Le diabète de type 1 (DT1) est une maladie auto-immune qui résulte en la destruction des cellules (ß des îlots de Langerhans par les cellules du système immunitaire. Des travaux précédents de notre laboratoire ont identifié la cytokine "Thymic Stromal Lymphopoietin" (TSLP) comme étant un stimulus tolérogénique pour les cellules dendritiques (DCs) chez le modèle murin du DT1, la souris "Non Obese Diabeiic" (NOD). Les DCs conditionnées à la TSLP (TSLP-DCs) présentent un phénotype semi-mature, sont capables d’induire une réponse Th2 ainsi qu’une conversion et une expansion des lymphocytes T régulateurs (Tregs) in vitro et protègent les souris NOD contre le DT1. Ces observations nous ont amené à investiguer les mécanismes qui entraînent cette protection contre le DT1. Les travaux décrits dans ce mémoire montrent que les TSLP-DCs injectées chez les souris NOD migrent vers la rate, de manière privilégiée. Ces observations nous ont amené à étudier l’influence des TSLP-DCs sur la réponse Th1/Th2 au niveau de la rate. Nous avons observé que les splénocytes CD4[indice supérieur +] et CD8[indice supérieur +] de souris injectées avec des TSLP-DCs exprimaient moins d’IFN? par rapport au souris témoins (splénocytes des souris injectées avec des LPS-DCs). Ces résultats suggèrent une diminution de la réponse Th1 chez ces splénocytes. Par contre, les résultats obtenus avec l’IL-10 ne nous ont pas permis de conclure quant à l’influence des TSLP-DCs sur la réponse Th2. Cependant, nous avons confirmé la capacité des TSLP-DCs à induire la conversion des lymphocytes T CD4[indice supérieur +]CD25[indice supérieur -] en Tregs CD4[indice supérieur +]CD25[indice supérieur +]Foxp3[indice supérieur +]. Nous avons aussi montré que ces Tregs partiellement convertis inhibent la prolifération de lymphocytes T 8.3-CD8[indice supérieur +] diabétogènes, et empêchent la production d’IFN?. Les Tregs convertis en présence de TSLP-DCs ou de LPS-DCs ont également été injectés à des souris 8.3-NOD.RAG2[indice supérieur -/-]. Les résultats ont révélé que seuls les Tregs différenciés en présence de TSLP-DCs ont la capacité d’empêcher le développement du DT1. Nos travaux suggèrent que la diminution de la réponse Th1 et l’induction d’une population efficiente de lymphocytes Tregs font partie des mécanismes utilisés par les TSLP-DCs pour protéger les souris NOD contre le DT1.

SerpinB2 (aka plasminogen activator type 2) is well described as an extracellular inhibitor of urokinase-type plasminogen activator (uPA). However, the majority of SerpinB2 is retained intracellularly, and many uPA-independent activities have been reported for SerpinB2 suggesting an alternate function. This thesis explores the role of SerpinB2 in epithelial tumour cell lines, highlights the problems associated with various expression systems and argues that SerpinB2 has no role in growth or apoptosis of tumour cells. A potential role for immune modulation and angiogenesis is suggested in in vivo models. Previous research using SerpinB2 transfected, clonally selected tumour cell lines suggested that SerpinB2 regulates the retinoblastoma tumour suppressor protein (Rb) by binding and protecting Rb from degradation. Despite the use of two techniques under numerous conditions and positive controls, no significant interaction between SerpinB2 and Rb was found. SerpinB2 was reported to bind Rb through a PENF homology motif located within the SerpinB2 C-D interhelical loop region. The PENF homology motif was postulated to represent the motif responsible for binding to the C-pocket of Rb. Epstein Barr Virus nuclear antigen 6 (EBNA6) is a known Rb binding protein, which contains two predicted PENF homology motifs. However, mutation of the two PENF homology motifs within EBNA6 did not reduce Rb binding. Furthermore, the SerpinB2 PENF homology motif is