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Background Higher blood pressure variability (BPV) is associated with the development of major vascular diseases, independent of mean blood pressure. However, despite data indicating that serum inflammatory markers are linked to hypertension, the association between serum inflammatory markers and BPV has not been studied in humans. Methods This is a post hoc analysis of the Multi-Ethnic Study of Atherosclerosis (MESA) study. The study exposure was tertiles of serum level of interleukin-6 (IL-6), C-reactive protein (CRP), d-dimer, plasmin–antiplasmin complex (PAP), fibrinogen antigen, and calibrated Factor VIII (%) at the baseline study visit. The primary outcome was visit-to-visit BPV measured as the residual standard deviation (rSD) of at least 4 study visits (2000–2018). Two logistic regression models were fit to the top tertile of rSD during follow-up: in Model 1, we adjusted for age, sex, and hypertension, and in Model 2, for patient age categories, sex, race/ethnicity, education, hypertension, diabetes, smoking, drinking, body mass index, lipid-lowering medication, and mean systolic blood pressure. Results Our analysis included 5,483 patients, with a mean (SD) age of 61.4 (10.0) years, 52.9% female, and 40.7% White. In unadjusted analyses, all markers of inflammation were associated with higher BPV, but after adjustment, only IL-6 retained significance (P < 0.001). The odds ratio for the highest tertile of BPV and IL-6 was 1.49 (95% confidence interval [CI] 1.28–1.74, P < 0.001). Conclusions Baseline serum IL-6 was associated with increased subsequent BPV in a large multiracial cohort. Further investigation is needed to better understand the relationship between chronic inflammation and BPV. [ABSTRACT FROM AUTHOR]

Background. The survival trends and the patterns of clinical practice pertaining to radiation therapy and surgical resection for WHO grade I, II, and III astrocytoma patients remain poorly characterized. Methods. Using the Surveillance, Epidemiology and End Results (SEER) database, we identified 2497 grade I, 4113 grade II, and 2755 grade III astrocytomas during the period of 1999-2010. Time-trend analyses were performed for overall survival, radiation treatment (RT), and the extent of surgical resection (EOR). Results. While overall survival of grade I astrocytoma patients remained unchanged during the study period, we observed improved overall survival for grade II and III astrocytoma patients (Tarone-Ware P,.05). The median survival increased from 44 to 57 months and from 15 to 24 months for grade II and III astrocytoma patients, respectively. The differences in survival remained significant after adjusting for pertinent variables including age, ethnicity, marital status, sex, tumor size, tumor location, EOR, and RT status. The pattern of clinical practice in terms of EOR for grade II and III astrocytoma patients did not change significantly during this study period. However, there was decreased RT utilization as treatment for grade II astrocytoma patients after 2005. Conclusion. Results from the SEER database indicate that there were improvements in the overall survival of grade II and III astrocytoma patients over the past decade. Analysis of the clinical practice patterns identified potential opportunities for impacting the clinical course of these patients. [ABSTRACT FROM AUTHOR]

Expression of HLA class II molecules on thyrocytes is a characteristic feature of autoimmune thyroid disease and may lead the thyroid cells to present autoantigens to CD4+ T lymphocytes. Since HLA-DM is a critical molecule in class II-restricted antigen processing and presentation, we assessed the expression of HLA-DMB, -invariant chain (Ii), class II transactivator (CIITA) and DRA in an untransformed, pure thyrocyte strain HTV-59A. Here we report that both HLA-DMB mRNA and the protein are expressed in thyrocytes and that CIITA expression is enhanced by interferon-gamma (IFN-γ) treatment and occurs before DMB, Ii and DRA up-regulation, suggesting CIITA expression is a requirement for antigen processing in thyrocytes. These results indicate that thyrocytes are capable of antigen processing and possibly antigen presentation to T cells. [ABSTRACT FROM AUTHOR]

We have investigated the effects of recombinant murine interferon-gamma (rIFN-γ) on type II collagen-induced arthritis (CA) in DBA/l mice. Therapeutic as well as prophylactic treatment with subcutaneous rIFN-γ, at 105 U/mouse six times a week, inhibited the development of CA without any obvious side effects. The accompanying suppression of anti-CII antibody responses may partly explain the inhibition of CA by rIFN-γ. The possible role of the anti-inflammatory effect of systemic IFN-γ in the inhibition of CA is discussed. [ABSTRACT FROM AUTHOR]

A possible role for retinal pigment epithelial cells (RPE) as local antigen presenting cells in immune inflammatory eye disease was investigated by studying the in vitro response of human RPE cells to stimulation with purified IFN-γ or Con A induced lymphokine. RPE cells cultured with a single dose of 50-1000 u/ml IFN-γ for up to 8 days to allow maximal Class II gene transcription, expressed HLA DP, DR and DQ antigens in a dose-dependent manner with 80% or more of cells positive for each antigen at the higher concentration. After removal of a suboptimal IFN-γ stimulus, HLA-DR antigen expression persisted for at least 15 days. HLA-DP and DQ antigens persisted only after maximal IFN-γ stimulation. Lymphokine from Con A stimulated tymphocytes induced higher levels of DR and DQ expression (80%) over DP (15%) implying complex interactions with other mediators present in the lymphocyte culture supernatant. Since RPE cells phagocytose and recycle autoantigenrich retinal rod outer segments and co-express HLA DR and DQ Class II antigens in response to IFN-γ stimulation, an immunoregulatory role in conditions in which retinal autoimmunity is implicated, such as chronic idiopathic posterior uveitis and retinal vasculitis is postulated for these cells. [ABSTRACT FROM AUTHOR]

Human peripheral blood lymphocytes were co-cultured with either allogeneic, autologous or purified protein derivative of tuberculin (PPD) pulsed autologous epidermal cells. In these mixed skin cell-lymphocyte culture reactions (MSLR), lymphocytes are stimulated to proliferate by epidermal cells. The supernatants of MSLR were examined for their capacity to induce class II MHC antigen expression on separately cultured epidermal cells. It is shown that supernatants from allogeneic and PPD pulsed autologous MSLR contained the factor(s) which stimulated HLA-DR antigen synthesis and expression by 30-40% of cultured epidermal cells. Kinetic analysis revealed a production rate maximum between 72 and 96 h of lympho-epidermal co-cultures. The factor mediating the induction of HLA-DR antigen expression on epidermal cells is thought to he γ-interferon, because it was sensitive to pH 2 as well as heat incubation. Furthermore, anti-γ-interferon monoclonal antibody abolished its activity. It is proposed, that HLA-DR antigen expression by keratinocytes observed in vivo in different dermatological inflammatory disorders originates from lympho-epidermal interactions and local γ-interferon production as documented here in experiments in vitro. [ABSTRACT FROM AUTHOR]

We obtained monoclonal antibodies specific for human type II collagen and characterized them using human collagen type I, II. Ill and V and tropocollagen A (3/4) (TCA) and iropocollagen B (1/4) (TCB) fragments of type II collagen which were obtained by digestion with tadpole collagenase. These antibodies were of the IgG2a class and specific for the conformational determinant of TCA fragment of type II collagen. When injected intravenously into DBA/IJ mice, one of the monoclonal antibodies induced arthritis, which was characterized by early onset, mildness in severity and preferential localization mainly in the peripheral joints of the lower extremities. These results suggest that, a I least, one of the arthritogenic determinants of type M collagen for collagen-induced arthritis of mice exists in the three quarter region from the N-terminus of type II collagen. [ABSTRACT FROM AUTHOR]