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PubMed2002

Acquired activated protein C resistance associated with anti-protein S antibody as a strong risk factor for DVT in non-SLE patients.

Anti-phospholipid (aPL) antibodies (Abs) are well known to be associated with thromboembolic events in patients with systemic lupus erythematosus (SLE). However, the clinical relevance of a PL Abs in patients without SLE (non-SLE) who have venous thromboembolism remains unclear. We evaluated 143 non-SLE patients with a first episode of clinically suspected deep vein thrombosis (DVT) by using objective tests for diagnosing DVT and laboratory tests including the activated protein C resistance (APC-R) test, the factor V Leiden test, and various aPL Abs. The prevalence of acquired APC-R, in which case there was no factor V Leiden mutation, was significantly higher in patients with DVT (15/58 cases, 25.9%, p < 0.0001) than in those without DVT (3/80 cases, 3.7%), and confirmed that acquired APC-R was a strong risk factor for DVT (odds ratio [OR], 8.95; 95% confidence intervals [CI], 2.45-32.7; p < 0.001). Multivariate logistic analysis revealed that the presence of LA, aCL, anti-beta2-glycoprotein I, anti-prothrombin and anti-protein C Abs was not reliable as a risk factor for DVT in non-SLE patients, and that the presence of anti-protein S Abs was the most significant risk factor for DVT (OR, 5.88; 95% CI, 1.96-17.7; p < 0.002). Furthermore, the presence of anti-protein S Abs was strongly associated with acquired APC-R (OR, 57.8; 95% CI, 8.53-391; p < 0.0001). These results suggest that acquired APC-R may reflect functional interference by anti-protein S Abs of the protein C pathway, which action may represent an important mechanism for the development DVT in non-SLE patients.

Activated Protein C Resistance↗

PubMed2003

[Study on corelation between InsP(3) generation and TCR/ CD3 complex-mediated [Ca(2+)]i responses in T cells from SLE patients].

AIM: To demonstrate whether function disorder of T cells from SLE patients was relative to abnormal biochemical pathways mediated by TCR/ CD3 complex and whether this abnormality was relative to the InsP(3) production. METHODS: Human T cells were isolated through Nylon-columns from heparinized peripheral blood from SLE patients and control individuals. Percentage of CD3(+) T cells was detected by flow cytometry. After cross-linking of anti-CD3 mAbs to sheep anti-mouse IgG and stimulating T cells, the changes of free calcium ion within T cells was observed successively for 10 minutes by an adhesion cytometry. Flow cytometry was used to detect the difference in positive rate between normal individual's and SLE patient's T cells. Level of InsP(3) was detected by a radioreceptor assay kit. RESULTS: (1)Flow cytometry analysis showed that CD3(+) T cells obtained through nylon column accounted for more than 90%.(2)The base line recordings of [Ca(2+)]i response from SLE patients were similar to that from normal control (P=0.105). Peak and plateau [Ca(2+)]i response in T cells of SLE patients were significantly higher than that in the control group (P<0.001). (3)The percentage of the CD3(+) T cells was similar in both individuals (P=0.665).(4)No differences in the anti-CD3 mAb-mediated InsP(3) generation were found between the two groups (P=0.537). CONCLUSION: TCR/ CD3-mediated [Ca(2+)]i responses in T cells from SLE patients is abnormal, and the abnormality has no relation to InsP(3) generation.

Animals↗

PubMed2004

Value of high resistance index - HRI calculated from Doppler spectrum of popliteal arteries in patients with systemic lupus erythematosus (SLE).

BACKGROUND: HRI is a new Doppler index calculated as a ratio between S -maximal systolic flow and D -maximal early diastolic reversed flow -HRI=D/S. The aim of the study is to evaluate the diagnostic significance of HRI calculated from the Doppler spectrum of popliteal arteries in patients with systemic lupus erythematosus (SLE) with and without secondary antiphospholipid syndrome (SAPS) compared with healthy controls. MATERIAL/METHODS: During 9-month period (May 2003 -January 2004), 93 patients (81 women and 12 men) with SLE (including 24 patients with SAPS) and 30 healthy controls (24 women and 6 men) underwent bilateral duplex Doppler examinations of lower limb arteries. The examinations were performed using HDI 3500 (ATL) with 5 -12 MHz linear transducer under standardized conditions: correct insonation angle and sample volume size, with the patient in a supine position, after 10 minutes rest. RESULTS: Mean HRI value obtained in the control group was 0.415 (range 0.305 -0.555; median 0.402). In the group of SLE patients without SAPS, mean HRI value was decreased to 0.320 (range 0 -0.584; median 0.334) and even lower -0.283 in SLE patients with SAPS (range 0.106 -0.545; median 0.291). CONCLUSIONS: Small arteries, arterioles and capillaries are the main affected vessels in SLE. This chronic process stimulates circulation through lower resistance collaterals, decreasing HRI value. The Doppler HRI calculation can be valuable in early diagnosis and monitoring of lower extremity vascular changes in patients suffering from SLE with and without SAPS.

