Sinais , Regulação para Cima , Doenças Vasculares/imunologia , Doenças Vasculares/metabolismoRESUMO
BACKGROUND: Cellular therapies for immunomodulation in vascularized composite allotransplantation (VCA) have gained importance due to their potential for minimization of immunosuppression. Adipose-derived (AD) mesenchymal stem cells (MSCs) especially have shown encouraging potential. We investigated the influence of timing and frequency of AD-MSC treatment on immunologic and graft survival as well as graft vasculopathy outcomes after VCA. METHODS: Lewis rats received full-mismatched Brown Norway rat hindlimb transplants. Recipient animals were assigned to groups receiving donor-derived AD-MSCs (10 cells/animal) either on postoperative day (POD) 1, POD 4, or repeatedly on POD 4, 8, and 15, and compared to untreated controls. RESULTS: Although AD-MSC administration on POD 1 or POD 4, 8, and 15 resulted in 50% long-term graft acceptance, recipients treated on POD 4, and controls rejected before POD 50. All treated animals revealed peripheral blood chimerism (4 weeks), most pronounced after repetitive cell administration (12.92% vs 5.03% [POD 1] vs 6.31% [POD 4]; P < 0.05; all P < 0.01 vs control 1.45%). Chimerism was associated with the generation of regulatory T cells (CD4CD25FoxP3). In vitro mixed lymphocyte reactions revealed modulation of the recipient immune response after AD-MSC treatment. Graft arteries at end point revealed significant differences of arterial intimal thickness between rejecting and AD-MSC-treated animals (P < 0.01). CONCLUSIONS: Taken together, our results point to the potential for repetitive AD-MSC administration in improving outcomes after VCA. Future studies are warranted into optimization of the dosing and frequency of AD-MSC therapy, either alone or used in, combination with other cell therapies (such as hematopoietic stem cells or bone marrow-derived MSC or dendritic cells) for optimization of appropriate conditioning or maintenance regimens.
Assuntos
Tecido Adiposo/citologia , Aloenxertos Compostos/irrigação sanguínea , Aloenxertos Compostos/transplante , Sobrevivência de Enxerto , Membro Posterior/irrigação sanguínea , Membro Posterior/transplante , Imunoterapia/métodos , Transplante de Células-Tronco Mesenquimais/métodos , Células-Tronco Mesenquimais/imunologia , Alotransplante de Tecidos Compostos Vascularizados/métodos , Animais , Proliferação de Células , Células Cultivadas , Aloenxertos Compostos/imunologia , Rejeição de Enxerto/imunologia , Rejeição de Enxerto/prevenção & controle , Membro Posterior/imunologia , Imunoterapia/efeitos adversos , Ativação Linfocitária , Masculino , Transplante de Células-Tronco Mesenquimais/efeitos adversos , Modelos Animais , Ratos Endogâmicos BN , Ratos Endogâmicos Lew , Linfócitos T Reguladores/imunologia , Fatores de Tempo , Quimeras de Transplante , Tolerância ao Transplante , Doenças Vasculares/imunologia , Doenças Vasculares/prevenção & controle , Alotransplante de Tecidos Compostos Vascularizados/efeitos adversosRESUMO
INTRODUCTION: Erectile dysfunction (ED) is highly prevalent among type 2 diabetes mellitus patients (T2DM). Although a link among systemic inflammation, endothelial dysfunction, and ED is described in clinical situations mainly related with coronary heart disease (CHD) risk, evidences of this link in T2DM patients are rather limited. AIMS: To evaluate the association between endothelial dysfunction and balance of pro-/anti-inflammatory mediators with ED presence and severity in T2DM. METHODS: We conducted a cross-sectional study of 190 T2DM patients without symptomatic CHD, 150 out of them with ED and 40 without ED. Serum levels of E-selectin, intercellular adhesion molecule-1, tumor necrosis factor-α (TNF-α), and interleukin (IL)-10 were measured using specific enzyme-linked immunosorbent assays (ELISAs). ED presence and severity were tested by the five-item version of the International Index of Erectile Function questionnaire. MAIN OUTCOME MEASURES: Differences in circulating levels of endothelial dysfunction (ICAM-1, E-selectin) and inflammatory/anti-inflammatory (TNF-α, IL-10, TNF-α : IL-10 ratio) markers between T2DM patients with and without ED, and assessment of biomarkers ED predictive value while adjusting for other known ED risk factors. RESULTS: Patients with ED were older and had longer duration of diabetes than patients without ED. E-selectin serum levels were significantly increased, while IL-10 were lower in patients with ED; because TNF-α levels tend to be higher, TNF-α : IL-10 ratio was more elevated in ED patients. No significant differences of ICAM-1 levels were observed between study groups. Endothelial activation markers and TNF-α, as well as diabetes duration, were negatively correlated with erectile function. On multivariate analysis including age, duration of diabetes, insulin treatment, hypertension, insulin resistance, fair-to-poor glycemic control, and metabolic syndrome, increments in E-selectin levels and TNF-α : IL-10 ratio predicted independently ED presence, while IL-10 increases were associated with lower risk of ED in T2DM patients. CONCLUSIONS: ED in T2DM patients without symptomatic CHD is associated with systemic endothelial dysfunction and a predominant, imbalanced low-grade inflammatory response.
