RESUMO
OBJECTIVE: To evaluate whether the presence of glomerulonephritis is or is not associated with the extent of arterial wall inflammatory cell infiltrate in Takayasu arthritis (TA). METHODS: Retrospective chart and pathology review of large artery and kidney specimens of TA autopsy cases. Kidney specimens were classified, according to their histopathological findings, in those with specific glomerular entities and those with non-specific, ischemic and/or hypertensive, glomerular changes. A control group of autopsy kidney specimens was utilized for comparison. Morphometric analysis was used to assess the extent of the arterial inflammatory infiltrates; results were compared among the different groups with kidney lesions. RESULTS: We included 25 kidney specimens from 25 autopsies. Specific glomerular entities were present in 14 specimens; 10 (40%) were classified as diffuse mesangial proliferative glomerulonephritis (DMPG [Group A]), and 4 (16%) as other associated glomerulopathies (Group B). Non-specific changes were observed in 11 (44%) specimens (Group C). The arterial inflammatory infiltrate proportion was 9.4 % for group A, 1.4% for group B, and 2.7% for group C. Furthermore, a larger proportion of vascular inflammation was confirmed for group A when compared with the other groups (p<0.05). Group A patients were younger than those in groups B and C (p<0.005) and exhibited shorter disease duration. CONCLUSION: The presence of DMPG was associated with a larger extent of vascular inflammatory cell infiltrate, suggesting a relationship between both phenomena.
Assuntos
Glomerulonefrite Membranoproliferativa/patologia , Glomérulos Renais/patologia , Arterite de Takayasu/patologia , Adolescente , Adulto , Causas de Morte , Criança , Comorbidade , Feminino , Glomerulonefrite Membranoproliferativa/epidemiologia , Humanos , Masculino , México/epidemiologia , Pessoa de Meia-Idade , Estudos Retrospectivos , Arterite de Takayasu/epidemiologiaRESUMO
Little is known about the immune system of patients with systemic lupus erythematosus (SLE) during periods of silent disease. To address this issue we analysed lymphoid populations andcytokine production of mononuclear cells obtained from SLE patients in remission. We studied 43 patients with inactive disease, 10 with active disease and 30 controls. Remission was defined as at least 1 year during which lack of clinical disease activity permitted withdrawal of all treatment. Remission length ranged from 1 to 30 years. Flow cytometry and ELISA were used to study lymphoid populations (CD4, CD8 and CD19) and cytokine production (IL-2, 4, 10, 12 and 18). Patients with short remission periods (up to 15 years) exhibited an increased percentage of B cells; production of IL-2, IL-10 and IL-12 was decreased; production of IL-18 was increased. Interestingly, patients from groups with long time of inactive disease had corrected most alterations, but had an impaired IL-18 expression. IL-12 production correlated strongly with the length of the remission period (r = 0.7565). The immune system of patients with inactive lupus has partially corrected the disturbances present during disease activity. This is accomplished gradually, sometimes until counter-regulatory alterations are developed. This may allow patients to remain without disease activity.
Assuntos
Citocinas/imunologia , Leucócitos Mononucleares/imunologia , Lúpus Eritematoso Sistêmico/imunologia , Adolescente , Adulto , Idoso , Ensaio de Imunoadsorção Enzimática , Feminino , Citometria de Fluxo , Humanos , Subpopulações de Linfócitos , Masculino , Pessoa de Meia-Idade , Remissão EspontâneaRESUMO
Accumulating evidence has implicated T cells in the pathogenesis of systemic lupus erythematosus (SLE). The CD69 antigen is an integral membrane protein rapidly induced on the surface of activated lymphocytes. We obtained CD4+ and CD8+ T cells from normal subjects and patients with SLE. The percentage of CD69 expression in freshly isolated cells and after in-vitro incubation with mitogens was quantified by three-colour immunofluorescent staining. Expression of this protein was increased in both CD4+ and CD8+ T-cell subsets from SLE patients when compared with normal cells, although the difference was significant only in the CD8+ T-cell subset (P = 0.05). Cellular activation increased CD69 expression. When stimulated with anti-CD2/CD2R or phytohaemagglutinin (PHA), the percentage and absolute numbers of CD69+ cells were lower in patients than in controls. Addition of anti-interleukin (IL)-10 monoclonal antibody (MoAb) increased the percentage of in-vitro CD69 expression in SLE cells. These results suggest that the peripheral blood lymphocytes from patients with SLE have an intrinsic defect that alters their activation process, including the expression of CD69, and might explain some of the T immunoregulatory abnormalities observed in these patients.