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Abstract: Immunology is a relatively new specialty. Ironically, the immune system impacts every physiological system in the body, but yet most textbooks of physiology do not include any functional aspects of the immune system. Indeed, with the exception of early descriptions of anaphylaxis and allergy, the majority of immune studies were focused on either the anatomy of lymph nodes and spleen, or of course on protection from microorganisms. The concept of autoimmunity is even newer and the first textbook on autoimmune disease was not published until 1963. For the past 50 years however, autoimmunity has virtually exploded from a field populated by a few, to recognition that autoimmune diseases can affect more than 10% of the population. There are many people that have contributed to this information explosion and the Journal of Autoimmunity devotes specific issues in recognition of the select few scientists that have contributed in a way that impacts not only their research peers, but also, and more importantly, the patients who suffer from autoimmune disease. Abul Abbas is one such individual. Abul is known not only for his outstanding research, but for his role in teaching and public service. His own scientific work is extraordinary and his impact is felt throughout the world. In this special issue a number of Abul's colleagues have specifically written papers to honor this unique individual. It is an extraordinary honor to be chosen for a special issue of a journal in recognition of one's career. [Copyright &y& Elsevier]

In recent years, there has been an increased recognition that vitamin D is not only a risk factor for poor musculoskeletal health but also a possible important contributor in the development of different autoimmune diseases. This has been linked to multiple immunosuppressive properties of vitamin D. Vitamin D has got pleiotropic effects and this reflects the wide spread presence of vitamin D receptors (VDRs) throughout the body. Currently, there is much ongoing research with regard to its emerging role in immunopathology. VDR has not only been found in tissues involved in calcium homeostasis but also in a variety of cell lines involved primarily in immune regulation, e.g., mononuclear cells, dendritic cells, antigen-presenting cells, and activated B lymphocytes and CD4+ T cells. There have been several reports linking the presence of low vitamin D to various autoimmune diseases. However, for autoimmune/inflammatory disease outcomes, firm conclusions regarding cause and effect cannot be based on epidemiological association studies, and prospective, long-term, well-designed studies, including large intervention trials, are needed across all life stages. In this paper, we will describe the evidence base for this potential role of vitamin D in different aspects of autoimmune diseases. Because of the enormous breadth of this emerging field, our aim in this review is not to provide an exhaustive list of all literature pertinent to vitamin D and immunopathology. Instead, we will frame the reasons and rationale behind the development of several immunoregulatory activities for 1,25(OH)2D3. [ABSTRACT FROM AUTHOR]

Rheumatoid arthritis (RA) is a common autoimmune disease and a systemic inflammatory disease which is characterized by chronic joint inflammation and variable degrees of bone and cartilage erosion and hyperplasia of synovial tissues. Considering the role of autoreactive T cells (particularly Th1 and Th17 cells) in pathophysiology of RA, it might be assumed that the regulatory T cells (Tregs) will be able to control the initiation and progression of disease. The frequency, function, and properties of various subsets of Tregs including natural Tregs (nTregs), IL-10-producing type 1 Tregs (Tr1 cells), TGF-β-producing Th3 cells, CD8+ Tregs, and NKT regulatory cells have been investigated in various studies associated with RA and collagen-induced arthritis (CIA) as experimental model of this disease. In this paper, we intend to submit the comprehensive information about the immunobiology of various subsets of Tregs and their roles and function in immunopathophysiology of RA and its animal model, CIA. [ABSTRACT FROM AUTHOR]

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 solublemediators 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. [ABSTRACT FROM AUTHOR]