Adult↗

PubMed1990

[Lymphocyte phenotypes and their correlation with clinical features in systemic lupus erythematosus (SLE)].

Lymphocyte phenotypes of peripheral blood from 32 SLE patients and 30 normal subjects were studied with 13 kinds of monoclonal antibodies using indirect immunofluorescence technique. The results showed that T4+, T8+, T3+ and T11+ cells decreased in active cases of SLE, while Ia+, IL2R1+ and PCA-1+ cells increased, other B-cell phenotypes (B1, B2, B4, IgM, IgG, IgD) showed no significant difference from those of the normal group. Thus, in inactive SLE after therapeutic management, the numbers of T3+, T11+, T4+, Ia+ and IL2R1+ cells no longer show any abnormality, but the numbers of T8+, PCA-1+ cells and the level of serum IgG are still higher than normal. From the above-mentioned results, it was shown that: 1. The key change in active SLE is the abnormality of immunoregulatory T cells, especially T4+ cells; 2. In active SLE, some of the T cells have been activated in vivo and these immunocompetent cells play an important role in immunoglobulin production of B cells; 3. The hyperactivity of humoral immunity is mainly related to the increase of PCA-1+ cells under the regulation of T cells; 4. Both the lymphocyte phenotypes and clinical features of SLE showed heterogeneity.

Adult↗

PubMed1989

Binding of anti-DNA antibodies to glomerular heparan sulfate: a new clue for the pathogenesis of SLE nephritis?

Antibodies against heparan sulfate (HS) were detected in sera from patients with active systemic lupus erythematosus (SLE) and in sera from MRL/l mice with a spontaneous SLE-like disease. By inhibition studies it was shown that this reactivity towards HS was due to cross-reactivity of anti-DNA antibodies. Immunoglobulin eluted from human and mouse kidneys with diffuse proliferative SLE glomerulonephritis also bound to HS. This crossreaction of anti-DNA antibodies was further substantiated by the finding that 17 out of 42 anti-DNA monoclonal antibodies (mAb) also bound to HS, 11 out of 17 HS positive mAb bound to heparan sulfate proteoglycan (HSPG) purified from human glomerular basement membranes (GBM) and 7 out of 42 bound directly to isolated human GBM-loops. The binding to HS, HSPG, and GBM could be inhibited in a dose-dependent manner by DNA. In a retrospective analysis of sera from 10 SLE patients, in which 6-16 serum samples per patient were studied, we found in all 5 episodes of onset or exacerbation of a SLE nephritis an anti-HS activity in the serum, prior to onset of the nephritis. In 4 episodes of onset or exacerbation of non-renal manifestations, anti-HS activity was only found in the serum during one episode. Based on these studies we postulate that binding of anti-DNA antibodies to HS within the GBM may be an important immunopathological event in the development of SLE nephritis.

Animals↗

PubMed1987

The effect of La(SSB) on PWM-induced immunoglobulin synthesis by anti-La(SSB) positive SLE patients and healthy controls.