Assuntos
Diabetes Mellitus Tipo 2/imunologia , Endotélio Vascular/imunologia , Disfunção Erétil/imunologia , Doenças Vasculares/imunologia , Adulto , Estudos Transversais , Diabetes Mellitus Tipo 2/sangue , Selectina E/sangue , Disfunção Erétil/sangue , Humanos , Inflamação/sangue , Inflamação/imunologia , Molécula 1 de Adesão Intercelular/sangue , Interleucina-10/sangue , Masculino , Pessoa de Meia-Idade , Fator de Necrose Tumoral alfa/sangue , Doenças Vasculares/sangueRESUMO
Se presenta el caso de una mujer joven, sin antecedentes de importancia, que muestra trombosis de grandes y pequeños vasos. A pesar del tratamiento con anticoagulación y corticoides en dosis altas, desarrolla necrosis cutánea y una importante respuesta inflamatoria sistémica con disfunción orgánica múltiple, por lo que .se le indicó plasmaféresis y, posteriormente, rituximab, con buena respuesta. Se discute el síndrome antifosfolípidos con énfasis en los anticuerpos antiprotrombina y la patogenia de la microangiopatía en el síndrome antifosfolípidos catastróficos.
We present the case of a young, otherwise healthy woman, who developed thrombosis of large and small vessels and capillaries. Despite anticoagulation treatment and high doses of glucocorticoids, she developed cutaneous necrosis and systemic inflammatory response with multiple organ dysfunction. Plasmapheresis and rituximab were administered with good response. We discuss the antiphospholipid syndrome, with emphasis on antiprothrombin antibodies and the pathogenesis of microangiopathy in antiphospholipid syndrome.
Assuntos
Humanos , Feminino , Adulto , Doenças Vasculares/complicações , Doenças Vasculares/imunologia , Doenças Vasculares/terapia , Síndrome Antifosfolipídica/complicações , Síndrome Antifosfolipídica/imunologia , Síndrome Antifosfolipídica/terapia , Anticorpos/imunologia , Doença Catastrófica , Protrombina/imunologia , Trombose/complicações , Trombose/imunologia , Trombose/terapiaRESUMO
The aim of this study was to evaluate the frequency and clinical associations of HLA-DR alleles in Brazilian Caucasian patients with polyarteritis nodosa (PAN) or microscopic polyangiitis (MPA). We evaluated 29 Caucasian patients with vasculitis classified as PAN or MPA according to the American College of Rheumatology (ACR) 1990 Criteria, Chapel Hill Consensus Conference (CHCC) nomenclature for vasculitis and EULAR recommendations for conducting clinical studies in systemic vasculitis. HLA-DR alleles were typed using polymerase chain reaction-amplified DNA, hybridized with sequence-specific low resolution primers. DNA obtained from 59 Caucasian healthy blood donors were used as control. In order to evaluate if a specific HLA may have influence on the clinical profile of those diseases, we also divided the patients according to Birmingham vasculitis score (BVAS) and Five-Factors Score (FFS) at the time of diagnosis. Increased frequency of HLA-DRB1*16 (p = 0.023) and DRB4*01 (p = 0.048) was found in patients with higher disease activity at the time of diagnosis (BVAS >/=22). Patients with less severe disease (FFS = 0) had a higher frequency of HLA-DRB1*03 (p = 0.011). Patients with gastrointestinal tract involvement had significantly increased frequency of HLA-DRB1*11 or B1*12 (p = 0.046), B1*13 (p = 0.021) and B3 (p = 0.008). In contrast, patients with renal disease, had higher frequency of DRB1*15 or DRB1*16 (p = 0.035) and B5 (p = 0.035). In the subgroup of patients with MPA, increased frequency of HLA-DRB1*15 was found in patients with BVAS >/=22 (p = 0.038) and FFS >/=1 (p = 0.039) suggesting that this allele is associated with more aggressive disease. Antineutrophil cytoplasmic antibodies (ANCA) negative MPA patients had significantly increased frequency of HLA-DRB1*11 or DRB1*12 when compared to ANCA positive patients (p = 0.023). Our results suggest that HLA-DR alleles may influence PAN and MPA clinical expression and outcome and that in MPA they participate in the mechanisms involved in the development to ANCA.
