The impact of teach-back training method (TBTM) on treatment adherence in hemodialysis patients: a randomized controlled trial.

Introduction: Ensuring adherence to treatment is vital for individuals undergoing haemodialysis. The demanding treatment frequency and duration often present challenges for patients in maintaining a consistent routine. Non-adherence can result in adverse health effects and an increased risk of hospitalization. This study aimed to evaluate the impact of teach-back training on treatment adherence among haemodialysis patients. Method: A randomized controlled trial involved 60 end-stage kidney disease patients undergoing haemodialysis. Participants were randomly assigned to either the control or intervention group. Data were collected using the End-Stage Renal Disease Adherence Questionnaire (ESRD-AQ), assessing adherence in four dimensions: HD incidence, medication use, fluid restriction, and diet recommendations. The intervention group received feedback-based training on diet and fluid restriction during four 45-60-min sessions, while the control group received regular indoor training. Result: Following the intervention, significant differences in mean scores for HD frequency, medication use, and fluid restriction were observed between the two groups (P<0.001). However, there was no significant difference in the mean score for food recommendations (P=0.108). Conclusion: The teach-back training method (TBTM) is an effective communication strategy that enhances treatment adherence in haemodialysis patients. This intervention has the potential to improve patient outcomes and overall quality of life by simplifying medical information and encouraging patient engagement.

Association of insulin resistance with polycystic ovary syndrome phenotypes and patients' characteristics: a cross-sectional study in Iran.

BACKGROUND: Polycystic ovary syndrome (PCOS) is the most common endocrine disorder in women. This disorder affects 6-15% of women of childbearing age worldwide. It is diagnosed with hyperandrogenism, polycystic ovaries, and chronic anovulation with insulin resistance. This study aimed to assess the prevalence of insulin resistance (IR) in 4 phenotypes of PCOS, and its relationship with demographic, clinical, and paraclinical individual characteristics in a sample of Iranian PCOS patients. METHODS: This particular cross-sectional investigation involved 160 female participants, aged between 18 and 45 years, who were receiving care at gynecology clinics in Urmia, northwestern Iran. All the participants had been diagnosed with PCOS and were categorized into one of four phenotypes. All the participants underwent clinical evaluations, paraclinical assessments, and ultrasound scans. IR was defined as HOMA-IR > 2.5. The statistical significance level was 0.05. RESULTS: Among the 160 participants, the prevalences of the 4 phenotypes were: A: 83 (51.9%), B: 37 (23.1%), C: 21 (13.1%), and D: 19 (11.9%). IR was detected in 119 participants (74.4%); its rate was significantly different between the 4 phenotypes (p-value: 0.008) as A: 62 (74.7%), B: 34 (91.9%), C: 12 (57.1%), D: 11 (57.9%). Linear and logistic regression analyses were performed to control confounding factors. In linear regression, PCOS phenotype, classic phenotype (A&B), economic status, and Hb levels were significantly related to HOMA-IR; in logistic regression Hb levels, exercise, economic status, and PCOS phenotypes were significantly associated with insulin resistance. CONCLUSIONS: The most prevalent PCOS phenotype in this study was A. PCOS phenotypes were significantly related to insulin resistance and HOMA-IR, with the highest levels of insulin resistance and HOMA-IR observed in phenotype B. Determining the phenotype of PCOS may be helpful for better management of PCOS and its associated complications. However, further investigations are recommended in this regard.

The Effect of Couple's Motivational Interviewing on Exposure to Secondhand Smoke Among Pregnant Women at Home.

Objective: Secondhand smoke (SHS) during pregnancy is associated with many maternal-fetal complications. Iran has a high male smoking prevalence rate. This study aimed to determine the effect of motivational interviewing with couples on exposure to SHS at home in pregnant women referring to health centers in Urmia in 2019. Materials and methods : A randomized control trial was performed on 112 non-smoking pregnant women with smoking husbands, randomly allocated into two groups (each with 56 members). The participants were asked to specify the daily average times and duration of exposure during the last week. Five motivational interviewing sessions were held for the members of the intervention group. Each session lasted90 minutes and two sessions were held per week. The data were collected before and four weeks after the intervention. The data were analyzed using the repeated-measures analysis of variance (ANOVA) by SPSS-20 at a significance level of 0.05. Results: Of 112 couples who were randomized, 102 (91.07%) completed the trial. There was a significant reduction in terms of the daily frequency and duration of SHS exposure of the husband one week and one month after the intervention in the intervention group. The daily frequency and duration of SHS exposure of people other than the spouse at home did not decrease over time. Conclusion: Following the results of the study, the couple-based motivational interviewing approach can be used to reduce SHS exposure in women at home.