The effect of affinity purified La(SSB) on immunoglobulin synthesis in vitro by mononuclear cells (MNC) from anti-La(SSB)-positive systemic lupus erythematosus (SLE) patients and healthy controls was studied. La(SSB) was prepared from calf thymus extract and characterized by SDS-polyacrylamide gel electrophoresis and immunoblotting. Silver staining of gels reveals nine major bands at 68 kD, 43-48 kD and 30-33 kD, of which six were recognized on immunoblots by sera from anti-La(SSB) positive SLE patients. Studies in vitro showed that La(SSB) alone did not stimulate total IgG or IgM synthesis in controls or SLE patients. Low concentrations of La(SSB) (optimal dose less than 0.02 ng/ml) suppressed pokeweed mitogen (PWM)-driven IgG synthesis by controls but not by anti-La(SSB) positive SLE patients. IgM responses were unaffected. Anti-La(SSB) and anti-DNA were detected in PWM-stimulated cultures from both study groups. In the presence of La(SSB) IgM anti-La(SSB) synthesis was enhanced in anti-La(SSB)-positive patients in a dose-dependent manner. In contrast, La(SSB) inhibited anti-La(SSB) production by controls (maximal at 2 ng/ml). La(SSB) had no effect on anti-DNA production in either group. Pre-incubation of control or anti-La(SSB)-positive SLE MNC with La(SSB) before addition to autologous PWM-driven cultures did not induce suppressor cells, although pre-incubation with Concanavalin A (ConA) did. Thus we suggest that La(SSB)-induced suppression of IgG synthesis in PWM-driven control cultures may not be due to induction of regulator cells, possibly missing from SLE cultures, but perhaps is a direct effect on B cells.

Adult↗

PubMed1984

Resistance to tolerance induction is not prerequisite to development of murine SLE.

Four different SLE-prone mice, NZB, (NZB x NZW)F1, MRL/MpJ-lpr/lpr, and male BXSB/MpJ, resisted the induction of tolerance to human IgG (HGG) at 5 wk, but not before 3 wk of age. However, female F1 hybrids between NZW and BXSB mice were easily made tolerant to HGG, although they develop an acute form of typical SLE similar to that seen in (NZB x NZW)F1 hybrid females. In addition, C57BL/6 mice bearing a mutant gene, lpr (lymphoproliferation), which produced significant amounts of various autoantibodies characteristic of murine SLE, were still as susceptible to tolerance induction as control C57BL/6 mice. In contrast, both (NZW x BXSB)F1 and (C3H x BXSB)F1 hybrid males carrying the abnormal Y chromosome of BXSB mice failed to become tolerant to HGG, although the extent of resistance to tolerance induction was less significant in (C3H x BXSB)F1 males than in (NZW x BXSB)F1 males. Our results suggest that 1) the defect in tolerance induction to heterologous IgG such as HGG is not necessarily required for the development of an SLE-like syndrome in mice; 2) the induction or enhanced production of autoantibodies by the lpr gene is not related to this cellular abnormality; but 3) a Y chromosome-associated factor from BXSB mice plays a significant role in the abnormality to resist tolerance induction as well as the acceleration of SLE. Our observations are consistent with the hypothesis that SLE may be based on highly specific abnormalities of immune responses to particular autoantigens, but not on a generalized breakdown of a tolerance mechanism.

Animals↗

PubMed1983

Reduced complement-mediated immune complex solubilizing capacity and the presence of incompletely solubilized immune complexes in SLE sera.

Reduced complement-mediated solubilization (CMS) of pre-formed immune complexes (IC) was demonstrated in sera from 11 out of 12 SLE patients. The presence of incompletely solubilized endogeneous IC in SLE sera was indicated by the following findings: (1) When IC positive SLE sera with reduced CMS capacity were mixed with normal donor sera they inhibited the CMS of the latter sera. (2) Resuspended PEG (2.75%) precipitates obtained from SLE sera inhibited the CMS of normal donor sera. (3) Non-solubilized or incompletely complement solubilized IC in SLE sera give a strong response in the PEG-CC assay for IC. The IC activity of SLE sera was clearly reduced in this assay when the endogeneous IC were solubilized prior to testing. In contrast, sera of 14 rheumatoid arthritis (RA) patients exhibited normal CMS. IC which could be further solubilized by complement were not demonstrable although all RA sera were IC positive.

Adult↗

PubMed1984

Characterization of mouse and human monoclonal antibodies cross-reactive with SLE serum antibodies to guanosine.

Two new monoclonal antibodies, one a mouse IgM and the other a human IgM that reacted with guanosine, were compared to human serum antibodies from patients with systemic lupus erythematosus (SLE). The human monoclonal antibody was polyspecific in its binding to the nucleoside bases, whereas the mouse monoclonal antibody was relatively specific for guanosine when compared by using an enzyme-linked immunosorbent assay (ELISA). Neither antibody bound polyguanylic acid or denatured single-stranded (ss) DNA, however. Serum IgG antibodies from seven patients with SLE cross-reacted with the mouse monoclonal antibody and showed considerable specificity for guanosine. In contrast, the human serum IgG antiguanosine antibodies also bound ssDNA but not dsDNA or polyguanylic acid. Serum IgG antibodies to guanosine measured by ELISA from the seven SLE patients had a decreased response when compared to the total serum IgG response to ssDNA, and most of the antibodies that bound guanosine also bound ssDNA. These studies provide new evidence that there are specific IgG antibodies to guanosine in SLE sera that are a small fraction of the antibodies to ssDNA. Further efforts to define the role of these guanosine antibodies in SLE may provide a better understanding of the basic mechanisms responsible for the development of SLE in man.

