Biomedical subjects

Ewa Robak

Publications and source records attributed to Ewa Robak.

17 recordsLinked to original sources

PubMed2006

Peripheral blood lymphocyte apoptosis and circulating dendritic cells in patients with systemic lupus erythematosus: correlation with immunological status and disease-related symptoms.

We investigated in vivo the relationship between the degree of peripheral blood lymphocyte apoptosis and circulating dendritic cells (DC) as well as the immunological status in 45 patients with systemic lupus erythematous (SLE). Apoptosis was detected by phosphatidylserine externalization and assays to detect caspase activation. The total DC count (tDC) and their myeloid, mDC1 (BDCA1+) and mDC2 (BDCA3+), and plasmacytoid, pDC (BDCA3+), subtypes were assessed. Moreover, several immunological parameters, such as complement proteins, interferons (IFN), tumor necrosis factor (TNF)-alpha, interleukin (IL)-4, and IL-6 levels were assessed. There were no significant differences in both the intensity of apoptosis and DC counts between active and inactive SLE as well as between untreated patients and those treated with steroids. The incidence of lymphocyte apoptosis correlated positively with T-cell count, both T-helper (p=0.004) and cytotoxic T cells (p=0.001), but not with B or natural killer (NK) cells. The intensity of apoptosis enhanced along with the increase in complement C3 (p=0.016) and decrease in IFN-gamma (p=0.040) levels. The apoptotic cell count correlated with tDC (p=0.031), mDC1 (p=0.007), and pDC (p=0.039) counts. Both tDC and mDC1 counts correlated positively with antinuclear antibody (ANA) titers (p=0.017 and 0.032, respectively). Moreover, tDC correlated with C4 (p=0.039) and pDC with both C3 (p=0.032) and C4 (p=0.007) levels. The DC counts correlated inversely with IFN-gamma (tDC, p=0.038; mDC1, p=0.009), IL-6 (mDC2, p=0.031), or serum IgG levels (tDC, p=0.006; mDC1, p<0.001; mDC2, p=0.001). We found a positive correlation between lymphocyte apoptosis and peripheral blood DC count as well as the level of complement proteins in patients with SLE. The enhanced lymphocyte apoptosis was accompanied by the decrease in concentration of some cytokines, such as IFN-gamma or IL-6, as well as serum IgG level. This finding may reflect pathogenetic events during development of the disease, which include a persistent signal derived from circulating apoptotic lymphocytes, mobilizing the complement system, and attracting peripheral blood DC.

Adult↗

PubMed2006

Circulating total and active metalloproteinase-9 and tissue inhibitor of metalloproteinases-1 in patients with systemic lupus erythomatosus.

We investigated the serum concentration of total metalloproteinase-9 (tMPP-9), active MMP-9 (aMMP-9), and tissue inhibitor of metalloproteinase-1 (TIMP-1) in a group of 41 patients with SLE and 20 healthy controls. Serum levels of tMMP-9 and TIMP-1 were assessed by an enzyme-linked immunosorbent assay (ELISA) and aMMP-9 by fluorometric assay. The tMMP-9 level was lower in SLE patients (mean 262 ng/mL) than in healthy volunteers (mean 325 ng/mL) (P = .048). Similarly, aMMP-9 level was lower in SLE patients (mean 121 ng/mL) than in control group (mean 169 ng/mL) (P = .0355) and lower in active SLE (mean 54 ng/mL) than in inactive disease (mean 99 ng/mL) (P = .033). TIMP-1 level was also lower in SLE patients (mean 181 ng/mL) than in control group (mean 233 ng/mL) (P = .004). In SLE patients, a positive correlation was found between tMMP-9 and aMMP-9 (rho = 0.568; P = .001). We also found a positive correlation of tMMP-9 and TIMP-1 with VEGF concentrations (rho = 0.450, P = .005 and rho = 0.387; P = .018, resp). tMMP-9, aMMP-9, and TIMP-1 serum levels are lower in SLE patients than in healthy control group.

Adolescent↗

PubMed2006

Purine nucleoside analogs as immunosuppressive and antineoplastic agents: mechanism of action and clinical activity.

