Autoimmune Diseases最新文献

Systemic lupus erythematosus (SLE) is an autoimmune inflammatory disease in which pathogenic autoantibodies and immune complexes are formed and mediate multiple organ and tissue damage. Thrombosis is one of the most common causes of death in patients with SLE. Anticoagulant therapy blocks the vicious cycle between inflammation and thrombosis, which may greatly improve the long-term prognosis of patients with SLE. However, the etiology and pathogenesis of this disease are very complicated and have not yet been fully clarified. Therefore, in the present review, we will highlight the characteristics and mechanisms of thrombosis and focus on the anticoagulant drugs commonly used in clinical practice, thus, providing a theoretical basis for scientific and reasonable anticoagulant therapy in clinical practice.

IgG4-related disease is a multiorgan immunological fibroinflammatory disorder characterized by lymphoplasmacytic infiltration and fibrosis in multiple organs accompanied by high serum IgG4 levels. The salivary glands are the most common organs involved in this disease. Recently, chronic sclerosing sialadenitis affecting salivary glands, formerly known as Küttner's tumor, and Mikulicz's disease have been classified as a class of IgG4-related diseases. The etiopathobiology of IgG4-related disease is not fully understood. It has recently been hypothesized that the inflammatory and fibrotic process and the increased serum IgG4⁺ levels in IgG4-related disease are the result of an interaction between B cells and T helper cells, suggesting that T cells may play a key role in the pathogenesis of this disease. The aim of this review is to discuss the proposed roles of different T cell subsets in the pathogenesis of IgG4-related disease focusing on their roles in immunopathogenesis of IgG4-related sialadenitis.

Results: Thirty-six patients were included in the final study. Cyclophosphamide was used in 24 patients (66.7%) and, comparatively, rituximab in 7 patients (19.4%) for induction. Seven patients (19.4%) had a documented relapse, and six patients (85.7%) had rituximab as induction therapy for relapse. The majority of patients were on azathioprine (61.1%, 57.1% relapse population) as maintenance therapy. Progression to ESRD occurred in 11 (30.6%), death in 4 (11.1%), established CKD in 15 (41.7%), and preservation of renal function in 6 (16.7%) patients by the end of the follow-up period.

Conclusions: While cyclophosphamide remains the choice of induction immunosuppression therapy, we favour rituximab as an induction agent in the relapse of AAV. Despite aggressive immunosuppression therapy, the incidence of ESRD and death remains high in these patients.

Results: Serum14-3-3η levels were significantly higher in all RA patients than in controls (P < 0.001), its sensitivity was 86.7% and 88.3% in early and established RA patients with a significant difference with RF and ACCP at early disease, and the specificity was 96.7%. There was a significant reduction of 14-3-3η levels 6 months after treatment in the first group (p=0.004), and there was a significant positive correlation between serum 14-3-3η levels and parameters of disease activity and severity.

Conclusion: 14-3-3η could be a novel, potent, and efficacious diagnostic, and prognostic marker for RA with high sensitivity, that may become a new therapeutic target for RA.

Objectives: Acute motor axonal neuropathy (AMAN) is a disease that leads to acute flaccid paralysis and may result from the binding of antibody and antigen to the spinal cord. The objective of this study is to evaluate the protective effect of hyperbaric oxygen treatment (HBOT) on axon degeneration of the spinal cord and sciatic nerve of the AMAN model rabbit. Axonal degeneration was assessed by evaluating glutathione (GSH) activity, interleukin-1β (IL-1β) expression, and clinical and histopathological features.

Methods: Twenty-one New Zealand rabbits were divided into three groups. The treatment group was exposed to 100% oxygen at 2.4 ATA 90 minutes for 10 days at a decompression rate of 2.9 pounds per square inch/minute. GSH level was evaluated using an enzyme-linked immune-sorbent assay. An expression of IL-1β in the spinal cord was determined by immunohistochemistry. Clinical appearances were done by motor scale and body weight. Histological features observed neuronal swelling and inflammatory infiltration in the sagittal lumbar region and the undulation of the longitudinal sciatic nerve.

Results: Rabbits exposed to HBO had high GSH activity levels (p < 0.05) but unexpectedly had high IL1β expression (p > 0.05). In addition, the HBO-exposed rabbits had a better degree of undulation, the size of neuronal swelling was smaller, the number of macrophages was higher, and motor function was better than the AMAN model rabbits (p < 0.05).

Conclusions: These findings indicate that HBO therapy can decrease axon degeneration by triggering GSH activity, increasing IL-1β level, and restoring tissues and motor status. In conclusion, HBO has a protective effect on axon degeneration of the spinal cord and sciatic nerve of the AMAN model rabbit.

Background: Psoriasis is a chronic inflammatory disorder of the skin and joint, affecting nearly 2-3% of the general population. It is assumed that imbalance between the types of natural microflora can accelerate the onset of the disease. Some fungi can play the role of superantigens and prolong chronic inflammation in the skin of psoriatic patients. The aim of the present investigation was to identify fungal species isolated from patients with psoriasis.