actually not well conserved between SerpinB2 proteins from multiple species, whereas other regions of the SerpinB2 C-D loop show a high level of conservation. These data do not support a role for SerpinB2 and the PENF homology motif in Rb binding. SerpinB2 has been proposed to have a role in regulating growth and apoptosis. To further investigate this proposed phenotype of SerpinB2, SerpinB2 was expressed in a range of epithelial tumour lines using transient transfection. No change in growth, apoptosis or Rb levels were found. After ≈2-3 month antibiotic selection for the SerpinB2-expressing plasmid, SerpinB2 protein was lost without the loss of the transgene, indicating selective pressure against long-term SerpinB2 protein expression. To further investigate long-term SerpinB2 expression adenovirus and lentivirus vectors were used. Infection of tumour cell lines with adenovirus vectors expressing SerpinB2 resulted in reduced cell growth, characterised by increased p53 (but not Rb) levels and G2 arrest or apoptosis. When SerpinB2 expressing lentivirus vectors were used to transduce the same tumour cell lines, high levels of long-term expression of functional SerpinB2 was achieved. However, SerpinB2-expressing cell lines showed no differences in growth, proliferation, Rb levels, or apoptosis induced by a range of agents. Growth and apoptosis observed with adenovirus SerpinB2 had all the characteristics of adenovirus-associated toxicity, which has been reported previously for specific proteins. These experiments highlighted the problems associated with SerpinB2 expression systems and suggest that SerpinB2 expression per se is not toxic nor has a role in regulating Rb, growth and apoptosis. Screening of a number of tumour cell lines identified the HPV16 transformed cervical cancer line as expressing high levels of SerpinB2. SerpinB2 was located both extracellularly and intracellularly with a cytoplasmic and nuclear distribution. A high molecular weight SerpinB2 species was identified in CaSki cells and was shown to be the N-linked glycosylated species. Sequencing showed the protein to be Type A SerpinB2 and the protein was shown to form an inhibitory complex with uPA. An abundant low molecular weight SerpinB2 species was also identified in CaSki cell supernatants and appeared to be a proteolytic fragment of SerpinB2. Treatment of CaSki with PMA, TNFα and IFNγ increased SerpinB2 levels. Lentiviral based shRNA failed to significantly down regulate SerpinB2 expression and increasing SerpinB2 levels with lentiviral expression did not change growth, apoptosis, Rb levels or E7 transcription. Lentiviral expression of SerpinB2 in (normally SerpinB2 negative) HPV16 transformed SiHa cells, also failed to show changes in Rb levels or E7 transcription. CaSki thus express wild-type and functional SerpinB2, but no evidence could found that SerpinB2 effects HPV16 E7 transcription or Rb levels. The data presented identifies CaSki as valuable source of biologically functional SerpinB2. SerpinB2 expression in breast cancer cells has been associated with positive prognosis. Tubo, a SerpinB2-negative murine breast carcinoma cell line, was transduced with lentivirus expressing SerpinB2 and grown subcutaneously in BALB/c mice. SerpinB2 expressing tumours appeared red and were larger than control tumours. Furthermore, SerpinB2 expressing tumours had a ≈2 fold higher density of blood vessels when compared to Tubo and Tubo expressing EGFP. Mice carrying tumours expressing SerpinB2 also showed reduced anti-tumour IgG2 responses. These data suggest that a role for SerpinB2 in regulating angiogenesis and antitumour immunity. In conclusion, this thesis challenges the notion that SerpinB2 regulates Rb, cell cycle, and apoptosis and suggests a potential role for SerpinB2 in tumour angiogenesis and immunity.

