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The role of cytokines in systemic lupus erythematosis: review article
Shideh Namazi , Vahid Ziaee , Nima Rezaei ,
Volume 73, Issue 6 (9-2015)
Abstract
Systemic lupus erythematosus (SLE) is a chronic autoimmune disease, involves almost all organs such as skin, heart, kidneys and central nervous system. The disease is characterized by vascular and connective tissue inflammation in a recurring pattern of remission and flare. Although the exact pathophysiology of disease has not been fully understood yet, the fundamental defect in SLE is attributed to dysfunction of T lymphocytes in controlling of B-cell that leads to polyclonal activation of B lymphocytes and production a large quantity of autoantibodies against nuclear and cytoplasmic components. These autoantibodies can damage tissues either directly or as a result of immune complex deposits. Several factors are involved in pathogenesis of SLE which can be divided into three major groups, environmental factors, genetic components, and immunological disturbances. They could breakdown body tolerance towards endogenous antigens and cause abnormal immunologic response to the healthy tissue, resulting in tissue damage. SLE occurs more frequently in female than male. It seems that immunological factors have important role in SLE. Inflammation and vascular endothelium irregularities are a number of main pathologies seen in SLE. Cytokines are protein mediators that play an essential role as regulator of innate and adaptive immune response against microbial agents or self-antigens. Influences of cytokines in autoimmune diseases such as SLE are poorly understood. Studies in both experimental animal models of lupus and patients with SLE have revealed a number of cytokine pathways that are important in the disease process. These studies showed that overexpression of inflammatory cytokines increases the proliferation of auto reactive B-cells and results in higher production of autoantibodies. Among them, the role of B-cell activating factor (BAFF), a proliferation-inducing ligand (APRIL), TNF-α, IFN-α, IL-6, IFN-γ, IL-23/IL-17, IL-10, IL-21 are prominent, which is associated with the generation of pathogenic autoantibodies and formation of immune complexes. In this paper, the role of cytokines and their encoding genes are described, while therapeutic applications are also briefly presented.
A review on Anaplasma phagocytophilum as a zoonotic agent: review article
Vahid Noaman,
Volume 76, Issue 12 (3-2019)
Abstract
Anaplasma phagocytophilum is a gram-negative intracellular bacterium that transmitted by hard ticks. A. phagocytophilum infect and multiply in the organs of ticks, in particular the salivary glands which enable the transmission to vertebrate hosts during feeding. The tick becomes infected by feeding on an infected host and there is transstadial but not transovarial passage of the organism. The majority of ticks are infected with the organism in enzootic areas. There are strains of A. phagocytophilum that have biological and ecological difference, including variations in host pathogenicity, vectors and geographical distribution. The organism has an interesting feature to grow in neutrophils by stopping the antibacterial activity of neutrophils. The bacterium is able to survive in the immune host, using complex mechanisms of antigenic variation. A. phagocytophilum infects humans and various animal species including dogs, sheep, cows, horses, wild deer and rodents. The disease is known as human granulocytic anaplasmosis in humans, canine granulocytic anaplasmosis in dogs, equine granulocytic anaplasmosis in horse and tick borne fever in ruminants. Cattle tick borne fever caused by A. phagocytophilum is characterized by high fever, reduced milk yield, inclusions in circulating neutrophils, leukopenia, abortions, reduced fertility, coughing, respiratory signs and swelling of the hind limbs. Clinical signs of human occur a week after the tick bites, the disease usually presents as an acute, sometimes fatal febrile syndrome, illness characterized by headache, chills, myalgias, arthralgia, malaise, and hematological abnormalities, such as neutropenia, lymphocytopenia, thrombocytopenia, leukopenia, and elevated hepatic aminotransferase levels and may lead to death. In this review article the history, bacteriology, epidemiology, pathogenesis, diagnosis, treatment and prevention of the disease caused by A. phagocytophilum is written based on the latest scientific findings. Several hard tick species are distributed in Iran and they are the most important ectoparasites of animals. A. phagocytophilum has been detected not only in Ixodes ricinus but also in cattle and sheep of Iran using molecular techniques. However, despite the zoonotic potential of the agent, there is no evidence in the identification of A. phagocytophilum in humans, and it seems necessary to research on the prevalence and epidemiology of the disease in the human population.

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