The purine nucleoside analogs (PNA) form an important group of cytotoxic drugs active in the treatment of neoplastic and autoimmune diseases. Three of them, fludarabine (FA), cladribine (2-chlorodeoxyadenosine, 2-CdA) and pentostatin (2'-deoxycoformycin, DCF) have established clinical activity in hematological malignancies and have been approved by FDA. These drugs are also investigated in some autoimmune diosorders. Recently four novel PNA: clofarabine (CAFdA), nelarabine, immucillin H (BCX-1777, forodesine) and 8-chloroadenosine (8-Cl-Ado) have been synthesized and introduced into clinical trials. All these drugs have chemical structure similar to adenosine or guanosine, however, the mechanism of their action is different. FA, 2-CdA and CAFdA mainly require phosphorylation by deoxynucleoside salvage pathways. The cytotoxic effect exerts the triphosphate metabolites, which are incorporated into DNA, and finally lead to programmed cell death. In contrast, DCF does not need to be phosphorylated and results in an increase of plasma deoxyadenosine (dAdo) levels and intracellular deoxyadenosine triphosphate (dATP). Nelarabine is an arabinosylguanine (ara-G) prodrug, which after conversion to ara-G is phosphorylated to ara-G triphosphate (ara-GTP). Accumulation of ara-GTP finally leads to apoptosis. Forodesine is a purine nucleoside phosphatase (PNP) inhibitor which blocks intracellular deoxyguanine (dGuo) cleaving to guanine (Guo), but instead converts it to deoxyguanosine triphosphate (dGTP), and similarly to other PNA resulting in apoptosis. 8-chloroadenosine (8-Cl-Ado) is a ribonucleoside analog. The mechanism of its action is quite different from other PNA and remains poorly understood. However, it is known that the drug inhibits RNA synthesis, but not DNA. These agents have significant cytotoxic activity against lymphoid and myeloid malignant cells. Moreover, they have deleterious effects on the normal resting lymphocytes. They result in prolonged lymphocyte depletion especially in the CD4 subset of T-cells. Several clinical trials have demonstrated that PNA used alone or in combination with other cytotoxic drugs or monoclonal antibodies shows good efficacy and acceptable toxicity profile in the treatment of lymphoid malignancies. 2-CdA and DCF are drugs of choice in the treatment of hairy cell leukemia. FA and 2-CdA have significant clinical activity in low-grade non-Hodgkin's lymphoma and chronic lymphocytic leukemia. 2-CdA exhibits some activity in progressive multiple sclerosis and other autoimmune disorders. This review will summarize current knowledge concerning the mechanism of action, pharmacological properties, clinical activity and toxicity of PNA accepted for use in clinical practice as well as new agents available for clinical trials.

Antineoplastic Agents↗

PubMed2006

[Acne rosacea--diagnostic challenge].

Acne rosacea is a common skin disorder which affects adults, usually women. Erythema, papules, pustules and telangiectases, the main clinical manifestations of the disease are located on the face. Currently opinions dealing with pathogenesis and clinical forms of rosacea are presented. As the clinical picture might be confusing, similar to other illnesses, differential diagnosis with other dermatoses like acne vulgaris, erysipelas, seborrhoeic and contact eczema as well as systemic diseases like lupus erythematosus, dermatomyositis, scleroderma, sarcoidosis and leukemia were discussed.

Acne Vulgaris↗

PubMed2005

Merkel cell carcinoma in a patient with B-cell chronic lymphocytic leukemia treated with cladribine and rituximab.

Merkel cell carcinoma (MCC) is an uncommon, neuroendocrine skin tumor with an aggressive clinical course. The etiology of the disease is unknown, although sun exposure and immunosuppression may play a role in its development. Coexistence of MCC with chronic lymphocytic leukemia (CLL) is extremely rare and to our knowledge it has been previously described in only 8 patients. We report a 51-year-old woman who presented with a red lump on the right cheek diagnosed as MCC. She had been diagnosed as having CLL 3 years earlier and was treated with 4 courses of cladribine (2-CdA) and subsequently with 4 courses of 2-CdA combined with rituximab. MCC was diagnosed on the basis of histological and immunohistochemical evaluation 2 months after the last course of 2-CdA and rituximab. Surgical excision with tumor-free margins was performed and local adjuvant radiotherapy was applied. Histopathological and immunohistochemical evaluation of the cervical lymph node specimens showed monotonous and diffuse infiltrate of small CD5+, CD20+, CD23+ lymphocytes and no MCC cells were present. To our knowledge, this is the first reported case of MCC occurring in CLL patients soon after treatment with 2-CdA and/or rituximab. The development of MCC in our patient may suggest that this complication rarely observed in CLL patients may have a link with strongly immunosuppressive therapy with 2-CdA and rituximab.