Animals↗

PubMed1981

In vitro study of complement dependent active adherence on SLE and RA leukocytes.

Immunological disorders may cause altered motility or attachment of leukocytes. Active adherence of buffy cost cells derived from normal subjects and with autoimmune diseases patients and complement dependency of this process was studied on glass surfaces. The adherence of leukocytes of both normal persons and of SLE and RA patients was decreased in the presence of normal human serum compared to serum-free medium. The effects of native and heat inactivated human sera on leukocytes of SLE and RA patients were compared. Adherence of SLE leukocytes was higher, whereas that of RA leukocytes was lower in unheated serum compared to heat inactivated human serum. Supernatants of leukocytes of SLE, RA patients and control subjects were harvested after incubation in serum-free medium. The C3 levels of supernatants were determined by rocket electrophoresis. Surface attached C3 was detected with immunofluorescence mainly on SLE leukocytes. The cellular effects of supernatants on control leukocytes, were consistent with the changes observed with leukocytes derived from SLE, RA or control patients.

Arthritis, Rheumatoid↗

PubMedDate not supplied

Signal transduction in T lymphocytes of SLE patients: lectin-activated phosphorylation on tyrosine.

A comparative study of signal transduction through tyrosine phosphorylation process in peripheral blood lymphocytes from SLE patients and healthy subjects reveal some modifications in the phosphorylation pattern of SLE T lymphocytes. Thus, the level of constitutive tyrosine phosphorylation in resting SLE T lymphocytes is higher than in lymphocytes from healthy subjects. In SLE T lymphocytes, a cellular proteic substrate with an apparent molecular weight of about 37 kDa is constitutively phosphorylated. Some differences in the pattern of phosphorylation are obvious in lectin (Con A, PHA)-activated T lymphocytes. Thus, Con A activation enhances the phosphorylation of cellular substrates with molecular weight in the range of 55-80 kDa from SLE T lymphocytes. Moreover, the 21 kDa substrate is also hyperphosphorylated after PHA activation of SLE lymphocytes.

Autoimmune Diseases↗

PubMed1994

[Clinical significance of anti-cardiolipin antibody in patients with systemic lupus erythematosus (SLE)].

Anti-cardiolipin antibody (aCL) in SLE patients reacts with cardiolipin/beta 2-GP1 complex. In order to disclose clinical significance of aCL in patients with SLE, aCL was determined by newly-developed anti-CL.beta 2-GP1 kit [Yamasa] EIA in 58 patients with SLE and the relationship between clinical manifestation of SLE and the presence of aCL was examined. Anti-cardiolipin antibody was positive in 20 patients (34.5%). In 20 SLE patients with positive aCL, livedo reticularis in 7, retinal vein thrombosis in 3, thrombophlebitis in 3 and other vasculo-occlusive episodes were observed as a characteristic clinical features of positive aCL. In contrast, a SLE patient complicated by ileal perforation due to necrotizing angiitis had negative aCL. Other clinical and laboratory features associated with aCL include recurrent fetal loss and thrombocytopenia.

Adolescent↗

PubMed1993

Increased proportion of responders to a murine anti-CD3 monoclonal antibody of the IgG1 class in patients with systemic lupus erythematosus (SLE).

A group of Venezuelan patients with SLE showed an increased proportion of responders to Leu-4, an anti-CD3 MoAb of the IgG1 class, compared with ethnically matched non-SLE patients and healthy controls. The rate of proliferative responses or IL-2 production induced by MoAb Leu-4, and the helper effect of macrophages from Leu-4 responders on T cells from a third-party donor were comparable in patients and controls. No significant differences in the binding of murine IgG1 molecules by macrophages from SLE patients and controls were observed. The proportion of monocytes/macrophages expressing Fc gamma RI was significantly higher in SLE patients. However, the expression of FcRII, the type capable of supporting Leu-4-mediated responses, and of Fc gamma RIII was comparable in monocytes from SLE patients and controls. Our results suggest that Venezuelan patients with SLE may have a genetic predisposition for the expression of the phenotypic variant of Fc gamma RII capable of binding murine IgG1 molecules.