GATA1 controls numbers of hematopoietic progenitors and their response to autoimmune neuroinflammation.

GATA-binding factor 1 (GATA1) is a transcription factor that governs the development and function of multiple hematopoietic cell lineages. GATA1 is expressed in hematopoietic stem and progenitor cells (HSPCs) and is essential for erythroid lineage commitment; however, whether it plays a role in hematopoietic stem cell (HSC) biology and the development of myeloid cells, and what that role might be, remains unclear. We initially set out to test the role of eosinophils in experimental autoimmune encephalomyelitis (EAE), a model of central nervous system autoimmunity, using mice lacking a double GATA-site (ΔdblGATA), which lacks eosinophils due to the deletion of the dblGATA enhancer to Gata1, which alters its expression. ΔdblGATA mice were resistant to EAE, but not because of a lack of eosinophils, suggesting that these mice have an additional defect. ΔdblGATA mice with EAE had fewer inflammatory myeloid cells than the control mice, suggesting that resistance to EAE is caused by a defect in myeloid cells. Naïve ΔdblGATA mice also showed reduced frequency of CD11b+ myeloid cells in the blood, indicating a defect in myeloid cell production. Examination of HSPCs revealed fewer HSCs and myeloid cell progenitors in the ΔdblGATA bone marrow (BM), and competitive BM chimera experiments showed a reduced capacity of the ΔdblGATA BM to reconstitute immune cells, suggesting that reduced numbers of ΔdblGATA HSPCs cause a functional deficit during inflammation. Taken together, our data show that GATA1 regulates the number of HSPCs and that reduced GATA1 expression due to dblGATA deletion results in a diminished immune response following the inflammatory challenge.

Transcription Factor RUNX3 Mediates Plasticity of ThGM Cells Toward Th1 Phenotype.

GM-CSF-producing T helper (Th) cells play a crucial role in the pathogenesis of autoimmune diseases such as multiple sclerosis (MS). Recent studies have identified a distinct population of GM-CSF-producing Th cells, named ThGM cells, that also express cytokines TNF, IL-2, and IL-3, but lack expression of master transcription factors (TF) and signature cytokines of commonly recognized Th cell lineages. ThGM cells are highly encephalitogenic in a mouse model of MS, experimental autoimmune encephalomyelitis (EAE). Similar to Th17 cells, in response to IL-12, ThGM cells upregulate expression of T-bet and IFN-γ and switch their phenotype to Th1. Here we show that in addition to T-bet, TF RUNX3 also contributes to the Th1 switch of ThGM cells. T-bet-deficient ThGM cells in the CNS of mice with EAE had low expression of RUNX3, and knockdown of RUNX3 expression in ThGM cells abrogated the Th1-inducing effect of IL-12. Comparison of ThGM and Th1 cell transcriptomes showed that ThGM cells expressed a set of TFs known to inhibit the development of other Th lineages. Lack of expression of lineage-specific cytokines and TFs by ThGM cells, together with expression of TFs that inhibit the development of other Th lineages, suggests that ThGM cells are a non-polarized subset of Th cells with lineage characteristics.

Comparing Geant4 physics models for proton-induced dose deposition and radiolysis enhancement from a gold nanoparticle.

Gold nanoparticles (GNPs) are materials that make the tumor cells more radiosensitive when irradiated with ionizing radiation. The present study aimed to evaluate the impact of different physical interaction models on the dose calculations and radiochemical results around the GNP. By applying the Geant4 Monte Carlo (MC) toolkit, a single 50-nm GNP was simulated, which was immersed in a water phantom and irradiated with 5, 50, and 150 MeV proton beams. The present work assessed various parameters including the secondary electron spectra, secondary photon spectra, radial dose distribution (RDD), dose enhancement factor (DEF), and radiochemical yields around the GNP. The results with an acceptable statistical uncertainty of less than 1% indicated that low-energy electrons deriving from the ionization process formed a significant part of the total number of secondary particles generated in the presence of GNP; the Penelope model produced a larger number of these electrons by a factor of about 30%. Discrepancies of the secondary electron spectrum between Livermore and Penelope were more obvious at energies of less than 1 keV and reached the factor of about 30% at energies between 250 eV and 1 keV. The RDDs for Livermore and Penelope models were very similar with small variations within the first 6 nm from NP surface by a factor of 10%. In addition, neither the G-value nor the REF was affected by the choice of physical interaction models with the same energy cut-off. This work illustrated the similarity of the Livermore and Penelope models (within 15%) available in Geant4 for future simulation studies of GNP enhanced proton therapy with physical, physicochemical, and chemical mechanisms.