Antibodies, Monoclonal↗

PubMed2005

[Diagnostic problems and evaluation of disease activity in systemic lupus erythematosus].

Systemic lupus erythematosus (SLE) is a chronic multisystem inflammatory disorder characterised by autoantibodies production. The diagnosis of disease requires evidence of 4 out of 11 clinical and/or laboratory symptoms proposed by American College of Rheumatology. For many years attention has been drawn to the problem of finding a valid and sensitive tool for measuring SLE activity and more than 60 different methods have been proposed. Unfortunately none of them has been generally accepted. Amongst the most frequently used are SLEDAI scale and its modifications, BILAG and SLAM. The systems have been validated in prospective studies, and their reproducibility, validity and sensitivity have been compared. At present they are widely used in clinical practice. In this review currently accepted methods of SLE activity evaluation are presented.

Diagnosis, Differential↗

PubMed2005

[Proinflammatory cytokines in inactive lupus erythematosus patients].

Systemic lupus erythematosus (SLE) is an autoimmune connective tisssue disease. Disregulation of proinflammatory cytokines' secrection plays a pivotal role in its etiopatogenesis. Most studies concerning serum levels of those cytokines were conducted in active SLE patients. To date, there are scarce date on proinflammatory cytokines' serum concentration in inactive SLE patients. The aim of the study was to evaluate serum level of IL-1beta, IL-6, IL-18 and TNF-alpha in inactive SLE patients. The study involved 25 SLE patients aged between 24-65 years (mean age 40.6 years) and 25 age- and sex-matched healthy volunteers. The activity of the disease was assesed by SLAM scale. Serum concentrations of IL-6 and IL18 were determined by ELISA while serum levels of TNF-alpha and IL-1beta were measured using chemiluminescensce assay. In all healthy volunteers and in 23 out of 25 SLE patients, serum level of IL-1beta was undetectable (< 5 pg/ml). Serum concentrations of IL-6, IL-18 and TNF-alpha were detectable in all SLE patients. In 9 out of 27 healthy subjects level of IL-18 was under detection limit. Serum levels of IL-6, IL-18 and TNF-alpha were significanly higher (p < 0.001) in SLE patients when compared to their concentrations in subjects from control group (3.45 pg/ml vs. 2.59 pg/ml for IL-6; 344.87 pg/ml vs. 50.31 pg/ml for IL-18; 7.72 pg/ml vs. 5.21 pg/ml for TNF-alpha, respectively). The evaluation of serum levels of proinflammatory cytokines may be a sensitive marker of disease activity which may be helpful in maintaining or withdrawing chronic therapy in SLE patients.

Adult↗

PubMed2005

[Progress and perspectives in the treatment of systemic lupus erythematosus].

Systemic lupus erythematosus (SLE) is an autoimmune disease that predominantly affects women in childbearing age. SLE tissue damage is mediated by autoantibodies, complement activation and immune complexes deposition. The disease is diagnosed on the basis of its clinical manifestations and the demonstration of characteristic immunological phenomena, especially antinuclear antibodies. Management of the disease includes regular monitoring of disease activity, avoidance of predisposing factors and therapy guided by the activity and severity of the leading organ manifestation. Treatment ranges from nonsteroidal antirheumatic drugs to intensive treatment with cytotoxic agents. Corticosteroids form the basis of all regimens. Antimalarials and azathioprine are important for treating mild and moderate SLE cases, especially for the long time. Cyclophosphamide given intravenously is the current gold standard for severe lupus nephritis. More recently new strategies for immunosuppression in SLE, that interfere with the syntesis of DNA and nucleotides have been developed (such as mycophenolate mofetil, fludarabine and cladribine). Other agents like cyclosporine and tacrolimus inhibit effect of the activation signals for T cells by inhibition of calcineurin. Some monoclonal antibodies against cytokines or components of the complement system interfere with the effector phase of the immune response. Abetimus (LJP-394) inhibits the production of anti-dsDNA antibodies and may prevent glomerulonephritis caused by anti-DNA containing immune complexes. Somatic gene therapy is also a novel approach in autoimmune disorders and my be a valuable method of SLE therapy in the future. The adrenal steroid prasterone (DHEA) has also shown benefitial effects in mild to moderate SLE. Finally, autologous stem cell transplantation can induce tolerance to self-antigens and cause significant improvement in SLE patients. However, new therapeutic strategies must be tested according to the established principles of clinical trial methods.