Assuntos
Antígenos HLA-DR/análise , Poliarterite Nodosa/imunologia , Doenças Vasculares/imunologia , Adolescente , Adulto , Idoso , Brasil , Criança , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Índice de Gravidade de Doença , Adulto JovemRESUMO
Although the molecular basis of sickle cell disease (SCD) is well established, the wide variability in clinical manifestations still puzzles haematologists and clinicians. Recently, SCD started to be considered by different groups as a chronic inflammatory condition, where the inflammatory tendency of each individual could drive more or less severe clinical features. Here we describe a haemoglobin SC disease patient (heterozygous to both HbS and HbC variants) that experienced several vaso-occlusive crises before underwent a successful kidney transplantation. Since then (16 years ago), she is on uninterruped immunosuppressive therapy, and do not experienced any severe vaso-occlusive crisis. Considering SCD associated morbidity as a result of exacerbated immune responses, we suggest that the immunosuppressive therapy directed to the kidney graft maintenance is actually also helping in the control of the chronic inflammatory responses associated to SCD.
Assuntos
Rejeição de Enxerto/prevenção & controle , Doença da Hemoglobina SC/tratamento farmacológico , Doença da Hemoglobina SC/imunologia , Imunossupressores/administração & dosagem , Modelos Imunológicos , Doenças Vasculares/imunologia , Doenças Vasculares/prevenção & controle , Adulto , Feminino , Rejeição de Enxerto/etiologia , Doença da Hemoglobina SC/complicações , Humanos , Falência Renal Crônica/etiologia , Falência Renal Crônica/cirurgia , Transplante de Rim/efeitos adversos , Resultado do Tratamento , Doenças Vasculares/etiologiaRESUMO
INTRODUCTION: Antiphospholipid antibodies lupus anticoagulant (LA) and anticardiolipin antibodies (aCL) play a role in promoting arterial and venous thrombosis in several vascular territories. Acute vestibular syndromes are a common complaint in general and neurology practice. Approximately 9% of cases are due to central nervous system vestibular areas lesions, often associated with vascular disorders. OBJECTIVE: Define the potential relationship between these antibodies and central or peripheral vestibular failure. PATIENTS AND METHODS: We report the presence of antiphospholipid antibodies in 16 patients with central vestibular symptoms. All patients were seen in the Neuro otology and Vascular Neurology clinics at the Institute for Neurological Research in Buenos Aires. Magnetic resonance imaging (MRI) and ancillary neuro otologic tests were used to determine the etiology of vestibular manifestations. Determinations of LA and aCL were done using standard criteria. RESULTS: We evaluated 16 patients (13 women and 3 men), aged 44 4 years (21 65). Thirteen patients did not have stroke risk factors. MRI lesions were found in 11 subjects (1 cerebellar infarct, 3 pontine ischemic changes, and 9 white matter abnormalities). All patients had signs consistent with dysfunction of vestibulo cerebellar structures or the vestibular nuclei. All patients had positive LA and 4 of them had also elevated aCL. CONCLUSION: Our findings suggest a potential association between the presence of a prothrombotic state and central vestibular dysfunction of vascular etiology. To the best of our knowledge, this is the first report of such an association in the absence of clinically evident autoimmune disease.