SerpinB2 (aka plasminogen activator type 2) is well described as an extracellular inhibitor of urokinase-type plasminogen activator (uPA). However, the majority of SerpinB2 is retained intracellularly, and many uPA-independent activities have been reported for SerpinB2 suggesting an alternate function. This thesis explores the role of SerpinB2 in epithelial tumour cell lines, highlights the problems associated with various expression systems and argues that SerpinB2 has no role in growth or apoptosis of tumour cells. A potential role for immune modulation and angiogenesis is suggested in in vivo models. Previous research using SerpinB2 transfected, clonally selected tumour cell lines suggested that SerpinB2 regulates the retinoblastoma tumour suppressor protein (Rb) by binding and protecting Rb from degradation. Despite the use of two techniques under numerous conditions and positive controls, no significant interaction between SerpinB2 and Rb was found. SerpinB2 was reported to bind Rb through a PENF homology motif located within the SerpinB2 C-D interhelical loop region. The PENF homology motif was postulated to represent the motif responsible for binding to the C-pocket of Rb. Epstein Barr Virus nuclear antigen 6 (EBNA6) is a known Rb binding protein, which contains two predicted PENF homology motifs. However, mutation of the two PENF homology motifs within EBNA6 did not reduce Rb binding. Furthermore, the SerpinB2 PENF homology motif is actually not well conserved between SerpinB2 proteins from multiple species, whereas other regions of the SerpinB2 C-D loop show a high level of conservation. These data do not support a role for SerpinB2 and the PENF homology motif in Rb binding. SerpinB2 has been proposed to have a role in regulating growth and apoptosis. To further investigate this proposed phenotype of SerpinB2, SerpinB2 was expressed in a range of epithelial tumour lines using transient transfection. No change in growth, apoptosis or Rb levels were found. After ≈2-3 month antibiotic selection for the SerpinB2-expressing plasmid, SerpinB2 protein was lost without the loss of the transgene, indicating selective pressure against long-term SerpinB2 protein expression. To further investigate long-term SerpinB2 expression adenovirus and lentivirus vectors were used. Infection of tumour cell lines with adenovirus vectors expressing SerpinB2 resulted in reduced cell growth, characterised by increased p53 (but not Rb) levels and G2 arrest or apoptosis. When SerpinB2 expressing lentivirus vectors were used to transduce the same tumour cell lines, high levels of long-term expression of functional SerpinB2 was achieved. However, SerpinB2-expressing cell lines showed no differences in growth, proliferation, Rb levels, or apoptosis induced by a range of agents. Growth and apoptosis observed with adenovirus SerpinB2 had all the characteristics of adenovirus-associated toxicity, which has been reported previously for specific proteins. These experiments highlighted the problems associated with SerpinB2 expression systems and suggest that SerpinB2 expression per se is not toxic nor has a role in regulating Rb, growth and apoptosis. Screening of a number of tumour cell lines identified the HPV16 transformed cervical cancer line as expressing high levels of SerpinB2. SerpinB2 was located both extracellularly and intracellularly with a cytoplasmic and nuclear distribution. A high molecular weight SerpinB2 species was identified in CaSki cells and was shown to be the N-linked glycosylated species. Sequencing showed the protein to be Type A SerpinB2 and the protein was shown to form an inhibitory complex with uPA. An abundant low molecular weight SerpinB2 species was also identified in CaSki cell supernatants and appeared to be a proteolytic fragment of SerpinB2. Treatment of CaSki with PMA, TNFα and IFNγ increased SerpinB2 levels. Lentiviral based shRNA failed to significantly down regulate SerpinB2 expression and increasing SerpinB2 levels with lentiviral expression did not change growth, apoptosis, Rb levels or E7 transcription. Lentiviral expression of SerpinB2 in (normally SerpinB2 negative) HPV16 transformed SiHa cells, also failed to show changes in Rb levels or E7 transcription. CaSki thus express wild-type and functional SerpinB2, but no evidence could found that SerpinB2 effects HPV16 E7 transcription or Rb levels. The data presented identifies CaSki as valuable source of biologically functional SerpinB2. SerpinB2 expression in breast cancer cells has been associated with positive prognosis. Tubo, a SerpinB2-negative murine breast carcinoma cell line, was transduced with lentivirus expressing SerpinB2 and grown subcutaneously in BALB/c mice. SerpinB2 expressing tumours appeared red and were larger than control tumours. Furthermore, SerpinB2 expressing tumours had a ≈2 fold higher density of blood vessels when compared to Tubo and Tubo expressing EGFP. Mice carrying tumours expressing SerpinB2 also showed reduced anti-tumour IgG2 responses. These data suggest that a role for SerpinB2 in regulating angiogenesis and antitumour immunity. In conclusion, this thesis challenges the notion that SerpinB2 regulates Rb, cell cycle, and apoptosis and suggests a potential role for SerpinB2 in tumour angiogenesis and immunity.