Efficacy of triamcinolone acetonide-impregnated Gelfoam nasal pack in management of chronic sinusitis with nasal polyps following endoscopic sinus surgery: a perfectly matched, placebo-controlled trial study.

PURPOSE: This perfectly matched, double-blinded, placebo-controlled trial study was performed to investigate the efficacy of triamcinolone acetonide (TAA)-impregnated Gelfoam nasal pack in management of different endotypes of chronic rhinosinusitis with nasal polyps (CRSwNP) following endoscopic sinus surgery (ESS). METHODS: One hundred and four patients with bilateral CRSwNP undergoing ESS were selected and randomized to receive TAA-soaked nasal packing in one nostril and saline-impregnated dressing contra-laterally. Validated Perioperative Sinus Endoscopy (POSE) scoring system was used to assess the participants' condition at postoperative months 1, 3, 6, 12, and 18. RESULTS: The treatment side of eosinophilic CRSwNP (EosCRSwNP) group had significantly better endoscopic scores than the contralateral control side in all follow-up visits (P < 0.05 for all comparisons) except for the first postoperative month. No significant difference was detected between the TAA- and saline-treated nostrils in the non-eosinophilic CRSwNP (nonEosCRSwNP) subgroup during the follow-up period. Intergroup comparisons revealed a borderline better POSE score for the treatment side of the EosCRSwNP group compared with the treatment nostril of the nonEosCRSwNP group at months 12 (P = 0.041) and 18 (P = 0.044). At the end of the study period, the treatment side of the EosCRSwNP group demonstrated better clinical response than the saline-treated side in terms of the total POSE scores (P = 0.019), middle turbinate synechia (P = 0.008), middle meatal narrowing (P = 0.010), ethmoid polypoid changes (P = 0.039), ethmoid polyposis (P = 0.027), ethmoid cavity secretions (P = 0.042), and sphenoid severity (P = 0.018). CONCLUSION: TAA-soaked Gelfoam dressing following bilateral ESS was found to be an effective method for treating CRSwNP particularly for the eosinophilic endotype of the disease.

IFN-ß Acts on Monocytes to Ameliorate CNS Autoimmunity by Inhibiting Proinflammatory Cross-Talk Between Monocytes and Th Cells.

IFN-ß has been the treatment for multiple sclerosis (MS) for almost three decades, but understanding the mechanisms underlying its beneficial effects remains incomplete. We have shown that MS patients have increased numbers of GM-CSF+ Th cells in circulation, and that IFN-ß therapy reduces their numbers. GM-CSF expression by myelin-specific Th cells is essential for the development of experimental autoimmune encephalomyelitis (EAE), an animal model of MS. These findings suggested that IFN-ß therapy may function via suppression of GM-CSF production by Th cells. In the current study, we elucidated a feedback loop between monocytes and Th cells that amplifies autoimmune neuroinflammation, and found that IFN-ß therapy ameliorates central nervous system (CNS) autoimmunity by inhibiting this proinflammatory loop. IFN-ß suppressed GM-CSF production in Th cells indirectly by acting on monocytes, and IFN-ß signaling in monocytes was required for EAE suppression. IFN-ß increased IL-10 expression by monocytes, and IL-10 was required for the suppressive effects of IFN-ß. IFN-ß treatment suppressed IL-1ß expression by monocytes in the CNS of mice with EAE. GM-CSF from Th cells induced IL-1ß production by monocytes, and, in a positive feedback loop, IL-1ß augmented GM-CSF production by Th cells. In addition to GM-CSF, TNF and FASL expression by Th cells was also necessary for IL-1ß production by monocyte. IFN-ß inhibited GM-CSF, TNF, and FASL expression by Th cells to suppress IL-1ß secretion by monocytes. Overall, our study describes a positive feedback loop involving several Th cell- and monocyte-derived molecules, and IFN-ß actions on monocytes disrupting this proinflammatory loop.

The Effect of Peer Education on Management of Chemotherapy Side Effects in Patients with Cancer.