Adolescent↗

PubMedDate not supplied

Superantigens and experimental SLE induced by idiotypic dysregulation.

OBJECTIVE: The effects of the superantigens (SAgs) Staphylococcal Enterotoxin B (SEB), Toxic Shock Syndrome Toxin-1 (TSST-1) and Mycoplasma Arthritidis Mitogen (MAM) were examined on the induction and on the course of experimental SLE-like disease. METHODS: Immunization of BALB/c mice with human anti-DNA mAb (MIV-7) carrying the pathogenic idiotype 16/6 emulsified in complete Freund's adjuvant (CFA), followed by a boost of MIV-7/PBS 3 weeks later, generated an experimental SLE via an idiotypic dysregulation. RESULTS: After immunization with MIV-7/SAg, replacing the MIV-7 boost by SAg, and then injecting SAg 7 weeks after the regular induction of the SLE-like disease, the mice failed to produce anti-hIgM and dsDNA Ab up to 6 months after the induction. The mice immunized with MIV-7/CFA and boosted with the SAg had high titers of anti-hIgM but no detectable anti-dsDNA Ab. In both experimental groups low titers of anti-CL Abs developed in 25/40 (62%) and 30/38 (79%) of the mice respectively, including the control mice immunized with non-pathogenic human IgM/SAg or PBS/SAg. The mice immunized according to the "classical" protocol showed increased titers of anti-dsDNA Ab (22%) and anti-CL Ab (28%) during 10 weeks of observation. In contrast SEB, TSST-1 and MAM induced a 29%, 1% and 17% reduction in the anti-DNA titers and a 32%, 15% and 12% reduction in the anti-CL titers, respectively. CONCLUSIONS: These data suggest that the SAg tested here cannot replace the effect of CFA in the induction of the primary humoral response. The SAgs TSST-1, SEB and MAM did not induce the SLE-like disease following idiotypic modulation. Moreover, they may have had a suppressive effect on the idiotypic network in our model. The appearance of anti-CL Abs in almost all the experimental groups including the naive mice supports the possibility that microbial SAgs can induce the production of autoantibodies by different mechanisms. The SAgs TSST-1, SEB and MAM reduced autoantibody production in the serologically established idiotypic-induced experimental SLE-like murine model. This beneficial effect may indicate new directions for research on the management of SLE.

Animals↗

PubMed1997

Association of interleukin 6 release from endothelial cells and pulmonary hypertension in SLE.

OBJECTIVE: To investigate how sera from 37 patients with systemic lupus erythematosus (SLE) stimulate interleukin (IL) 6 release from IL-1beta pretreated endothelial cells and compare these effects to those of sera from 16 normal controls. METHODS: Endothelial cells pretreated 18 h with IL-1beta (5 U/ml) were incubated 2 h with sera diluted 10-fold with phosphate buffered saline (PBS). IL-6 concentrations in endothelial culture supernatants collected after incubation were measured by ELISA. RESULTS: Compared with PBS, sera from controls and 24 patients with SLE suppressed IL-6 release from IL-1beta pretreated cells. However, sera from 13 patients with SLE augmented IL-6 release. Of note, sera from 5 patients with pulmonary hypertension induced the highest level of IL-6 release. IgG from control sera suppressed IL-6 release, whereas F(ab')2 did not. Both IgG and F(ab')2 from the sera of patients with SLE with pulmonary hypertension augmented IL-6 release from IL-1beta pretreated cells. CONCLUSION: IgG antiendothelial cell antibodies from patients with SLE may be associated with the pathogenesis of SLE and pulmonary hypertension.

Adolescent↗

PubMedDate not supplied

Persistent expression of a soluble form of Fas/APO1 in continuously activated T cells from a patient with SLE.