SerpinB2 (aka plasminogen activator type 2) is well described as an extracellular inhibitor of urokinase-type plasminogen activator (uPA). However, the majority of SerpinB2 is retained intracellularly, and many uPA-independent activities have been reported for SerpinB2 suggesting an alternate function. This thesis explores the role of SerpinB2 in epithelial tumour cell lines, highlights the problems associated with various expression systems and argues that SerpinB2 has no role in growth or apoptosis of tumour cells. A potential role for immune modulation and angiogenesis is suggested in in vivo models. Previous research using SerpinB2 transfected, clonally selected tumour cell lines suggested that SerpinB2 regulates the retinoblastoma tumour suppressor protein (Rb) by binding and protecting Rb from degradation. Despite the use of two techniques under numerous conditions and positive controls, no significant interaction between SerpinB2 and Rb was found. SerpinB2 was reported to bind Rb through a PENF homology motif located within the SerpinB2 C-D interhelical loop region. The PENF homology motif was postulated to represent the motif responsible for binding to the C-pocket of Rb. Epstein Barr Virus nuclear antigen 6 (EBNA6) is a known Rb binding protein, which contains two predicted PENF homology motifs. However, mutation of the two PENF homology motifs within EBNA6 did not reduce Rb binding. Furthermore, the SerpinB2 PENF homology motif is actually not well conserved between SerpinB2 proteins from multiple species, whereas other regions of the SerpinB2 C-D loop show a high level of conservation. These data do not support a role for SerpinB2 and the PENF homology motif in Rb binding. SerpinB2 has been proposed to have a role in regulating growth and apoptosis. To further investigate this proposed phenotype of SerpinB2, SerpinB2 was expressed in a range of epithelial tumour lines using transient transfection. No change in growth, apoptosis or Rb levels were found. After ≈2-3 month antibiotic selection for the SerpinB2-expressing plasmid, SerpinB2 protein was lost without the loss of the transgene, indicating selective pressure against long-term SerpinB2 protein expression. To further investigate long-term SerpinB2 expression adenovirus and lentivirus vectors were used. Infection of tumour cell lines with adenovirus vectors expressing SerpinB2 resulted in reduced cell growth, characterised by increased p53 (but not Rb) levels and G2 arrest or apoptosis. When SerpinB2 expressing lentivirus vectors were used to transduce the same tumour cell lines, high levels of long-term expression of functional SerpinB2 was achieved. However, SerpinB2-expressing cell lines showed no differences in growth, proliferation, Rb levels, or apoptosis induced by a range of agents. Growth and apoptosis observed with adenovirus SerpinB2 had all the characteristics of adenovirus-associated toxicity, which has been reported previously for specific proteins. These experiments highlighted the problems associated with SerpinB2 expression systems and suggest that SerpinB2 expression per se is not toxic nor has a role in regulating Rb, growth and apoptosis. Screening of a number of tumour cell lines identified the HPV16 transformed cervical cancer line as expressing high levels of SerpinB2. SerpinB2 was located both extracellularly and intracellularly with a cytoplasmic and nuclear distribution. A high molecular weight SerpinB2 species was identified in CaSki cells and was shown to be the N-linked glycosylated species. Sequencing showed the protein to be Type A SerpinB2 and the protein was shown to form an inhibitory complex with uPA. An abundant low molecular weight SerpinB2 species was also identified in CaSki cell supernatants and appeared to be a proteolytic fragment of SerpinB2. Treatment of CaSki with PMA, TNFα and IFNγ increased SerpinB2 levels. Lentiviral based shRNA failed to significantly down regulate SerpinB2 expression and increasing SerpinB2 levels with lentiviral expression did not change growth, apoptosis, Rb levels or E7 transcription. Lentiviral expression of SerpinB2 in (normally SerpinB2 negative) HPV16 transformed SiHa cells, also failed to show changes in Rb levels or E7 transcription. CaSki thus express wild-type and functional SerpinB2, but no evidence could found that SerpinB2 effects HPV16 E7 transcription or Rb levels. The data presented identifies CaSki as valuable source of biologically functional SerpinB2. SerpinB2 expression in breast cancer cells has been associated with positive prognosis. Tubo, a SerpinB2-negative murine breast carcinoma cell line, was transduced with lentivirus expressing SerpinB2 and grown subcutaneously in BALB/c mice. SerpinB2 expressing tumours appeared red and were larger than control tumours. Furthermore, SerpinB2 expressing tumours had a ≈2 fold higher density of blood vessels when compared to Tubo and Tubo expressing EGFP. Mice carrying tumours expressing SerpinB2 also showed reduced anti-tumour IgG2 responses. These data suggest that a role for SerpinB2 in regulating angiogenesis and antitumour immunity. In conclusion, this thesis challenges the notion that SerpinB2 regulates Rb, cell cycle, and apoptosis and suggests a potential role for SerpinB2 in tumour angiogenesis and immunity.

Diss. (sammanfattning) Linköping : Linköpings universitet, 2005. / Härtill 4 uppsatser.

