Multiple sclerosis (MS) is an autoimmune disease characterized by recurrent episodes of demyelination and axonal lesion mediated by CD4+ T cells with a proinflammatory Th1 and Th17 phenotype, macrophages, and soluble inflammatory mediators. Identification of Th17 cells led to breaking the dichotomy of Th1/Th2 axis in immunopathogenesis of autoimmune diseases such as MS, and its experimental model, experimental autoimmune encephalomyelitis (EAE). Th17 cells are characterized by expression of retinoic acid‐related orphan receptor (ROR)γt and signal transducer and activator of transcription 3 (STAT3) factors. Th17‐produced cytokine profile including interleukin (IL)‐17, IL‐6, IL‐21, IL‐22, IL‐23 and tumour necrosis factor (TNF)‐α, which have proinflammatory functions, suggests it as an important factor in immunopathogenesis of MS, because the main feature of MS pathophysiology is the neuroinflammatory reaction. The blood brain barrier (BBB) disruption is an early and central event in MS pathogenesis. Autoreactive Th17 cells can migrate through the BBB by the production of cytokines such as IL‐17 and IL‐22, which disrupt tight junction proteins in the central nervous system (CNS) endothelial cells. Consistent with this observation and regarding the wide range production of proinflammatory cytokines and chemokines by Th17 cells, it is expected that Th17 cell to be as a potent pathogenic factor in disease immunopathophysiology. Th17‐mediated inflammation is characterized by neutrophil recruitment into the CNS and neurons killing. However, the majority of our knowledge about the role of Th17 in MS pathogenesis is resulted in investigation into EAE animal models. In this review, we intend to focus on the newest information regarding the precise role of Th17 cells in immunopathogenesis of MS, and its animal model, EAE.

This study supports the contributing and beneficial effects of vitamins D and E in the treatment of atopic dermatitis.

Rheumatoid arthritis (RA) is a chronic inflammatory disease characterized by the sequestration of various leukocyte subpopulations within both the developing pannus and synovial space. The chronic nature of this disease results in inflammation of multiple joints, with subsequent destruction of the joint cartilage and erosion of bone. Identification of T helper (Th)17 cells led to breaking the dichotomy of the Th1/Th2 axis in immunopathogenesis of autoimmune diseases such as RA, and its experimental model, collagen-induced arthritis (CIA). Th17 cells produce cytokines, including interleukin (IL)-17, IL-6, IL-21, IL-22 and tumor necrosis factor (TNF)-a, with proinflammatory effects, which appear to have a role in immunopathogenesis of RA. Regarding the wide ranging production of pro-inflammatory cytokines and chemokines by Th17 cells, it is expected that Th17 cell could be a potent pathogenic factor in disease immunopathophysiology. Thus the identification of effector mechanisms used by Th17 cells in induction of disease lesions may open new prospects for designing a new therapeutic strategy for treatment of RA.

Rheumatoid arthritis (RA) is a chronic, autoimmune, and complex inflammatory disease leading to bone and cartilage destruction, whose cause remains obscure. Accumulation of genetic susceptibility, environmental factors, and dysregulated immune responses are necessary for mounting this self-reacting disease. Inflamed joints are infiltrated by a heterogeneous population of cellular and soluble mediators of the immune system, such as T cells, B cells, macrophages, cytokines, and prostaglandins (PGs). Prostaglandins are lipid inflammatory mediators derived from the arachidonic acid by multienzymatic reactions. They both sustain homeostatic mechanisms and mediate pathogenic processes, including the inflammatory reaction. They play both beneficial and harmful roles during inflammation, according to their site of action and the etiology of the inflammatory response. With respect to the role of PGs in inflammation, they can be effective mediators in the pathophysiology of RA. Thus the use of agonists or antagonists of PG receptors may be considered as a new therapeutic protocol in RA. In this paper, we try to elucidate the role of PGs in the immunopathology of RA.

Alzheimer's disease (AD) is a neurodegenerative disorder and leading cause of dementia, which begins with impaired memory. The neuropathological hallmarks of AD include destructive alterations of neurons by neurofibrillary tangles, neuritic amyloid plaques, and neuroinflammatory process in the brain. Chemokines have a major role in inflammatory cell attraction and glial cell activation and/or modulation in the central nervous system. Moreover, the clinical and immunopathological evidence could show dual key role of chemokines in their pro- and anti-inflammatory properties in AD. However, their effects in neurodegeneration and/or neuroprotection remain an area of investigation. This review article provides an overview of characteristic, cellular source and activity of chemokines, and their roles in neuronal glial cell interaction in AD.