Assuntos
Anticorpos Antifosfolipídeos/metabolismo , Doenças Vasculares/imunologia , Doenças Vestibulares/imunologia , Núcleos Vestibulares/patologia , Adulto , Idoso , Anticorpos Anticardiolipina/metabolismo , Feminino , Humanos , Inibidor de Coagulação do Lúpus/metabolismo , Imageamento por Ressonância Magnética , Masculino , Pessoa de Meia-Idade , Fatores de Risco , Doenças Vasculares/patologia , Doenças Vestibulares/patologiaAssuntos
Anticorpos Antifosfolipídeos/sangue , Autoanticorpos/sangue , Glicoproteínas/imunologia , Adulto , Fatores Etários , Idoso , Idoso de 80 Anos ou mais , Envelhecimento/imunologia , Anticorpos Anticardiolipina/sangue , Anticorpos Anticardiolipina/efeitos dos fármacos , Anticorpos Antifosfolipídeos/efeitos dos fármacos , Anticoagulantes/sangue , Anticoagulantes/farmacologia , Autoanticorpos/efeitos dos fármacos , Autoimunidade , DNA/imunologia , Feminino , Glicoproteínas/sangue , Glicoproteínas/farmacologia , Humanos , Prevalência , Doenças Vasculares/etiologia , Doenças Vasculares/imunologia , beta 2-Glicoproteína IAssuntos
Humanos , Glândulas Suprarrenais/irrigação sanguínea , Doença de Chagas/imunologia , Leucócitos/imunologia , Adesão Celular , Glândulas Suprarrenais/imunologia , Coração/parasitologia , Doença de Chagas/parasitologia , Doenças Vasculares/imunologia , Doenças Vasculares/parasitologia , Imunidade Celular , Miocárdio/imunologia , Veias/imunologia , Veias/parasitologiaAssuntos
Glândulas Suprarrenais/irrigação sanguínea , Doença de Chagas/imunologia , Leucócitos/imunologia , Glândulas Suprarrenais/imunologia , Adesão Celular , Doença de Chagas/parasitologia , Coração/parasitologia , Humanos , Imunidade Celular , Miocárdio/imunologia , Doenças Vasculares/imunologia , Doenças Vasculares/parasitologia , Veias/imunologia , Veias/parasitologiaRESUMO
Direct and indirect immunofluorescence tests performed on skin biopsy specimens and serum have enriched the diagnostic skills of the practicing pathologist. Specific patterns of immunoglobulin and complement deposition have clarified the diagnostic entities within the group of vesicobullous diseases. The pemphigus group of diseases is characterized by antibodies, usually IgG, directed against the intercellular substance of squamous epihelium. The pemphigoid group of bullous diseases is characterized by antibody, usually IgG directed against the basement membrane zone. The basement membrane zone deposition of immunoglobulin or complement is linear and localized to the lamina lucida. In dermatitis herpetiformis, granular or speckled IgA deposition in the upper papillary dermis is characteristic; however, other patterns of deposition may occur. Abnormal microfibrillar bundles in the upper papillary dermis have recently been identified in patients with dermatitis herpetiformis.Immunofluorescence studies of patients with lupus erythematosus are important not only in diagnosis but also in prognosis. The diseased skin of lupus patients contains deposits of immunoglobulin, ussually IgG or IgM, at the basement membrane zone in more than 90 per cent of the cases. In discoid lupus erythemathoss, clinically normal skin does not contain such deposits. However, in systemic lupus erythematosus, normal sun exposed skin contains these deposits in approximately 80 per cent of the cases and normal nonsun exposed skin contains them in 50 per cent the cases. Direct immunofluorescence of normal skin may demonstrate basement membrane zone deposition of immunoglobulin in mixed connective tissue disease and other autoimmune diseases with anti-DNS antibodies.The skin of psoriatic patients may demonstrate in vivo bound IgG within the stratum corneum. Similar circulating antistratum corneum antibodies are found in normal subjects; however, these antibodies do not appear to have access to epidermal binding sites. Patients with lichen planus characteristically have large globular deposits of immunoglobulin and complement in the epidermis and dermis in diseased skin. Granular deposition of IgM and IgG at the basement membrane zone in lichen planus may lead to cofusion with lupus erythematosus.Deposition of immunoglobulin and complement is found in and about vessels in early lesions of cutaneous vasculitis. Negative findings in older lesions may be due to immune co.