Thesis (Ph. D.)--University of Missouri-Columbia, 2007. / "May 2007" The entire dissertation/thesis text is included in the research.pdf file; the official abstract appears in the short.pdf file (which also appears in the research.pdf); a non-technical general description, or public abstract, appears in the public.pdf file. Vita. Includes bibliographical references.

Thesis (Ph.D.)--University of Alabama at Birmingham, 2008. / Title from first page of PDF file (viewed on June 24, 2009). Includes bibliographical references (p. 88-101).

Thesis (Ph. D.)--Ohio State University, 2007. / Full text release at OhioLINK's ETD Center delayed at author's request

OBJETIVO: Avaliar a expressão dos perfis de citocinas Th1, Th2 e Th17 em pacientes com LES e verificar possíveis associações com os níveis séricos de vitamina D. MÉTODOS: Estudo transversal com inclusão de 172 pacientes acompanhados no ambulatório de reumatologia do Hospital de Clínicas de Porto Alegre. Os níveis de vitamina D foram medidos por quimiluminescência. Níveis séricos <20 ng/ml foram considerados como deficiência de vitamina D e níveis ≥20 ng/ml foram considerados normais. As citocinas foram medidas no soro após o descongelamento das amostras em uma única ocasião, usando Kit CBA (cytometric beads array) Th1/Th2/Th17. RESULTADOS: Cento e sessenta e um (94%) pacientes eram mulheres e 128 (74,4%) foram classificados como euro-descendentes. A idade média foi de 40,5±13,8 anos e a idade média no momento do diagnóstico foi de 31,5±13,4 anos. Na entrada do estudo, os pacientes tiveram mediana (intervalo interquartil) de atividade da doença (SLEDAI- systemic lupus erythematosus disease activity index) de 2 (1-4) e cronicidade (SLICC damage index- systemic lupus international collaborating clinics) de 0 (0-1). O nível médio de vitamina D foi de 25,4±11,04 ng/ml. Cinquenta e nove (34,3%) pacientes apresentavam deficiência de vitamina D e 113 (65,7%) tinham níveis considerados normais. Nenhuma associação e correlação estatisticamente significativa foram encontradas. Os níveis de INF-α e SLEDAI mostraram uma correlação positiva fraca (rs=0,22, p=0,04). Análise de regressão linear foi realizada para controlar possíveis fatores de confusão. CONCLUSÃO: A deficiência de vitamina D é prevalente em pacientes com LES, entretanto, não foram encontradas correlações e associações entre níveis de vitamina D e perfil de citocinas. Confirmamos a correlação existente entre o IFN-α e SLEDAI, conforme a literatura. Efeito in vitro de vitamina D no perfil de citocinas não foi reproduzido no presente estudo. Estudos longitudinais podem ajudar a esclarecer a influência da vitamina D na fisiopatogenia do LES. / OBJECTIVES: To evaluate the expression of Th1, Th2 and Th17 cytokine profiles in SLE patients and verify possible associations with serum vitamin D levels. METHODS: Cross-sectional study with 172 SLE patients, followed at the outpatient clinic of rheumatology at Hospital de Clínicas de Porto Alegre were included. The levels of vitamin D were measured by chemiluminescence. Serum levels <20 ng/ml were considered as vitamin D deficiency. Normal vitamin D levels were defined as ≥20ng/ml. Cytokines were measured in serum after thawing the samples on a single occasion, using Kit CBA (cytometric beads array) Th1/Th2/Th17. RESULTS: One hundred sixty one (94%) patients were women and 128 (74.4%) were classified as European derived. The mean age of patients was 40.5±13.8 years and the mean age at diagnosis was 31.5±13.4 years. At the time of study entry, patients had median (IQR) of active disease (SLEDAI- systemic lupus erythematosus disease activity index) of 2 (1-4) and chronicity (SLICC damage index- systemic lupus international collaborating clinics) of 0 (0-1). Mean vitamin D levels were 25.4±11.04 ng/ml. Fifty-nine (34.3%) patients had vitamin D deficiency and 113 (65.7%) had normal levels. No association and statistically significant correlations was found. The levels of INF-α and SLEDAI showed a weak positive correlation (rs=0.22, p=0.04). Linear regression analysis was performed to control for possible confounding factors. CONCLUSION:Vitamin D deficiency is prevalent in patients with SLE, however, no statistically significant correlations and associations between vitamin D levels and cytokine profile were found. We confirm the correlation between IFN-α and SLEDAI, according to the literature. In vitro effect of vitamin D on the cytokine profile was not reproduced in this study. Longitudinal studies may help clarify the influence of vitamin D in the pathogenesis of SLE.