BACKGROUND: Chemotherapy drugs may have numerous side effects for patients. Thus, this study was conducted with the aim to determine the effect of peer education on the management of chemotherapy side effects in patients with cancer. MATERIALS AND METHODS: This randomized, controlled trial was conducted on 80 patients with cancer in 2018. They were allocated to two groups of intervention and control. The self-care education on chemotherapy side effects was provided by the peers to the individuals in the intervention group. The data collection tools included a demographic characteristics form and the Self-Care Diary (SCD). Data analysis was performed using independent t-test and Chi-square test in SPSS software. RESULTS: The results showed that the mean scores of the effectiveness of self-care behaviors were significantly higher in the intervention group compared to the control group after the intervention (p < 0.05). CONCLUSIONS: Peer education is recommended for cancer patients undergoing chemotherapy.

CRISPR-mediated rapid generation of neural cell-specific knockout mice facilitates research in neurophysiology and pathology.

Inducible conditional knockout mice are important tools for studying gene function and disease therapy, but their generation is costly and time-consuming. We introduced clustered regularly interspaced short palindromic repeats (CRISPR) and Cre into an LSL-Cas9 transgene-carrying mouse line by using adeno-associated virus (AAV)-PHP.eB to rapidly knockout gene(s) specifically in central nervous system (CNS) cells of adult mice. NeuN in neurons and GFAP in astrocytes were knocked out 2 weeks after an intravenous injection of vector, with an efficiency comparable to that of inducible Cre-loxP conditional knockout. For functional testing, we generated astrocyte-specific Act1 knockout mice, which exhibited a phenotype similar to mice with Cre-loxP-mediated Act1 knockout, in an animal model of multiple sclerosis (MS), an autoimmune disorder of the CNS. With this novel technique, neural cell-specific knockout can be induced rapidly (few weeks) and cost-effectively. Our study provides a new approach to building inducible conditional knockout mice, which would greatly facilitate research on CNS biology and disease.

The effects of nanocurcumin supplementation on inflammation in hemodialysis patients: A randomized controlled trial.

INTRODUCTION: Serum levels of several pro-inflammatory cytokines are higher in hemodialysis patients compared to healthy people. Curcumin has been shown to be able to decrease cytokines levels in nonuremic subjects. Our goal was to evaluate the effect of nanocurcumin administration on cytokines levels in hemodialysis patients. METHODS: The study was performed over a 3 months period on 54 hemodialysis patients who had been randomized to receive either nanocurcumin or placebo. Serum levels and gene expressions of tumor necrosis factor-alpha (TNF-α) and interleukin 6 (IL-6) were evaluated using enzyme-linked immunosorbent assay (ELISA) and real-time polymerase chain reaction (RT-PCR). FINDINGS: Serum levels of IL-6 and TNF-α were similar in the two groups at baseline but were lower after 12 weeks of treatment with nanocurcumin compared to placebo (P = 0.024 for IL-6 and 0.02 for TNF). In the group given nanocurcumin, serum levels of both cytokines decreased substantially (P < 0.001 for each), whereas they were unchanged in the group given placebo. Gene expression for each cytokine in peripheral blood mononuclear cells (PBMCs) was reduced at 12 weeks vs. baseline in the group given nanocurcumin, and changes in gene expression correlated with changes in serum level for each of the two cytokines. DISCUSSION: The results indicate that nanocurcumin supplementation reduces both serum levels and gene expression of IL-6 and TNF-α in hemodialysis patients. The feasibility and potential clinical benefits of nanocurcumin treatment to reduce inflammation in hemodialysis patients warrant further study.

Montelukast alleviates inflammation in experimental autoimmune encephalomyelitis by altering Th17 differentiation in a mouse model.

Montelukast is a leukotriene receptor antagonist that is known to prevent allergic rhinitis and asthma. Blocking the Cysteinyl leukotriene receptor (CysLTR1), one of the primary receptors of leukotrienes, has been demonstrated to be efficacious in ameliorating experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis (MS), through disrupting chemotaxis of infiltrating T cells. However, the role of CysLTR1 in the pathogenesis of MS is not well understood. Here, we show that MS patients had higher expression of CysLTR1 in the circulation and central nervous system (CNS). The majority of CD4+ T cells expressed CysLTR1 in MS lesions. Among T-cell subsets, Th17 cells had the highest expression of CysLTR1, and blocking CysLTR1 signalling abrogated their development in vitro. Inhibition of CysLTR1 by montelukast suppressed EAE development in both a prophylactic and therapeutic manner and inhibited myelin loss in EAE mice. Similarly, the in vivo results showed that montelukast inhibited Th17 response in EAE mice and that Th17 cells treated with montelukast had reduced encephalitogenic in adoptive EAE. Our findings strongly suggest that targeting Th17 response by inhibiting CysLTR1 signalling could be a promising therapeutic strategy for the treatment of MS and CNS inflammatory diseases.