Anti-Inflammatory Agents, Non-Steroidal↗

PubMed2004

Multiple myeloma in a patient with systemic lupus erythematosus, myasthenia gravis and non-familial diffuse palmoplantar keratoderma.

The coexistence of autoimmune diseases and malignancies including lymphoproliferative diseases is often reported in the literature. Here we report an unusual case with two autoimmune diseases--myasthenia gravis (MG) and systemic lupus erythematosus (SLE) associated with unique palmoplantar keratoderma (PK) which preceded the development of multiple myeloma (MM) for twenty and seven years respectively. MG associated with non-malignant thymoma developed in 1981 and was successfully treated with thymectomy and physostigmine. Thirteen years later SLE was diagnosed and until now it is also accompanied by skin lesions corresponding to non-familial, diffuse palmoplantar keratoderma which is resistant to treatment. In 2001 the patient revealed inguinal and abdominal lymphadenopathy first diagnosed as extramedullary plasmacytoma and then as multiple myeloma on the basis of bone marrow infiltration and monoclonal gammopathy. Therapy with VAD regimen achieved complete remission of the MM and significant improvement of the skin changes lasting for six months. We failed to collect sufficient numbers of CD 34+ cells for peripheral blood stem cell transplantation. Now the malignancy is in partial remission after CHOP therapy and the skin lesions have returned to their initial status. To our knowledge, this is the first case to be reported with coexistence of these four diseases.

Adult↗

PubMed2003

Allergic diseases, drug adverse reactions and total immunoglobulin E levels in lupus erythematosus patients.

BACKGROUND: The association of allergic diseases, drug adverse reactions and elevated total immunoglobulin E (IgE) concentration in systemic lupus erythematosus patients remains controversial. The aim of the study was to investigate the prevalence of those features in active and inactive systemic lupus erythematosus patients, and in the control group as well. METHODS: Total IgE concentration was evaluated by enzyme-linked immunosorbent assay. RESULTS AND CONCLUSIONS: The results of our study revealed that concomitant allergic diseases were not more frequent in systemic lupus erythematosus patients than in the general population. Total IgE concentration was significantly higher during the active stage of the disease. Drug reactions were very frequent but not connected with IgE elevation. Our results indicate that IgE may play a role in lupus pathogenesis, especially in the active phase of the disease.

Acute Disease↗

PubMed2003

Vascular endothelial growth factor and its soluble receptors VEGFR-1 and VEGFR-2 in the serum of patients with systemic lupus erythematosus.

We investigated the serum concentration of vascular endothelial growth factor (VEGF) and its two soluble receptors, sVEGFR-1 and sVEGFR-2, in a group of 60 patients with systemic lupus erythematosus (SLE), and 20 healthy controls, using an enzyme-linked immunosorbent assay. We examined a possible association between serum levels of these proteins and certain clinical and laboratory parameters as well as SLE activity. VEGF, sVEGFR-1 and sVEGFR-2 were detectable in all patients with SLE and in all normal individuals. The VEGF level was higher in active SLE (mean, 300.8 pg/ml) than in inactive SLE (mean, 165.9 pg/ml) (p < 0.05) or in the control group (mean, 124.7 pg/ml) (p < 0.04). The highest sVEGFR-1 concentrations were also detected in active SLE patients (mean, 42.2 pg/ml) and the lowest in inactive disease (mean, 32.0 pg/ml) (p < 0.01). In contrast, the levels of sVEGFR-2 were lower in SLE (mean, 12557.6 pg/ml) than in the control group (mean, 15025.3 pg/ml) (p < 0.05). We found a positive correlation between sVEGFR-1 concentration and the SLE activity score p = 0.375 (p < 0.004) and a negative, but statistically insignificant correlation between sVEGFR-2 and SLE activity (p = -0.190, p > 0.05). Treatment with steroids and cytotoxic agents did not influence VEGF or its soluble receptors levels. In conclusion, in SLE patients the levels of VEGF and sVEGFR-1 are higher in patients with active SLE than in inactive disease or healthy persons. In contrast, the level of sVEGFR-2 is lower in active SLE than in inactive disease. The imbalance between VEGF and its soluble receptors may be important in SLE pathogenesis.