OBJECTIVE: To report a patient with SLE whose T cells expressed disproportionally increased amounts of an alternatively spliced form of Fas/APO1 transcript and secreted a soluble form of Fas. METHODS: We established continuously activated, short-term T cell lines from 16 patients with SLE and from 6 normal controls. The structure, expression and function of Fas was examined using RT-PCR and sequencing, flow cytometry (surface expression of Fas), ELISA (measurement of soluble Fas) and a PI-based cytotoxicity assay (functional analysis). RESULTS: A soluble form of Fas which originates from an alternatively spliced transcript and lacks the transmembrane domain of the original molecule was the dominant product of the Fas-gene in one line (S18B) derived from a patient with very active SLE. Compared to a control line, the S18B cells displayed decreased surface Fas expression but increased accumulation of Fas inside the cell. The amount of soluble Fas in the culture supernatant of S18B was found to be 1.8 times higher than that of a control line. Culture supernatants from S18B cells inhibited anti-Fas mAb-medicated T cell death. CONCLUSION: Continuously activated T cells from one patient with SLE displayed increased amounts of soluble Fas that inhibits anti-Fas mediated cell death. Although the frequency of this abnormality among patients with SLE and other diseases is unknown, increased production of soluble Fas may have contributed to the pathogenesis of SLE in the patient presented here.

Adolescent↗

PubMedDate not supplied

Anti-neutrophil cytoplasmic antibodies in 566 European patients with systemic lupus erythematosus: prevalence, clinical associations and correlation with other autoantibodies. European Concerted Action on the Immunogenetics of SLE.

OBJECTIVES: To evaluate, in a cohort of 566 patients with systemic lupus erythematosus (SLE) drawn from 11 European centres: (i) the prevalence of ANCAs and their subspecificities in a large series of European SLE patients; (ii) the possible associations of ANCA with the most common clinical manifestations of the disease; and (iii) whether ANCAs correlate with some of the autoantibodies commonly found in SLE. METHODS: ANCA detection was performed by indirect immunofluorescence (IIF), and by ELISA for lactoferrin (LF), myeloperoxydase (MPO), proteinase3 (PR3) and lysozyme (LZ) subspecificities. RESULTS: The prevalence of ANCA was 16.4% (IIF). The prevalence of LF was 14.3%, LZ 4.6%, MPO 9.3%, and PR3 1.7%. Our results show that ANCA is associated with certain clinical manifestations of SLE. In particular, positive correlations were found between IIF ANCA and serositis (p = 0.026), livedo reticularis (p = 0.01), venous thrombosis (p = 0.03) and arthritis (p = 0.04), while anti-LF antibodies were associated with serositis (p = 0.05) and livedo reticularis (p < 10(-3). Nevertheless, multivariate analysis demonstrated that other autoantibodies, such as aCL and SSA/Ro, are more closely correlated than ANCA with some of the aforementioned clinical features. CONCLUSION: Our results demonstrate that ANCA are detectable in SLE sera and that some of them are associated with particular clinical manifestations. Whether ANCA plays a direct pathogenetic role in the vascular damage of SLE or only represents an epiphenomenon or a marker of disease activity remains to be elucidated.

Adolescent↗

PubMed1993

13-cis-retinoic acid affects oxidation and DNA damage in oxidative-positive SLE lymphocytes but may not be useful for therapy.

13-cis-Retinoic acid (13-CRA), a water-soluble vitamin A analog and 5'-lipoxygenase inhibitor, was tested in vitro for effects on excess oxidative metabolism and DNA damage in mitogen-stimulated lymphocytes from patients with systemic lupus erythematosus (SLE), because other 5'-lipoxygenase enzyme inhibitors were shown to lower the excess oxidative metabolism in SLE cells. Excess chemiluminescence (CL) was abolished within minutes after the addition of 1 x 10(-6) M 13-CRA in five of five CL-positive mitogen-stimulated SLE lymphocytes, and was lowered in five of eight samples after 48 to 72 h culture. Similarly, low concentrations of 13-CRA for 48-72 h largely prevented the S1 nuclease-sensitive DNA changes/DNA damage observed in CL-positive lupus lymphocytes in vitro. However, 13-CRA did not affect DNA damage in four of four CL-negative lymphocyte samples. 13-CRA, like other retinoic acid compounds, was known to stimulate B-cell activities in vivo and in vitro but effects on dividing lupus T cells had not been studied. 13-CRA further inhibited the diminished PHA-stimulated lupus T-cell growth in tissue culture at a concentration of 9 x 10(-6) M in three of five lupus lymphocyte samples. 13-CRA has positive and negative effects on multiple aspects of the immune system and it is not clear whether 13-CRA will have positive or adverse clinical effects on SLE patients. Close attention to vitamin A and vitamin "supplements" in patients with SLE may answer this question.

Cells, Cultured↗