OBJETIVO: Avaliar a expressão dos perfis de citocinas Th1, Th2 e Th17 em pacientes com LES e verificar possíveis associações com os níveis séricos de vitamina D. MÉTODOS: Estudo transversal com inclusão de 172 pacientes acompanhados no ambulatório de reumatologia do Hospital de Clínicas de Porto Alegre. Os níveis de vitamina D foram medidos por quimiluminescência. Níveis séricos <20 ng/ml foram considerados como deficiência de vitamina D e níveis ≥20 ng/ml foram considerados normais. As citocinas foram medidas no soro após o descongelamento das amostras em uma única ocasião, usando Kit CBA (cytometric beads array) Th1/Th2/Th17. RESULTADOS: Cento e sessenta e um (94%) pacientes eram mulheres e 128 (74,4%) foram classificados como euro-descendentes. A idade média foi de 40,5±13,8 anos e a idade média no momento do diagnóstico foi de 31,5±13,4 anos. Na entrada do estudo, os pacientes tiveram mediana (intervalo interquartil) de atividade da doença (SLEDAI- systemic lupus erythematosus disease activity index) de 2 (1-4) e cronicidade (SLICC damage index- systemic lupus international collaborating clinics) de 0 (0-1). O nível médio de vitamina D foi de 25,4±11,04 ng/ml. Cinquenta e nove (34,3%) pacientes apresentavam deficiência de vitamina D e 113 (65,7%) tinham níveis considerados normais. Nenhuma associação e correlação estatisticamente significativa foram encontradas. Os níveis de INF-α e SLEDAI mostraram uma correlação positiva fraca (rs=0,22, p=0,04). Análise de regressão linear foi realizada para controlar possíveis fatores de confusão. CONCLUSÃO: A deficiência de vitamina D é prevalente em pacientes com LES, entretanto, não foram encontradas correlações e associações entre níveis de vitamina D e perfil de citocinas. Confirmamos a correlação existente entre o IFN-α e SLEDAI, conforme a literatura. Efeito in vitro de vitamina D no perfil de citocinas não foi reproduzido no presente estudo. Estudos longitudinais podem ajudar a esclarecer a influência da vitamina D na fisiopatogenia do LES. / OBJECTIVES: To evaluate the expression of Th1, Th2 and Th17 cytokine profiles in SLE patients and verify possible associations with serum vitamin D levels. METHODS: Cross-sectional study with 172 SLE patients, followed at the outpatient clinic of rheumatology at Hospital de Clínicas de Porto Alegre were included. The levels of vitamin D were measured by chemiluminescence. Serum levels <20 ng/ml were considered as vitamin D deficiency. Normal vitamin D levels were defined as ≥20ng/ml. Cytokines were measured in serum after thawing the samples on a single occasion, using Kit CBA (cytometric beads array) Th1/Th2/Th17. RESULTS: One hundred sixty one (94%) patients were women and 128 (74.4%) were classified as European derived. The mean age of patients was 40.5±13.8 years and the mean age at diagnosis was 31.5±13.4 years. At the time of study entry, patients had median (IQR) of active disease (SLEDAI- systemic lupus erythematosus disease activity index) of 2 (1-4) and chronicity (SLICC damage index- systemic lupus international collaborating clinics) of 0 (0-1). Mean vitamin D levels were 25.4±11.04 ng/ml. Fifty-nine (34.3%) patients had vitamin D deficiency and 113 (65.7%) had normal levels. No association and statistically significant correlations was found. The levels of INF-α and SLEDAI showed a weak positive correlation (rs=0.22, p=0.04). Linear regression analysis was performed to control for possible confounding factors. CONCLUSION:Vitamin D deficiency is prevalent in patients with SLE, however, no statistically significant correlations and associations between vitamin D levels and cytokine profile were found. We confirm the correlation between IFN-α and SLEDAI, according to the literature. In vitro effect of vitamin D on the cytokine profile was not reproduced in this study. Longitudinal studies may help clarify the influence of vitamin D in the pathogenesis of SLE.