Adolescent↗

PubMed2002

Langerhans cell histiocytosis in a patient with systemic lupus erythematosus: a clonal disease responding to treatment with cladribine, and cyclophosphamide.

Langerhans cell histiocytosis (LCH) is a rare neoplastic disease of specific dendritic cells which belong to the monocyte-macrophage system. The association of LCH with autoimmune disease is extremely rare and to our knowledge its coexistence with systemic lupus erythematosus (SLE) has not been described so far. We report a case of LCH affecting liver, spleen and abdomen lymph nodes, which developed in an adult female six years after diagnosis of SLE treated for a long time with prednisone. Histology showed infiltration of characteristic Langerhans cells with folded, grooved or lobulated nuclei with fine chromatin. In the background there were eosinophils, lymphocytes and CD-68-positive histiocytes. The neoplastic cells were S100p-immunopositive, but stained negatively for CD1a--probably as the result of overfixation of consulted material. CD-68 was present mostly in macrophages. Ultrastructurally, the tumour cells presented structures consistent with Birbeck granules. Clonal origin of neoplastic cells was shown using the HUMARA-PCR assay. The disease was refractory to treatment with high doses of prednisone and vincristine but complete response was achieved after treatment with caldribine combined with cyclophosphamide.

Antineoplastic Combined Chemotherapy Protocols↗

PubMed2002

Aggressive primary plasma cell leukemia with skin manifestations, trisomy 8 and molecular oligoclonal features.

Plasma cell leukemia (PCL) is a very rare variant of multiple myeloma (MM) occurring in about 2% of newly diagnosed patients. Plasma cell leukemia may develop during the course of MM (secondary PCL) or it can occur without any prior sign of MM (primary PCL). We report a case of aggressive primary PCL with unusual clinical, cytogenetic and molecular features. A 36-year-old male patient was first seen because of fever and bone pain. On the skin of his chest, back, abdomen, and palpebras, there were nodular infiltrations resembling urticaria. White blood cell count was 10.8 x 10(9)/l with 41% plasmacytes. Bone marrow aspiration was hypercellular, 93.5% of cells were atypical plasmacytes and plasmablasts. The cytogenetic analysis of G-banded chromosomes in bone marrow cells yielded the trisomy 8. The skin biopsy specimen showed intensive infiltrates of uninucleated blastic cells similar to those found in the bone marrow. Immunophenotyping of bone marrow and skin neoplastic cells showed CD45+, CD45Ro+, CD68+, CD38+ and cytoplasmic kappa light chain +. The neoplastic cells stained negatively for lambda light chain, CD3, CD20, CD30, EMA, CD15, CD34, CD56 and factor VIII. The pattern of IgL genes rearrangement in the bone marrow aspirate, peripheral blood mononuclear cells, and skin specimens was examined by PCR analysis. All studied specimens showed three different IgK gene configurations suggesting that the neoplastic cells originated as a result of oligoclonal lymphoproliferation process. The patient received two courses of VAD (vincristine, doxorubicin, dexamethasone) without improvement and three courses of CHOP with only temporary stabilization of the disease. He died 5 months after the diagnosis of PCL because of disease progression and pneumonia.

Adult↗

PubMed2002

[Drug eruptions].

In the following paper, there have been discussed the mechanisms of reactions which may result from adverse drug effects. In particular, the paper shows a clinical picture of skin lesions and various dermatological entities in which drugs are triggering factors.

Drug Eruptions↗

PubMedDate not supplied

Pneumocystis carinii mimicking neonatal lupus erythematosus-related pneumonitis.

Neonatal lupus erythematosus (LE) is a rare disease associated with the transplacental passage of maternal autoantibodies to infants who manifest congenital heart block, skin disease, and less commonly, hematologic and hepatic disease. Pulmonary disease is a rare manifestation of neonatal LE and has presented as transient pneumonitis. In this report we describe an infant with neonatal LE who had the classic skin and hematologic findings of the disease in addition to pulmonary disease which might be attributed to neonatal LE-related pneumonitis, but in fact was caused by a concomitant Pneumocystis carinii infection. This case demonstrates the importance of looking for other causes of pulmonary disease in neonatal LE patients.

Diagnosis, Differential↗

PubMedDate not supplied

Proinflammatory interferon-gamma--inducing monokines (interleukin-12, interleukin-18, interleukin-15)--serum profile in patients with systemic lupus erythematosus.