Investigation of p16 protein expression and its association with histopathologic parameters in breast cancer.

We investigated the association between p16 expression and histopathologic parameters including size, neural and vascular invasion, and lymph node involvement in breast cancer. 58 specimens from patients with different grades of breast cancer were included. Hematoxylin and eosin and immunohistochemistry staining for p16 was performed. 5 patients (8.6%) had grade I, 23 (39.7%) had grade II, and 30 (51.7%) had grade III breast cancer. Assessment of the tumor size showed that 5 (8.6%) tumors had a size of ≤2cm, 29 (50%) were between 2-5 cm and 24 (41.4%) had a size of ≥5cm. Moreover, 45 (77.6%) of the included patients had axillary lymph node involvement. Investigation of association between p16 positivity with pathological parameters in three groups with positivity to p16 (1-25%, 26-75%, >75%) showed that there was no association between p16 positivity and other parameters including histologic score (p=0.44), tumor size (p=0.77), neural invasion (p=0.79), perivascular invasion (p=0.98) and the number of involved LNs (p=0.49). From the group including eight patients with >75% p16 positivity, seven (87.5%) were found with neural invasion and two (25%) with perivascular invasion. P16 positivity was not associated with size, neural and vascular invasion, and LN involvement in breast cancer.

A distinct GM-CSF+ T helper cell subset requires T-bet to adopt a TH1 phenotype and promote neuroinflammation.

Elevation of granulocyte-macrophage colony-stimulating factor (GM-CSF)­producing T helper (TH) cells has been associated with several autoimmune diseases, suggesting a potential role in the pathogenesis of autoimmunity. However, the identity of GM-CSF­producing TH cells has not been closely examined. Using single-cell RNA sequencing and high-dimensional single-cell mass cytometry, we identified eight populations of antigen-experienced CD45RA−CD4+ T cells in blood of healthy individuals including a population of GM-CSF­producing cells, known as THGM, that lacked expression of signature transcription factors and cytokines of established TH lineages. Using GM-CSF-reporter/fate reporter mice, we show that THGM cells are present in the periphery and central nervous system in a mouse model of experimental autoimmune encephalomyelitis. In addition to GM-CSF, human and mouse THGM cells also expressed IL-2, tumor necrosis factor (TNF), IL-3, and CCL20. THGM cells maintained their phenotype through several cycles of activation but up-regulated expression of T-bet and interferon-γ (IFN-γ) upon exposure to IL-12 in vitro and in the central nervous system of mice with autoimmune neuroinflammation. Although T-bet was not required for the development of THGM cells, it was essential for their encephalitogenicity. These findings demonstrate that THGM cells constitute a distinct population of TH cells with lineage characteristics that are poised to adopt a TH1 phenotype and promote neuroinflammation.

IL-9 Controls Central Nervous System Autoimmunity by Suppressing GM-CSF Production.

Multiple sclerosis and experimental autoimmune encephalomyelitis (EAE) are inflammatory diseases of the CNS in which Th17 cells play a major role in the disease pathogenesis. Th17 cells that secrete GM-CSF are pathogenic and drive inflammation of the CNS. IL-9 is a cytokine with pleiotropic functions, and it has been suggested that it controls the pathogenic inflammation mediated by Th17 cells, and IL-9R-/- mice develop more severe EAE compared with wild-type counterparts. However, the underlying mechanism by which IL-9 suppresses EAE has not been clearly defined. In this study, we investigated how IL-9 modulates EAE development. By using mice knockout for IL-9R, we show that more severe EAE in IL-9R-/- mice correlates with increased numbers of GM-CSF+ CD4+ T cells and inflammatory dendritic cells (DCs) in the CNS. Furthermore, DCs from IL-9R-/- mice induced more GM-CSF production by T cells and exacerbated EAE upon adoptive transfer than did wild-type DCs. Our results suggest that IL-9 reduces autoimmune neuroinflammation by suppressing GM-CSF production by CD4+ T cells through the modulation of DCs.

miR-23b Suppresses Leukocyte Migration and Pathogenesis of Experimental Autoimmune Encephalomyelitis by Targeting CCL7.

