The etiology of several autoimmune diseases, including multiple sclerosis (MS), has still not been completely clarified. MS is defined as an autoimmune disease with clinical features of a chronic, inflammatory and demyelinating autoimmune disorder which affects the central nervous system. The course of the disease includes phases of remission and relapses which can be exacerbated in both severity and duration. Chemokines, which are a subfamily of the cytokines, act as chemoattractants for a wide variety of cells, including immune cells. CXCL10 is a small protein that is defined as an ‘inflammatory' chemokine and binds to CXCR3 to mediate immune responses through the activation and recruitment of leukocytes such as T cells, eosinophils, monocytes and NK cells. The aim of this review is to address recent findings regarding the relationship between CXCL10 and MS.

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The etiology of the most autoimmune disorders is largely yet to be understood. However, major target antigens have been determined against some of clinically important molecules of human autoimmune diseases, such as insulin in type 1 diabetes mellitus (T1DM). T1DM is believed to be resulted from immune-mediated destruction of insulin-producing β-cells in pancreatic islets of Langerhans. Chemokines are small glycoproteins (weighing 8-10 kDa) that are chemotactive for a wide variety of cell types especially immune system cells and their target cells express appropriate G protein receptors. CXCL10 is a 10-kDa protein and is functionally categorized as an "inflammatory" chemokine. Recently, accumulating reports have shown that the serum and/or the tissue expressions of CXCL10 are increased in various autoimmune diseases like T1DM. Thus, in this article we will focus on the crucial role(s) played by CXCL10 in pathogenesis of T1DM. Therefore, we tried our best to collect the current reports regarding relationship between the serum concentrations of CXCL10 in T1DM.

Several environmental and genetic factors are believed to influence the onset of diabetes and its complications. It has also been established that cytokines play a key role in the pathogenesis of type 2 diabetes. Previous studies have revealed that the polymorphism at the stromal-derived factor 1β (SDF-1β) 3'A regulates the expression of SDF-1 (CXCL12). This study was aimed to explore this polymorphism in parallel with SDF-1 serum levels in type 2 diabetic patients. In this assessment, peripheral blood samples were collected from 200 type 2 diabetic patients and 200 healthy controls. DNA was extracted, and a PCR-RFLP screening was applied to examine the SDF-1β 3'A polymorphism. We also applied the ELISA technique to measure serum levels of SDF-1. Our results showed that there were no significant correlations between SDF-1β 3'Α polymorphism in type 2 diabetic patients when compared to controls. However, our results showed that the serum levels of SDF-1 were significantly increased in the patients when compared to controls. Based on the results of this study, we concluded that SDF-1β 3'Α polymorphism does not play a role in the pathogenesis of type 2 diabetes but that elevated serum levels of SDF-1 may be important for the etiology of type 2 diabetes but are unrelated to the SDF-1β 3'Α polymorphism.

Investigations revealed substantial parts accomplished by chemokines specifically eotaxins and their specific receptors. They are functionally involved in the modulation of the pathologic state of tissue inflammation which is as a result of allergic reactions. Chemokines as small proteins with approximately 8-10 kDa molecular weight are considered and fit in the bigger family of cytokines, containing basic heparin-binding polypeptide mediators. Chemokines actively interfere in the processes of selective, oriented leukocyte (including eosinophil) recruitment. As eminent from their name, more specifically, eotaxins are specialized for eosinophils' oriented locomotion toward allergic inflamed regions. To date, three members are defined for eotaxin subfamily as follows: eotaxin-1 (CCL11), eotaxin-2 (CCL24), and eotaxin-3 (CCL26), all of them bind to and activate CCR3 but have a low level of homology and appear to exhibit different physiological potentials. Allergy is described as a clinical state in which a pathologic hypersensitivity reaction is always initiated throughout an immunologic mechanism; similar to other immunologic reactions, an allergic reaction could also either be antibody or cell mediated. This type of allergic reactions occurs in all age groups and damages several different organs, having a significant impact on the emotional and social health of patients and their families and relatives. Concerning introductory comments introduced above, the authors of the present review attempted to collect and provide the latest evidences and information regarding the correlation between expression of eotaxin family members and allergy, in a wider extent, in two important allergic disorders: atopic asthma (AA) and atopic dermatitis (AD). Overall, concerning the most recent articles published within the database in the life sciences literature regarding the fundamental role(s) played by eotaxins in the pathogenesis of AA and AD, the authors of the current article propose that eotaxins (CCL11, CCL24, and CCL26) play key role(s) during symptomatic inflammatory responses raised in response to allergic crisis of these two clinical states.

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