Concentrations of three interferon-gamma - inducing monokines, IL-12, IL-18 and IL-15, were investigated in the serum of 60 patients with systemic lupus erythematosus (SLE) and 20 healthy subjects. IL-12 and IL-18 were detectable in the serum of all patients with SLE and in all healthy controls. The level of IL-12 was significantly higher in SLE patients (median 264.9 pg/ml) than in the control group (median 163.6 pg/ml, p < 0.02). Similar differences were observed in the level of IL-18 (median values 602.2 pg/ml and 252.7 pg/ml, respectively, p < 0.001). Correlations between serum levels of IL-12 and IL-18 and SLE activity were not statistically significant (p > 0.05). We found a significant, positive correlation between IL-12 and IL-18 (rhô = 0.419, p < 0.001) in SLE patients. The level of IL-18 was higher in the SLE patients with antinuclear antibodies (ANA) (median 660.0 pg/ml) than in ANA-negative patients (median 326.5 pg/ml, p < 0.03), as well as in patients with immunoglobulin deposits at the dermal-epidermal junction (median 746.0 pg/ml and 444.0 pg/ml respectively, p < 0.04). The level of IL-12 was also higher in patients with skin immunoglobulin deposits (328.9 pg/ml) than those without this phenomenon (257.0 pg/ml, p < 0.05). The levels of both cytokines in the patients treated with immunosuppressive drugs and those patients not treated were similar. The serum levels of IL-15 were low and not significant both in SLE patients (median 2.9 pg/ml), and in healthy controls (median 1.6 pg/ml). In conclusion, serum levels of IL-12 and IL-18 are higher in SLE patients than in healthy controls which may indicate a role in the disease pathogenesis. However, they do not correlate with disease activity and seem to be unresponsive to immunosuppressive treatment.

Adolescent↗

PubMedDate not supplied

Relationship between peripheral blood dendritic cells and cytokines involved in the pathogenesis of systemic lupus erythematosus.

Recent studies indicate that dendritic cells (DC) and several cytokines are implicated in the induction of autoimmune diseases. In this study we investigated the relationship between the total number of DC (tDC), and their plasmacytoid (pDC) and myeloid (mDC) subpopulations, with serum concentrations of interferons (IFN-alpha and IFN-gamma) and selected cytokines (TNF-alpha, IL-4, IL-6), in patients with systemic lupus erythematosus (SLE) and healthy persons. Subpopulations of DC were determined by the following antigen expression profiles: BDCA-1+\CD11c+\HLA-DR+ (for mDC) and BDCA-2 +\CD123+\HLA-DR+ (for pDC), using flow cytometry. Serum levels of interferons and cytokines were assessed by an enzyme-linked immunosorbent assay (ELISA). The study was performed in 36 SLE patients and 19 healthy volunteers. The mean number of tDC was lower in SLE patients (13.9 +/- 6.4\microL) than in healthy persons (24.1 +/- 12.6\microL) (P < 0.001). The number of pDC was also significantly lower in SLE (6.6 +/- 3.6\microL) than in the control group (12.0 +/- 8.3\microL) (P < 0.02). Moreover, the mean pDC count was lower in active than in inactive disease (5.5 +/- 3.6\microL vs 7.6 +/- 3.4\microL; P < 0.04). The mean serum levels of IFN-alpha and IFN-gamma were significantly higher in SLE patients (63.8 pg\mL and 6.6 pg\mL, respectively) than in the control group (2.7 pg\mL and 0.5 pg\mL, respectively) (P < 0.008 and P < 0.001, respectively). Serum levels of TNF-alpha and IL-6 were also higher in SLE patients (mean 7.3 pg\mL and 18.4 pg\mL, respectively) than in healthy controls (4.2 pg\mL and 0.5 pg\mL, respectively) (P < 0.02 and P < 0.001, respectively). The mean serum IL-4 concentrations were similar in SLE and healthy persons (0.2 pg\mL and 0.31 pg\mL, respectively; P -/+ 0.119). A negative correlation was found between pDC number and the serum level of IFN-alpha (rho -/+ -- 0.386, P -/+ 0.02) and between mDC and IFN-gamma (rho -/+ -- 0.377, P -/+ 0.024). In conclusion, the correlation between peripheral blood DC subsets and serum levels of IFN-alpha and IFN-gamma suggests a possible relationship between these cytokines in the pathogenesis of SLE.

Case-Control Studies↗