Methods: From March 2016 to May 2019, 289 patients with prior diagnosis of psoriasis were included in this survey. Direct microscopy with potassium hydroxide (KOH 10%), culture, urea hydrolysis, hair perforation test, and growth on rice grains were used to identify clinical isolates, phenotypically. For molecular identification of Candida species and Malassezia species, PCR-RFLP and PCR-sequencing were used, respectively.

Results: Forty-six out of 289 psoriatic patients had fungal infections (15.9%). Dermatophytes (54.3%), Candida spp. (19.5%), Malassezia spp. (15.2%), Aspergillus spp. (6.5%), and Fusarium spp. (4.3%) were the causative agents of fungal infections. Among Malassezia and Candida species, M. restricta (10.8%) and C. glabrata (8.7%) were the most prevalent species, respectively.

Conclusion: Our findings suggested that fungal pathogens, particularly dermatophytes, may play an important role in the pathogenicity of psoriasis. Also, due to the high rate of yeast colonization in the clinical samples of psoriatic patients, concomitant use of anti-inflammatory drugs and antifungals may represent an effective therapeutic approach for better management of chronic lesions among these patients. Mycological tests should be applied to indicate the incidence of fungal diseases in psoriatic patients.

[This corrects the article DOI: 10.1155/2015/197893.].

Objectives: Rheumatoid arthritis affects about 1% of the world's population. This is a chronic autoimmune disease. It is predominant in females with progressive joint damage. Immune cells are involved, especially Th1/Th17 lymphocytes and their inflammatory cytokines. These proteins have different functions in the immune system, such as IL-16 is a chemotactic factor; IL-18 can activate NFκB transcription producing inflammatory proteins; IL-31 can activate the JAK/STAT pathway which leads to the production of inflammatory factors in chronic diseases; IL-33 promotes IL-16 secretion which causes lymphocyte recruitment, and IL-32 and IL-34 appear to increase TNF secretion by macrophages activation in AR. The aim of this study was to evaluate serum levels of IL-16, IL-18, IL-31, IL-32, IL-33, and IL-34 and compare them with the severity and treatment of RA patients if there are any correlations.

Methods: A total of 140 RA patients and 40 healthy donors were recruited from the Department of Rheumatology at Hospital das Clínicas from the Federal University of Pernambuco. 60 AR patients were naïve for any treatment. Serum cytokine levels were determined using an ELISA kit.

Results: Serum IL-16 (p = 0.0491), IL-18 (p < 0.0001), IL-31 (p = 0.0004), and IL-32 (p = 0.0040) levels were significantly increased in RA patients compared with healthy donors. It was observed that patients using leflunomide had the lowest IL-18 levels, close to controls levels (p = 0.0064).

Conclusion: IL-16, IL-18, IL-31, and IL-32 are increased in the serum of RA patients. IL-18 is at lower levels in those AR who are taking leflunomide as treatment.

Much public research suggests that autoimmune diseases such as rheumatoid arthritis (RA) are induced by aberrant "self" immune responses attacking autologous tissues and organ components. However, recent studies have reported that autoimmune diseases may be triggered by dysbiotic composition changes of the intestinal bacteria and an imbalance between these bacteria and intestinal immune systems. However, there are a few solid concepts or methods to study the putative involvement and relationship of these inner environmental factors in RA pathogenesis. Fortunately, Collagen-Induced Arthritis (CIA) and Collagen Antibody-Induced Arthritis (CAIA) models have been widely used as animal models for studying the pathogenesis of RA. In addition to RA, these models can be extensively used as animal models for studying complicated hypotheses in many diseases. In this review, we introduce some basic information about the CIA and CAIA models as well as how to apply these models effectively to investigate relationships between the pathogenesis of autoimmune diseases, especially RA, and the dysbiosis of intestinal bacterial flora.

Background: Pernicious anemia (PA) is an autoimmune disease (AID) which is caused by lack of vitamin B12 (cobalamin) due to its impaired uptake. PA is a multifactorial disease which is associated with a number of other AID comorbidities and which is manifested as part of autoimmune polyglandular syndrome. Due to the shortage of family studies on PA, we planned to address the problem by assessing familial risks for concordant PA between family members and for discordant PA in families of other AID patients.

Methods: We collected data on patients diagnosed with AIDs from the Swedish hospitals and family data from a population register. We calculated standardized incidence ratios (SIRs) in families for concordant and discordant risks.

Results: The number of PA patients in the offspring generation (for which the familial risk was calculated) was 7701; 278 (3.6%) patients had a family history of PA. The population prevalence of PA was 0.9/1000. The familial risk for PA was 3.88 when any first-degree relative was the proband, equal for men and women. The familial risk was two times higher between siblings than between offspring and parents which may be due to complex genetic background. Associations of PA with 14 discordant AIDs were significant; these included some AIDs that have previously been described as comorbidities in PA patients and several yet unreported associations, including rheumatoid arthritis and other AIDs.

Conclusions: The familial risks for PA were high suggesting multifactorial genetic etiology. The results call for further population-level studies to unravel mechanisms of familial PA which may help to understand the etiology of this disease.