MicroRNAs (miRNAs) are small, non-coding RNAs involved in immune response regulation. Specific miRNAs have been linked to the development of various autoimmune diseases; however, their contribution to the modulation of CNS-directed cellular infiltration remains unclear. In this study, we found that miR-23b, in addition to its reported functions in the suppression of IL-17-associated autoimmune inflammation, halted the progression of experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis (MS), by directly inhibiting the migration of pathogenic leukocytes to the CNS. We demonstrated that miR-23b was specifically decreased during the acute phase of EAE and that overexpression of miR-23b resulted in a defect in leukocyte migration and strong resistance to EAE. Furthermore, we found that miR-23b suppressed leukocyte migration of EAE by targeting CCL7, a chemokine that attracts monocytes during inflammation and metastasis. Finally, in the adoptive transfer model, miR-23b reduced the severity of EAE by inhibiting the migration of pathogenic T cells to the CNS rather than diminishing the encephalitogenesis of T cells. Taken together, our results characterize a novel aspect of miR-23b function in leukocyte migration, and they identify miR-23b as a potential therapeutic target in the amelioration of MS and likely other autoimmune diseases.

Factors associated with extubation time in coronary artery bypass grafting patients.

Background and Objectives. Cardiovascular diseases are the leading cause of death worldwide, with coronary artery disease being the most common. With increasing numbers of patients, Coronary Artery Bypass Grafting (CABG) has become the most common operation in the world. Respiratory disorder is one of the most prevalent complications of CABG. Thus, weaning off the mechanical ventilation and extubation are of great clinical importance for these patients. Some post-operative problems also relate to the tracheal tube and mechanical ventilation. Therefore, an increase in this leads to an increase in the number of complications, length of hospital stay, and treatment costs. Since a large number of factors affect the post-operative period, the present study aims to identify the predictors of extubation time in CABG patients using casualty network analysis. Method. This longitudinal study was conducted on 800 over 18 year old patients who had undergone CABG surgery in three treatment centers affiliated to Shiraz University of Medical Sciences. The patients' information, including pre-operative, peri-operative, and post-operative variables, was retrospectively extracted from their medical records. Then, the data was comprehensively analyzed through path analysis using MPLUS-7.1 software. Results. The mean of extubation time was 10.27 + 4.39 h. Moreover, extubation time was significantly affected by packed cells during the Cardiopulmonary Bypass (CPB), packed cells after CPB, inotrope use on arrival at ICU, mean arterial pressure 1st ICU, packed cells 1st ICU, platelets 1st ICU, Blood Urea Nitrogen 1st ICU, and hematocrit 1st ICU. Conclusion. Considering all of the factors under investigation, some peri-operative and post-operative factors had significant effects. Therefore, considering the post-operative factors is important for designing a treatment plan and evaluating patients' prognosis.

Expression of GM-CSF in T Cells Is Increased in Multiple Sclerosis and Suppressed by IFN-ß Therapy.

Multiple sclerosis (MS) is an autoimmune disease of the CNS. Studies in animal models of MS have shown that GM-CSF produced by T cells is necessary for the development of autoimmune CNS inflammation. This suggests that GM-CSF may have a pathogenic role in MS as well, and a clinical trial testing its blockade is ongoing. However, there have been few reports on GM-CSF production by T cells in MS. The objective of this study was to characterize GM-CSF production by T cells of MS patients and to determine the effect of IFN-ß therapy on its production. GM-CSF production by peripheral blood (PB) T cells and the effects of IFN-ß were characterized in samples of untreated and IFN-ß-treated MS patients versus healthy subjects. GM-CSF production by T cells in MS brain lesions was analyzed by immunofluorescence. Untreated MS patients had significantly greater numbers of GM-CSF(+)CD4(+) and CD8(+) T cells in PB compared with healthy controls and IFN-ß-treated MS patients. IFN-ß significantly suppressed GM-CSF production by T cells in vitro. A number of CD4(+) and CD8(+) T cells in MS brain lesions expressed GM-CSF. Elevated GM-CSF production by PB T cells in MS is indicative of aberrant hyperactivation of the immune system. Given its essential role in animal models, abundant GM-CSF production at the sites of CNS inflammation suggests that GM-CSF contributes to MS pathogenesis. Our findings also reveal a potential mechanism of IFN-ß therapy, namely suppression of GM-CSF production.